Surgical Management of Lumbosacral Spinal Epidural Abscesses

Surgical Management of Lumbosacral Spinal Epidural Abscesses

Surgical Management of Lumbosacral Spinal Epidural Abscesses Carlos A. Bagley, MD, Kimberly J. Dudukovich, PA-C, Jean-Paul Wolinsky, MD, and Ziya L. G...

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Surgical Management of Lumbosacral Spinal Epidural Abscesses Carlos A. Bagley, MD, Kimberly J. Dudukovich, PA-C, Jean-Paul Wolinsky, MD, and Ziya L. Gokaslan, MD, FACS Infections involving the epidural space of the spinal canal are rare, yet potentially devastating entities. The incidence of spontaneous epidural abscesses ranges from 0.2 to 1.3 per 10,000 hospital admissions, most commonly affecting those who are immunosuppressed. The overall incidence of epidural abscesses has been found to be on the rise in recent years, due in part to the overall aging of the population, increasing medical use of potent immunosuppressants, increasing numbers of interventional procedures involving the spinal column, and increasing rates of intravenous drug abuse. The cervical spine is affected in approximately 20% of spinal epidural abscesses, and is the least commonly affected vertebral region. In this article we review the clinical presentation and surgical management of epidural abscesses involving the cervical spine. Oper Tech Neurosurg 7:206-211 © 2005 Elsevier Inc. All rights reserved. KEYWORDS epidural abscess, cervical spine, surgical management

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nfections involving the epidural space of the spinal canal are rare yet potentially devastating entities. The incidence of spontaneous epidural abscesses ranges from 0.2 to 1.3 per 10,000 hospital admissions.1-4 This problem typically affects those who are immunosuppressed, either related to a disease process (ie, HIV) or iatrogenically (ie, transplant recipients). Other risk factors include intravenous drug abuse, diabetes mellitus, corticosteroid use, trauma, advanced age, and rheumatologic or immunologic diseases.5-8 Men are affected almost twice as often as women.9 Some authors have also found morbid obesity to be a risk factor.10 In recent years the incidence of epidural abscesses has been increasing. The increase reflects the overall aging of the population, increasing medical use of potent immunosuppressants, increasing numbers of interventional procedures involving the spinal column, and increasing rates of intravenous drug abuse. Furthermore, advances in radiographic techniques (ie, magnetic resonance imaging [MRI]) have improved the recognition and diagnosis of this clinical entity.1,11,12 The lumbar spine is the second most commonly affected vertebral region. In a recent meta-analysis of the literature, about 30% of epidural abscesses occurred in the lumbar spine.13 Other authors report lumbar spine involvement in about 48% of all cases, compared with 21% and 31% for the Department of Neurosurgery, Johns Hopkins Hospital, Baltimore, MD. Address reprint requests to Ziya L. Gokaslan, MD, FACS, Department of Neurosurgery, Meyer Building 7-109, Johns Hopkins Hospital, 600 North Wolfe Street, Baltimore, MD 21287-7713; [email protected].

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1092-440X/04/$-see front matter © 2005 Elsevier Inc. All rights reserved. doi:10.1053/j.otns.2005.06.006

cervical and thoracic regions, respectively.14 This preference for the lumbar spine may result from the larger size of the spinal canal in this region in addition to the well-developed epidural venous plexus in this area. The causative organisms for spinal infections can be classified as pyogenic or granulomatous, based on the host immune response.4 Pyogenic organisms are the most common; Staphylococcus aureus is the isolate in 60% of cases.4,15,16 Gram-negative infections by organisms such as Escherichia coli also may occur and tend to be found in immunocompromised patients.4,17 Granulomatous infections occur with either Mycobacterium species or fungi. Mycobacterium species are typically caused by M. tuberculosis; coccidiomycosis, blastomycosis, histoplasmosis, and Cryptococcus spinal fungal infections have also been described.4,18

