ACUTE SPINAL EPIDURAL ABSCES Walter R. Slade, Jr, MD, and Frank Lonano, RPA Brooklyn, New York
Acute spinal epidural abscess is an uncommon disease. Recommended management has been mainly surgical. We recently treated three cases within 4 weeks. Lowered immune resistance played a role in two of the cases. We suggest that acquired immunodeficiency syndrome will increase the incidence of this uncommon entity and advise that acute spinal epidural abscess can be successfully treated by nonsurgical means in some cases. Key words * spinal epidural abscess * abscess Acute spinal epidural abscess is uncommon, with an estimated incidence of between 1 in 100 000 and 1 in 400 000.1-3 With few exceptions, recommended treatment has been surgical.4-6 However, the dictum "once the diagnosis is established, laminectomy is imperative" needs to be evaluated in relation to other therapeutic tools. In 1762, Morgagni7 described a case of epidural abscess without vertebral involvement. Almost 200 years later, in 1941, Browder and others8 were able to find slightly more than 200 cases in the literature. More recently, several isolated cases have been reported.9-12 This increasing frequency may reflect a relationship between acute spinal epidural abscess and acquired immunodeficiency syndrome or just increased awareness. From the Neurology Service, Brooklyn, VAMC, Department of Neurology, SUNY, and the Health Science Center of Brooklyn, New York. Requests for reprints should be addressed to Dr Walter R. Slade, Jr, Chief, Neurology Service (127), VA Medical Center, Brooklyn, NY 11209. JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 82, NO. 10
We report three cases of acute spinal epidural abscess, suggest possible reasons for increasing incidence, and question laminectomy as primary therapy.
CASE REPORTS Case 1 A 67-year-old man was admitted with neck pain radiating into the fingers, accompanied by weakness of both hands and the right lower extremity. He had been admitted previously for a generalized seizure, fever, chills, and neck pain and was discharged 5 days later on oral cephradine. He was admitted to another hospital with hand paresthesias and neck pain. After an extensive evaluation (spine radiographs, complete blood count, lumbar puncture, and blood, spinal fluid, and urine cultures), Escherichia coli were isolated from his urinary tract and he was treated with trimethoprim/sulfamethoxazole. Nine days after discharge he was admitted to neurology because radiographs revealed pathology of C-6 and C-7 vertebrae. Examination revealed localized neck pain increasing on movement, marked right upper extremity weakness, decreased pinprick sensation in the right upper extremity, and sensory impairment below the umbilicus. Computerized tomography of the cervical spine revealed end plate destruction of C-6 and C-7, with evidence of an adjacent anterior paraspinal soft tissue mass (Figure 1). Myelography revealed a complete block at C-6 level, with the mass extending to T-1 (Figure 2). A laminectomy with abscess drainage was performed. After a difficult postoperative course on antibiotics, the patient improved and began physiotherapy. He was discharged on December 28, 1987, without neurologic deficit. To date he is asymptomatic and neurologically normal. 713
ACUTE SPINAL EPIDURAL ABSCESS
Figure 2. Myelography showing complete block.
Figure 1. X-ray of cervical spine. Case 2 A 22-year old male intravenous drug user was admitted with excruciating lower back pain, urinary frequency, and constipation duning the week prior to admission. Examination revealed a 3/4 systolic murmur, bilateral weakness of the thigh flexors, and tenderness over L-4 and L-5 vertebrae. His temperature was 1020F. Blood cultures revealed Staphylococcus aureus. Spine radiographs and myelography revealed changes of osteomyelitis and an epidural mass at L-4 and L-5. He was treated with penicillin; the weakness resolved and pain subsided. He was discharged symptom-free after 47 days of intravenous antibiotic therapy. He has been symptom-free since discharge on December 20, 1987.
Case 3 A 47-year-old man with a history of alcohol abuse was admitted with fever, chills, and neck and right shoulder pain. Examination revealed mastoid tenderness and neck pain on palpation and movement. There was also a decrease in the neck range of motion. Radiographs 714
revealed a narrowing of C-6 and C-7 disc space. Leukocytosis was present (39 000 mm3). Spinal fluid revealed a glucose of 90 ,ugm%, protein 83 ,ugm%, and 2 lymphocytes/cc. The patient was initially diagnosed with mastoiditis, but on the second hospital day a computerized scan revealed an anteriorly placed epidural mass displacing the cord posteriorly. The patient's pain increased, and antibiotics were increased. His neurologic status was carefully monitored, as the patient had right shoulder bursitis. After 6 weeks of antibiotic therapy, a second computerized scan revealed complete abscess resolution. He was discharged on oral antibiotic therapy on January 16, 1988. There has been no recurrence of signs or symptoms to date.
