The Journal of The American Paraplegia Society

ISSN: 0195-2307 (Print) (Online) Journal homepage: http://www.tandfonline.com/loi/yscm19

Spinal Epidural Abscess Complicating Vertebral Osteomyelitis: An Insidious Cause of Deteriorating Spinal Cord Function Hang J. Lee , John R. Bach & Robert E. White To cite this article: Hang J. Lee , John R. Bach & Robert E. White (1992) Spinal Epidural Abscess Complicating Vertebral Osteomyelitis: An Insidious Cause of Deteriorating Spinal Cord Function, The Journal of The American Paraplegia Society, 15:1, 19-21, DOI: 10.1080/01952307.1992.11735858 To link to this article: https://doi.org/10.1080/01952307.1992.11735858

Published online: 02 Jun 2016.

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SPINAL EPIDURAL ABSCESS COMPLICATING VERTEBRAL OSTEOMYELITIS: AN INSIDIOUS CAUSE OF DETERIORATING SPINAL CORD FUNCTION 1

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Hang J. Lee, M.D.; John R. Bach, M.D.; 3 Robert E. White, M.D.

ABSTRACT Spinal epidural abscess may complicate vertebral osteomyelitis. The purpose of this report is to discuss its course in two patients with sensory/motor and cognitive impairment and to demonstrate the need for its early detection. Delayed detection may lead to spinal cord injury or meningitis. It may also delay functional return and hinder intensive rehabilitation efforts. Two patients are presented. (} Amer Paraplegia Society 7992;7'5:79-21)

KEY WORDS: spinal epidural abscess, vertebral osteomyelitis, spinal cord injury, brain injury INTRODUCTION

Vertebral osteomyelitis is uncommon but may occur in at-risk populations, especially in the young and in the elderly.1,2,3 Vertebral osteomyelitis most often occurs from a hematogenous source. Unequivocal primary sources include, in order of frequency, the genitourinary tract, the skin, and the respiratory tract. 2 Vertebrae with cellular marrow and an abundant vascular supply are most often affected. 4 Pyogenic VO frequently involves two adjacent bony plates and the corresponding intervertebral disc. Extension can occur longitudinally to other vertebrae, anteriorly as a paras pinal abscess, or posteriorly. The latter can result in serious complications including spinal epidural abscess and possible spinal cord injury or meningitis. 2 Spinal epidural abscesses have been reported in 5 to 18% of patients with vertebral osteomyelitis5 and Baker1 found that vertebral osteomyelitis was present in 38% of patients with spinal epidural abscesses. The most common location for a spinal epidural abscess is in thoracic or lumbar areas with the cervical region being the least common site.l,3,6 Although the usual initial manifestations are back pain, localized tender.~----

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1 Assistant Professor of Clinical Physical Medicine and Rehabilitation, Department of Physical Medicine and Rehabilitation, The New Jersey Medical School-UMDNJ, Newark, NJ. 2 Associate Professor of Physical Medicine and Rehabilitation, The New Jersey Medical School-UMDNJ, Newark, NJ3 Assistant Professor of Physical Medicine and Rehabilitation, The New Jersey Medical School-UMDNJ, Newark, NJ_ This work was performed on patients referred to University Hospital, Newark,NJ Address correspondence to: Hang J. Lee, M.D. Department of Rehabilitation Medicine University Hospital B-239 The New Jersey Medical School - UMDNJ 150 Bergen Street Newark, NJ 07103

ness/spasm, and low grade fever1,2,4,6-8 symptoms may develop insidiously and be difficult to interpret. This is particularly true in the presence of significant sensory/motor or cognitive impairment such as occurs in patients with spinal cord or traumatic head injury.9 Patients with spinal cord injury may thus develop extensive spinal epidural abscesses below the initial level of spinal cord injury. 8 We report two cases of vertebral osteomyelitis which resulted in spinal epidural abscesses during the acute rehabilitation process. CASE STUDIES

CASE 1: A 67 -year-old male was involved in a motor vehicle accident in September 1990. After two weeks of acute care he was ttansferred to a rehabilitation facility with the diagnosis of C5 partial quadriplegia. The patient's condition improved during the first two weeks of rehabilitation; then lower extremity function decreased and significant bilateral lower extremity weakness was noted. He was rehospitalized at which time magnetic resonance imaging (MRI) of the lumbar spine demonstrated a posterior lesion with compression of the cord at T9 and T10. The lesion extended inferiorly to the level of L1 and L2 (Figure 1) and a tentative diagnosis of spinal epidural abscess was made. There was also evidence of a possible fracture of the L1 vertebral body. Surgical exploration confirmed the diagnosis of spinal epidural abscess and the patient underwent multiple thoracic decompressive laminectomies. Culture of the abscess yielded Escherichia coli sensitive to ceftriaxone which the patient then received intravenously for 6 weeks. The erythrocyte sedimentation rate (ESR) decreased from Submitted for publication, April16, 1991; accepted in revised form July 1,1991.