Diagnosis The clinical findings in cases of spinal epidural abscesses vary from moderate back pain and fever to severe neurologic deficits. Despite advances in treatment, many patients are left with residual neurologic deficits. The progression of symptoms tends to be insidious, often delaying the diagnosis of the infection. Patients left untreated may progress from back ache to nerve root pain in 3 days, to radicular weakness in 4 to 5 days, and finally to paralysis in 24 hours.19,20 This progression of symptoms may be related to direct spinal cord compression from the epidural compression as well as spinal vein thrombophlebitis and spinal cord infarction.21 The duration of symptoms in cases of epidural abscesses

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Figure 1 (A) T1-weighted contrast enhanced and (B) T2-weighted lumbosacral MRI show an epidural abscess collection associated with severe discitis/osteomylitis at the disk space between L2 and L3.

ranges from 2 days to 6 months.4 Patients harboring spinal infections often become symptomatic with nonspecific complaints. Focal back pain, fever, radicular pain and weakness are common presenting symptoms. However, as many as half of all patients found to have an epidural abscess do not have a history of recent fevers.22,23 Laboratory values such as serum C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are often elevated in cases of epidural abscess.4 The ESR is almost always elevated, and the CRP has been found to be universally elevated in the presence of an infection.4,23-25 These values are nonspecific for spinal infections but quite useful in monitoring the response to therapy. MRI is the radiographic modality of choice for the diagnosis of spinal epidural abscesses (Fig. 1). The advantages offered include the abilities to evaluate the disk and soft tissue structures noninvasively, and to assess the entire neuroaxis rapidly to determine the full extent of the abscess collection. When MRI is unavailable or contraindicated, computed tomography (CT) myelography can be used to aid in the diagnosis of spinal epidural infections. They appear as an extradural compressive mass with or without a myelographic block. It is often necessary to perform injections both above and below the lesion to determine the extent of epidural compression. CT myelography, however, is invasive and associated with the risk of iatrogenic seeding of the subarach-

noid space if the myelographic needle passes through a dorsally situated collection before entering the thecal sac.

Surgical Indications Most spinal epidural abscesses can be managed effectively with intravenous antibiotics alone. Multilevel disease and multiple underlying medical conditions that preclude general anesthesia are additional reasons to consider nonoperative management. Numerous reports of cases and series have shown that these lesions can be adequately managed nonoperatively in the absence of neurologic deficits or spinal instability, and when the offending organism has been identified by other means (ie, blood cultures).7,12,26 Furthermore, the advances in imaging and antibiotic therapy have greatly increased efficacy of conservative management and decreased the associated morbidity. Nonetheless, when there is neurologic deficit, lack of response to an appropriate course of antibiotics, or evidence of spinal instability, surgical intervention is warranted to decompress the neural elements, to stabilize the spinal column, and to obtain additional cultures. Three general principles must be applied when any infection that involves the lumbosacral spinal column or epidural space is treated surgically. First, the infected tissue must be debrided thoroughly to decrease the bacterial load. Second, the affected area must be provided with an adequate blood