DISCUSSION Although the clinical picture and diagnostic correlates are well established, diagnosis of acute spinal epidural abscess is often difficult (Table 1). Usually evidence of infection distinguishes inflammatory from noninflammatory entities, but prior partial antibiotic therapy may initially mask fever and leukocytosis. Meningitis is the most difficult to differentiate in phase 1, during which fever, neck stiffness, headache, and movement discomfort are common findings. Localized tenderness may be the only clue helpful in differentiating the two. The clinical picture has been well described by Heusner,13 who delineated the phases as noted in Table 2. The duration of phases varies. In phase 1, a careful history, examination, and sensitivity to patients at risk for acute spinal epidural abscess are important (Table JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 82, NO. 10
ACUTE SPINAL EPIDURAL ABSCESS
TABLE 1. DIFFERENTIAL DIAGNOSIS OF ACUTE SPINAL EPIDURAL ABSCESS Meningitis Acute subdural abscess Spinal epidural hematoma Vascular lesions Osteomyelitis Acute transverse myelitis Disc protrusion Tumor
TABLE 2. PHASES OF ACUTE EPIDURAL ABSCESS Midline back pain, fever, focal tenderness Phase 1 Phase 2 Radicular pain, abnormal reflexes, leukocytosis, nuchal rigidity Phase 3 Weakness of voluntary muscles and sphincters, sensory abnormalities Phase 4 Paralysis
3). In phase 2, diagnosis should be made based on focal neurologic findings and adequate history. This is the phase during which treatment should be administered to avoid risk of irreversible neurologic deficit. The sources of infection are the bloodstream, osteomyelitis, and other contiguous spread-psoas abscess, decubiti, operative wounds, and epidural catheters. The cases described illustrate three of the four phases of acute spinal epidural abscess and suggest that there may be options other than surgical management. In the case that required surgery, medical management was not used correctly, as the correct diagnosis was not initially made. If osteomyelitis is diagnosed, early routine radiographs may be deceiving as the disease may not yet be visible. In case 1, spinal fluid failed to reveal typical findings because antibiotics masked the diagnosis. The patient in case 1 was in phase 3 when the diagnosis was made. The presence of neurologic deficit and the cervical location indicated that laminectomy was the management of choice. The patient in case 2 had a lumbar spinal epidural abscess associated with osteomyelitis. Conservative therapy was instituted. The patient in case 3 was in phase 2 and was managed medically. Bursitis caused a problem in differential diagnosis, but frequent neurologic evaluations permitted conservative therapy.
CONCLUSION Acute spinal epidural abscess may not be as uncommon as reported. Suspicion should be raised JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 82, NO. 10
TABLE 3. INCREASED RISK FACTORS FOR ACUTE SPINAL EPIDURAL ABSCESS Intravenous drug abuse Septicemia, especially associated with spine trauma Operative wounds in close proximity to the spine Decubiti over spinal area Epidural mechanical entry Acquired immunodeficiency syndrome
when a patient presents with any of the signs and symptoms listed in Table 2, especially patients with increased risk factors. The recommended diagnostic aids are magnetic resonance imaging, computerized tomography, and myelography. Magnetic resonance imaging is believed to be the most effective technique in demonstrating early osteomyelitis. We find that computerized tomography and myelography demonstrate both the lesion and the block degree. The suspicion of spinal epidural abscess should not be abandoned until all diagnostic tests have been evaluated. Laboratory data may be altered by prior therapy. Once the diagnosis is confirmed, there are management choices other than surgery. 14,15 Although surgery is indicated in a patient with rapidly progressing phase 3 disease, in phases 1 or 2, conservative management with neurologic monitoring is recommended. Epidural abscesses in the lumbar area are, by location, more amenable to conservative management compared with those in the cervical area. There are fewer risks of irreversible neurologic deficit in acute spinal epidural abscess located in the lumbar area because of anatomic relationships between the epidural space and vital neural elements. In the cervical spinal canal, the spinal cord occupies a greater percentage of space, whereas the spinal cord is present for only a small percentage of the longitudinal lumbar spinal canal. The nerve roots are more resistant to compression and less likely to suffer from infarction and functional compression associated with spinal epidural abscess, allowing for a more conservative approach in managing acute spinal epidural lumbar abscesses. Acknowledgement The authors thank Kenneth Roistacher, MD (Infectious Diseases), Fred Schialaba, MD (Neurosurgery), and the Radiology service for assistance in diagnosis and management.
Literature Cited 1. Baker AS, Ojemann RG, Swartz NM, Richardson EP, Jr. Spinal epidural abscess. N Engl J Med. 1976;293:463-468.