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Fig 1. Figure 1. An MRI following surgical drainage of a spinal epidural abscess demonstrates small amount of air accumulation in the epidural space at the level of T11 to L 1 and wedging of the L1 vertebral body.

140 to 35 mm per hour by the end of the 6-week course. The patient remained afebrile. Repeated cultures of drainage from the surgical site were negative for bacterial growth. During the hospital stay, the patient received physical and occupational therapy. His tipper and lower extremity strength improved to fair range throughout. During the fifth week of hospitalization he was placed in a lumbosacral support body jacket for sitting. He tolerated this well for short periods of time and was returned to a regional rehabilitation center for continuation of the rehabilitation process. CASE 2: A 30-year-old Asian male sustained traumatic brain injury and bilateral acetabular fractures in a high speed motor vehicle accident in January 1990. Radiographs of the cervical spine and computerized tomography (CT) of the skull and the spine from upper cervical levels to L3 were read as normal. A CT scan of the head without contrast was also normal; however, severe brain injury was manifested by extensor posturing. The patient was able to move all four extremities spontaneously but was unable to follow commands or communicate. Diffuse axonal injury was diagnosed in view of his negative CT scans and general unresponsiveness. A small serosal tear of the bladder was diagnosed by cystogram and treated by Foley catheter drainage. The acetabular fractures were repaired by open reduction and internal fixation. His rehabilitation program included physical, cognitive and linguistic therapy. He developed improved

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Fig 2. An MRI of the cervical spine demonstrating an epidural inflammatory process with osteomyelitis of C5 and C6.

physical and cognitive function until 6 weeks after admission when he developed gradual quadriparesis. Neurological examination at this time revealed decreased sensation to pinprick below C7 on the right and below C6 on the left. On manual muscle testing the strength of the deltoid was ~5, biceps ~5, triceps 2/5, and 0-1/5 in wrist flexors and hand intrinsics. The muscle strength in both lower extremities was 0/5. An MRI disclosed vertebral osteomyelitis with destruction and collapse of C5/C6 and a spinal epidural abscess from C4 to C7 compressing the cord anteriorly (Figure 2). Operative decompression, debridement and spinal fusion with halo stabilization was urgently performed. Staphylococcus aureus was isolated from the spinal epidural abscess and treated with 6 weeks of intravenous nafcillin. No further progression of his neurological deficit was noted and he began to improve. He underwent comprehensive rehabilitation during the next several months and improved to the point of being able to ambulate independently indoors with a walker and to independently perform most activities of daily living. He is now able to read his engineering texts and he hopes to return to work within a year. DISCUSSION Ambrose et aF found that because early symptoms and signs were minimal, an average of 4 months elapsed from the onset of vertebral osteomyelitis to establishment of the diagnosis. The definitive diagnosis of vertebral osteomyelitis and spinal epidural abscess