208 supply to allow the wound to heal adequately and the patient’s immune system to fight the infection. Finally, spinal stability should be maintained or restored by the surgical approach taken. This is especially relevant in cases of extensive disease over multiple levels requiring extensive laminectomies, or when there is significant anterior column destruction from an associated osteomyelitis or discitis. The optimal method for the surgical treatment of lumbosacral spinal epidural abscesses remains controversial. In cases of postoperative abscesses, adequate drainage can often be obtained through the surgical wound. Traditionally, surgical intervention has involved multilevel laminectomies with or without fusion of the involved segments. When a ventral abscess collection is extensive or when the anterior spinal column is significantly involved with the infectious process, the pathology may need to be addressed more directly to adequately restore stability of the spinal column and to decompress the neural elements. Destruction of the vertebral body and disk space in the setting of osteomyelitis or diskitis also may necessitate an anterior approach, possibly involving a corpectomy with reconstruction of the anterior column. Surgical decompression affords the advantage of being able to obtain a sample for Gram stain and culture. The lack of an appropriate response to an adequate course of empiric or presumed specific antibiotics may be the sole indication for surgery. Surgical techniques range from anterior debridement and interbody fusion, posterior debridement and internal fixation, and a single- or two-staged anterior decompression and debridement followed by posterior instrumentation. The approach selected should address the site of the most significant pathology as well as any spinal instability from the infectious process itself or iatrogenically from the surgical intervention. Most lumbosacral epidural abscesses occur posterior to the thecal sac and are optimally approached dorsally.1 Posterior decompression is mainly reserved for cases with isolated posterior involvement, little to no anterior column or ventral canal involvement, or liquefied abscesses. The typical posterior approach involves either a limited laminotomy or a more extensive laminectomy over the affected levels. Care must be taken to avoid destabilizing the spine by overaggressively resecting the pars interarticularis or disrupting the facet joints. Abscesses mainly composed of purulent liquid material also may be decompressed effectively through a limited laminotomy. Epidural collections composed of mainly thick, granulation tissue, however, require more extensive bony removal with complete laminectomies of the affected levels. When an extensive anterior reconstruction is required or the quality of the bone of the anterior column is poor, posterior instrumentation may be warranted to supplement segmental stabilization. Anterior debridement without instrumentation followed by delayed posterior stabilization has also been used successfully.27,28 An increasing number of lumbosacral epidural abscesses occur anteriorly, with associated discitis or osteomyelitis, and are therefore optimally approached ventrally.14,19 Several authors have reported cases of neurologic deterioration after decompressive laminectomy in patients with anterior spinal infections.3,29,30 Lumbosacral abscesses may develop as an extension of a psoas or other paravertebral abscess. The approach taken should consider any soft tissue abscess compo-

C.A. Bagley et al. nents so that both can be debrided during the same approach. The imaging characteristics of the epidural collection also must be considered when planning an anterior lumbosacral approach. Purulent, liquid material may be decompressed through a smaller approach than a more chronic, granulomatous collection. Several anterior surgical approaches have been described to access pathology in this region. A thoracic thoracotomy at about the level of the tenth rib may be used for ventral exposures of the upper lumbar vertebrae. A transabdominal or a retroperitoneal approach may be used to expose the lower ventral lumbosacral spine. All surgical approaches involve wide debridement of the necrotic, infected tissue followed by reconstruction of the spinal column. When a significant component of osteomyelitis is present, multilevel corpectomy is warranted to remove the infected nidus. The bone should be debrided back to normal, healthy-looking bone to ensure adequate debridement and sufficient strength of the remaining vertebrae for anterior spinal column support. This strategy allows extensive neural decompression, which may improve outcomes in patients with severe neurologic deficits.31 Great familiarity with the visceral and vascular anatomy anterior to the lumbosacral region is a necessity for any ventral approach to this region. The abdominal aorta and the inferior vena cava typically bifurcate between the vertebral body of L4 and the disk space between L5 and S1. Several presacral vessels that arise in the region of the bifurcation may need to be identified and ligated in an anterior exposure of the lower lumbosacral spine. Mobilizing the vascular structures that lie anterior to the spinal column may be formidable in the setting of infection. The presence of an infection also may make the vessel walls extremely friable, thereby increasing the risk of injury. Additional neural structures of concern in this region include the hypogastric nerves and plexi, which lie ventrolateral to the vertebral column and sympathetic trunk. Injury to these autonomic nerves may cause impotence or retrograde ejaculation. The upper lumbar spine may be approached via a transthoracic approach at the level of the tenth rib. Lesions involving the first or second lumbar vertebra may require removal of the lateral attachment of the diaphragm to gain adequate exposure. The iliopsoas muscle may need to be mobilized to obtain a complete exposure. During this initial exposure, abscesses of the psoas can be drained concurrently. Copious irrigation of the wound with antibiotic irrigation is imperative for cases of spinal infections. When generous debridement of the infected tissue is possible, the wound may be closed primarily with temporary suction drains left in place. When this approach is not possible, packing the wound open should be considered. Packing the wound, however, prolongs hospitalization and increases patient discomfort. Typically, this maneuver is unnecessary and a primary closure may be performed. Recently, the popularity of minimally invasive approaches to the management of epidural abscess has increased with improvements in imaging techniques, optics, and surgical instruments. Techniques using a limited laminectomy or laminotomy followed by insertion of a silicon catheter or a Foley embolectomy catheter have been used successfully.14,32 Percutaneous, CT-guided aspiration of a posteriorly situated thoracolumbar epidural abscess has been described.33 Video-

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assisted, endoscopic aspiration through a key-hole laminotomy has been used successfully to decompress a liquefied abscess.34 In these cases, the patients were either too ill to tolerate an extensive surgical procedure or had such extensive disease that direct decompression would have dramatically destabilized the spinal column, warranting a multilevel fusion procedure. By limiting the extent of bony removal, the risk of developing subsequent instability is theoretically minimized. Furthermore, the limited exposure required and the low blood loss can allow systemically ill patients to tolerate surgical decompression. Limitations of these techniques include patients with severe spinal canal stenosis and abscesses mainly composed of chronic, granular tissue. Percutaneous, needle aspiration techniques are associated with the added risk of unintentionally introducing the infectious material into the thecal sac.

Instrumentation in the Setting of infection Traditional dictum teaches that an active spinal infection is a contraindication to implantation of spinal instrumentation and the use of allograft material. Intuitively, the exposure of the instrumentation results in impregnation of its surface with bacteria and thus increases the risk of persistent or recurrent infections. In vitro studies, however, demonstrate that bacteria do not easily adhere to the metal. In vivo, a glycocalyx biofilm forms on the surface of the hardware after the initial inflammatory reaction. This film establishes a means by which bacteria might adhere to the surface of these devices and continue to pose a clinical problem.35 Clinical studies, however, indicate that with adequate debridement of the infectious nidus and an appropriate course of bacteriospecific antibiotics, the complication rate is acceptably low. A growing body of literature suggests that allograft and titanium instrumentation may be used safely in the setting of an active infection and may, in fact, improve patient outcomes. Several authors have reported that autograft or allograft used with spinal instrumentation and followed by a prolonged postoperative course of bacteriospecific antibiotics has been associated with no deleterious effects in select patients.3,5,36-39 Severe cases of osteomyelitis or discitis of the lumbosacral spine associated with an epidural abscess may require aggressive debridement and the use of interbody grafting. In this setting the use of autologous bone graft has been rather routine since its application in the presence of an active infection was first described by Wiltberger in 1952.40 Autograft options include iliac crest, fibular autograft, and vascularized rib, all of which have been used with excellent success rates.3,38,41,42 The postoperative reinfection and complication rates are comparable to those cases associated with the use of autograft struts. Recently, the popularity of titanium cages as a means to reconstruct the anterior column has increased. With the newly developed distractable cages, the ability to restore sagittal alignment and achieve satisfactory fusion rates has improved significantly, even in the presence of spinal infections (Fig. 2).38,43,44 The incidence of graft dislodgement and subsidence is also less with the use of these rigid devices when compared with the use of auto- or allograft materials.44 The use of cage devices and allograft avoids the potential donorsite morbidity associated with allograft harvesting.

Figure 2 Sagittally reconstructed postoperative CT scan of a patient who failed medical management of an epidural abscess associated with spondylodiscitis. The patient underwent a staged anterior reconstruction with an expandable titanium cage and lateral plate followed by posterior multisegmental fixation and fusion with pedicle screws and autologous and local bone graft.