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requires isolation of the etiological organism. This requires needle aspiration of the intervertebral disc space, percutaneous needle biopsy of the infected bone, or open bone biopsy during surgery for drainage of the abscess. 4·6·10 Blood cultures are usually negative.6,7 Leukocytoses is usually absent but the erythrocyte sedimentation rate is almost always increased. 6·7 Although many types of microorganisms including viruses and fungi may cause vertebral osteomyelitis, its etiology is usually bacteriaP.4,6,1l The most common etiologic agent is Staphylococcus aureus, followed by streptococci and gram negative bacilli.l,2,4 While x-ray changes may not develop for several weeks following vertebral infection, radionuclide scans with technetium pyrophosphate are positive early. 6 The first x-ray changes appear after 2 to 8 weeks. These changes are characterized by soft tissue swelling, piecemeal destruction of vertebral plateau bone, and narrowing of the disc space. 2 Routine radiographs and tomograms are helpful in distinguishing between bone destruction associated with metastases and the changes of osteomyelitis. Metastases destroy bone, but the cortical endplates and disk spaces are generally preserved. Vertebral osteomyelitis involves the disk space and adjacent endplates and gives rise to characteristic changes in MRI studies. An MRI, therefore, is the examination of choice for diagnosing discitis, osteomyelitis and spinal epidural abscess.l2 Major considerations in the differential diagnosis are meningitis, spinal subdural abscess, acute transverse myelopathy, intervertebral disc abnormalities, vascular lesions, and spinal cord tumors. 1 Heusner 13 described the progression of the clinical picture of a spinal epidural abscess in four phases: spinal ache, root pain, weakness, and paralysis. Vertebral osteomyelitis can also lead to the development of kyphosis due to destruction of disc and adjacent vertebral bodies.l4 Vertebral osteomyelitis can be treated by antibiotics without surgery; however, the required duration of treatment has not been clearly defined. Six weeks of parenteral antibiotics has led to relapse in only one of 20 cases. 2 At least 4 to 6 weeks of parenteral antibiotic treatment are needed and bed rest should be continued until resolution ofthe spinal pain and reduction of ESR indicate clearing of the infection.6,14 Indications for surgical debridement and bone grafting are extensive destruction of the vertebral bodies with sequestra and abscess formation, signs of cord compression, and, possibly, recurrence ofthe disease. 2

for most patients with thoracic or lumbar osteomyelitis. Once the infection is inactive, the patient can ambulate with orthoses until X-ray show bony fusion_l4 CONCLUSION Diagnosis of vertebral osteomyelitis and spinal epidural abscess is often difficult in patients with spinal cord injury or traumatic brain injury because of its particularly insidious development in patients with impaired sensory or cognitive functions. Therefore, it is essential to be aware of these potentially devastating conditions in order to interpret correctly, and in a timely manner, their subtle symptoms and signs to limit their untoward consequences on subsequent rehabilitation. REFERENCES 1. Baker AS, Ojemann RG, Swartz MN, Richardson EP. Spinal epidural abscess. N Eng! J Med 1975;293:463-468. 2. Waldvogel FA, Vasey H. Osteomyelitis: the past decade. N Eng! J Med 1980;303:360-370. 3. Silvani V, Brambilla G, Rainoldi F, Gaetani P, Denaro V. Vertebral osteomyelitis with chronic cervical extradural abscess in a heroin addict. Neurochirugia 1987;30:91-94. 4. Poletti CE, Hesselink ,JH, Richardson EP, Shahani BT. Case record. N Eng! J Med 1982;306:729-737. 5. Sapico FL, Montmerie J. Pyogenic vertebral osteomyelitis: report of nine cases and review of the literature. Rev Infec Dis 1976;1:754-776. 6. Hirschmann JV. Osteomyelitis. In: Braunwald E, et a!, eds. Harrison's principles of internal medicine. New York: McGraw Hilll987:1910-12. 7. Ambrose GB, Alpert M, Neer CS. Vertebral osteomyelitis. A diagnostic problem. JAMA 1966;197:619622. 8. Malik GM, Sapico FL, Montgomerie JZ. Severe vertebral osteomyelitis in patients with spinal cord injury. Arch Intern Med 1982;142:807-808. 9. Musher DM, Thorsteinsson SB, Minuth JN, Luchi RJ. Vertebral osteomyelitis. Still a diagnostic pitfall. Arch Intern Med 1976;136:106-110. 10. Sugarman B. Osteomyelitis in spinal cord injury. Arch Phys Med Rehabil 1984;65:132-134. 11. Aad I, Bay JW, Peterson JM. Nocardia! osteomyelitis of the spine with epidural spinal cord compression: a case report. Neurosurg 1984; 15:254-256. 12. Hyman RA, Gorey MT. Imaging strategies for MR of the spine. Radiologic Clinics of North America 1988;26:505529. 13. Heusner AP. Non tuberculous spinal epidural infection. N Engl J Med 1948;239:845-854. 14. Abramovitz JN, Batson RA, Yablon JS. Vertebral osteomyelitis: the surgical management of neurologic complications. Spine 1985;9:418-420.

External stabilization by traction or brace is indicated for an unstable cervical spine but is unnecessary

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Spinal epidural abscess complicating vertebral osteomyelitis: an insidious cause of deteriorating spinal cord function.

Spinal epidural abscess may complicate vertebral osteomyelitis. The purpose of this report is to discuss its course in two patients with sensory/motor...
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