Surgical Outcomes The natural history of untreated epidural abscesses of the lumbosacral spine is that of continued progression and possible death. In the preantibiotic era, the mortality rate was as high as 70%.45 Advances in antimicrobial and surgical therapies have significantly reduced this rate. In the contemporary era, most appropriately treated patients (more than 78%) will recover fully or with minimal weakness.45 The duration of paresis and the rapidity of progression of symp-

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210 toms, however, affect the outcome of lumbosacral epidural abscesses, underscoring the need for prompt diagnosis and treatment. Six main factors affect the outcome of patients with spinal epidural abscesses: the duration of the patient’s symptoms, age, degree of thecal sac compression, abscess location, sepsis presentation, and surgical findings.5,46 Younger patients tend to have better outcomes than elder patients, presumably because their overall health status is better and because they lack significant comorbidities such as diabetes mellitus. The single most significant prognostic factor in favorable postoperative outcomes is preoperative motor function. Patients with more severe deficits at surgery tend to have the worst neurologic outcomes. The timing of surgical intervention to relieve compression caused by an epidural abscess is critical. Many studies have demonstrated that there is an about a 24-hour window when surgical intervention can be expected to reverse severe neurologic deficits. Few patients with paralysis longer than 36 hours experience meaningful neurologic recovery.12,19,23,31 Other authors, however, have found that some patients do recover significant function when decompressed as long as 72 hours after the onset of symptoms.5 Several authors have attempted to determine which radiographic criteria may be associated with an increased risk of neurologic deterioration. Patients with a spinal epidural abscess that causes severe spinal cord compression, defined as at least 50% spinal canal compromise on radiographic imaging, had a 50% to 70% chance of a poor outcome.5,47 Abscesses longer than 3 cm have been found to correlate with lack of complete motor recovery.47 Tung and co-workers retrospectively analyzed a group of patients with spinal epidural abscesses to develop a three-point grading system to identify which patients were most at risk for poor neurologic outcomes. The enhancement pattern of the epidural inflammatory tissue (homogeneous or peripherally enhancing), severity of spinal canal narrowing (greater or less than 50%), and length of the abscess (greater or less than 3 cm) were assigned one or zero points based on their presence or absence, respectively. Patients with scores of 0 or 1 had excellent outcomes (no weakness, ambulating independently, and complete recovery of premorbid function), whereas all those with a score of 3 had poor outcomes. Satisfactory outcomes were achieved in only 50% of patients with a score of 2.47 In general, the prognosis for patients with lumbosacral abscesses is superior to those with cervical or thoracic lesions. This outcome partially reflects the increased size of the spinal canal at this level. Furthermore, the compression is on the cauda equina or nerve roots rather than on the spinal cord.5 Neurologic dysfunction may result from direct neural compression in addition to the epidural mass causing “venous compression and thrombosis, thrombophlebitis, and ischemic myelitis” resulting in spinal cord infarction at the level of the conus medularis.19 At follow-up, only about 27% of patients with lumbosacral abscesses will have residual limb weakness, compared to more than 42% of patients with cervical or thoracic lesions.47 Despite the advances in the management and diagnosis of spinal epidural abscesses, the mortality rate associated with this condition is 10% to 14%.6,46 Overall, the rate of poor outcomes is 18% to 63% in surgically managed patients.5,48

These high rates largely reflect the delay in the initiation of therapy. This fact underscores the need for prompt recognition and treatment, especially in patients with predisposing risk factors.

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Managing lumbosacral spinal epidural abscesses 24. Baldwin N, Scott AR, Heller SR, O’Donoghue D, Tattersall RB: Vertebral and paravertebral sepsis in diabetes: An easily missed cause of backache. Diabet Med 2:395-397, 1985 25. Carragee EJ, Kim D, van der Vlugt T, Vittum D: The clinical use of erythrocyte sedimentation rate in pyogenic vertebral osteomyelitis. Spine 22:2089-2093, 1997 26. Akalan N, Ozgen T: Infection as a cause of spinal cord compression: A review of 36 spinal epidural abscess cases. Acta Neurochir (Wien) 142:17-23, 2000 27. Dimar JR, Carreon LY, Glassman SD, Campbell MJ, Hartman MJ, Johnson JR: Treatment of pyogenic vertebral osteomyelitis with anterior debridement and fusion followed by delayed posterior spinal fusion. Spine 29:326-332, 2004 28. Fukuta S, Miyamoto K, Masuda T, et al: Two-stage (posterior and anterior) surgical treatment using posterior instrumentation for pyogenic and tuberculotic spondylitis. Spine 28:E302-E308, 2003 29. Abramovitz JN, Batson RA, Yablon JS: Vertebral osteomyelitis. The surgical management of neurologic complications. Spine 11:418-420, 1986 30. Arnold PM, Baek PN, Bernardi RJ, Luck EA, Larson SJ: Surgical management of nontuberculous thoracic and lumbar vertebral osteomyelitis: Report of 33 cases. Surg Neurol 47:551-561, 1997 31. Young WF, Weaver M, Snyder B, Narayan R: Reversal of tetraplegia in patients with cervical osteomyelitis— epidural abscess using anterior debridement and fusion. Spinal Cord 39:538-540, 2001 32. Schultz KD Jr, Comey CH, Haid RW Jr: Technical note. Pyogenic spinal epidural abscess: A minimally invasive technique for multisegmental decompression. J Spinal Disord 14:546-549, 2001 33. Louw JA: Spinal tuberculosis with neurological deficit. Treatment with anterior vascularised rib grafts, posterior osteotomies and fusion. J Bone Joint Surg Br 72:686-693, 1990 34. Roselli R, Iacoangeli M, Pompucci A, et al: Anterior cervical epidural abscess treated by endoscopy-assisted minimally invasive microsurgery via posterior approach. Minim Invasive Neurosurg 41:161-165, 1998

211 35. Naderi S, Acar F, Mertol T: Is spinal instrumentation a risk factor for late-onset infection in cases of distant infection or surgery? Case report. Neurosurg Focus 15:E15, 2003 36. Acosta FL Jr, Chin CT, Quinones-Hinojosa A, Ames CP, Weinstein PR, Chou D: Diagnosis and management of adult pyogenic osteomyelitis of the cervical spine. Neurosurg Focus 17:E2, 2004 37. Dietze DD Jr, Fessler RG, Jacob RP: Primary reconstruction for spinal infections. J Neurosurg 86:981-989, 1997 38. Khanna RK, Malik GM, Rock JP, Rosenblum ML: Spinal epidural abscess: Evaluation of factors influencing outcome. Neurosurgery 39: 958-964, 1996 39. Ogden AT, Kaiser MG: Single-stage debridement and instrumentation for pyogenic spinal infections. Neurosurg Focus 17:E5, 2004 40. Wiltberger BR: Resection of vertebral bodies and bone-grafting for chronic osteomyelitis of the spine. Spine 1:33-43, 1976 41. Bradford DS: Instrumentation of the lumbar spine. An overview. Clin Orthop Relat Res 203:209-218, 1986 42. Liljenqvist U, Lerner T, Bullmann V, Hackenberg L, Halm H, Winkelmann W: Titanium cages in the surgical treatment of severe vertebral osteomyelitis. Eur Spine J 12:606-612, 2003 43. Hee HT, Majd ME, Holt RT, Pienkowski D: Better treatment of vertebral osteomyelitis using posterior stabilization and titanium mesh cages. J Spinal Disord Tech 15:149-156, 2002 44. Lee MC, Wang MY, Fessler RG, Liauw J, Kim DH: Instrumentation in patients with spinal infection. Neurosurg Focus 17:E7, 2004 45. Currier BL, Kim CW, Heller JG, Eismont FJ: Cervical spinal infections, in Clark CR (ed): The Cervical Spine. Baltimore: Lippincott Williams and Wilkins, 2005, pp 858-890 46. Bluman EM, Palumbo MA, Lucas PR: Spinal epidural abscess in adults. J Am Acad Orthop Surg 12:155-163, 2004 47. Tung GA, Yim JW, Mermel LA, Philip L, Rogg JM: Spinal epidural abscess: Correlation between MRI findings and outcome. Neuroradiology 41:904-909, 1999 48. Baker AS, Ojemann RG, Swartz MN, Richardson EP Jr: Spinal epidural abscess. N Engl J Med293:463-468, 1975