715
ACUTE SPINAL EPIDURAL ABSCESS
2. Hancock DO. A study of 48 patients with acute extradural abscess. Paraplegia. 1973;10:285-288. 3. Lasker JR, Wharter DH. Cervical epidural abscess. Neurology. 1987;37:1747-1753. 4. Yerner EP, Musher PM. Spinal epidural abscess. Med Clin North Am. 1985;69(2):375-384. 5. Feldenzer JA, Waters DC, Knake JE, Hoff JT. Anterior cervical epidural abscess: the use of intraoperative spinal sonography. Surg Neurol. 1986;25:105-108. 6. Peterson JA, Paris P, Williams AC. Acute epidural abscess. Am J Emerg Med. 1987;5:287-290. 7. Morgagni JB. 1762. Desedibus et Causis Morobum Per Anatomic Indagatis. Naples: Typographia Simoniana 5 vols. The Seats and Causes of Diseases Investigated by Anatomy. Naples, Italy: Typographia Simoniana; 1962. 8. Browder J, Meyers R. Pyogenic infections of the spinal epidural space: a consideration of the anatomic and physiologic pathology. Surgery. 1941 ;10:296-308.
716
9. Yerner EF, Musher DM. Spinal epidural abscess. Med Clin North Am. 1985;69(2):375-384. 10. Schmutzhard E, Alchner F, Dierckx RA, Gerstenbrand F, Willeit J. New perspectives in acute spinal epidural abscess. Acta Neurochir (Wein). 1 986;80(3-4):1 05-108. 11. Firsching R, Frowein RA, Niltner K. Acute spinal epidural empyema. Acta Neurochir (Wein). 1985;74(1-2):68-71. 12. Peterson JA, Paris P, Williams AC. Acute epidural abscess. Am J Emerg Med. 1987;5(4):287-290. 13. Heusner AP. Nontuberculous spinal epidural infections. N Engl J Med. 1948;239:845-854. 14. Leys D, Lesoin F, Vaud C, et al. Decreased morbidity from acute bacterial spinal epidural abscesses using computered tomography and non-surgical treatment in selected patients. Ann Neurol. 1 985;1 7:350-355. 15. Bouchez B, Arnoj J, Delfosse JM. Acute spinal epidural abscess. J Neurol. 1985;281 :343-344.
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 82, NO. 10
Acute spinal epidural abscess is an uncommon disease. Recommended management has been mainly surgical. We recently treated three cases within 4 weeks. Lowered immune resistance played a role in two of the cases. We suggest that acquired immunodeficiency syndrome will increase the incidence of this uncommon entity and advise that acute spinal epidural abscess can be successfully treated by nonsurgical means in some cases. Key words * spinal epidural abscess * abscess Acute spinal epidural abscess is uncommon, with an estimated incidence of between 1 in 100 000 and 1 in 400 000.1-3 With few exceptions, recommended treatment has been surgical.4-6 However, the dictum "once the diagnosis is established, laminectomy is imperative" needs to be evaluated in relation to other therapeutic tools. In 1762, Morgagni7 described a case of epidural abscess without vertebral involvement. Almost 200 years later, in 1941, Browder and others8 were able to find slightly more than 200 cases in the literature. More recently, several isolated cases have been reported.9-12 This increasing frequency may reflect a relationship between acute spinal epidural abscess and acquired immunodeficiency syndrome or just increased awareness. From the Neurology Service, Brooklyn, VAMC, Department of Neurology, SUNY, and the Health Science Center of Brooklyn, New York. Requests for reprints should be addressed to Dr Walter R. Slade, Jr, Chief, Neurology Service (127), VA Medical Center, Brooklyn, NY 11209. JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 82, NO. 10
We report three cases of acute spinal epidural abscess, suggest possible reasons for increasing incidence, and question laminectomy as primary therapy.
CASE REPORTS Case 1 A 67-year-old man was admitted with neck pain radiating into the fingers, accompanied by weakness of both hands and the right lower extremity. He had been admitted previously for a generalized seizure, fever, chills, and neck pain and was discharged 5 days later on oral cephradine. He was admitted to another hospital with hand paresthesias and neck pain. After an extensive evaluation (spine radiographs, complete blood count, lumbar puncture, and blood, spinal fluid, and urine cultures), Escherichia coli were isolated from his urinary tract and he was treated with trimethoprim/sulfamethoxazole. Nine days after discharge he was admitted to neurology because radiographs revealed pathology of C-6 and C-7 vertebrae. Examination revealed localized neck pain increasing on movement, marked right upper extremity weakness, decreased pinprick sensation in the right upper extremity, and sensory impairment below the umbilicus. Computerized tomography of the cervical spine revealed end plate destruction of C-6 and C-7, with evidence of an adjacent anterior paraspinal soft tissue mass (Figure 1). Myelography revealed a complete block at C-6 level, with the mass extending to T-1 (Figure 2). A laminectomy with abscess drainage was performed. After a difficult postoperative course on antibiotics, the patient improved and began physiotherapy. He was discharged on December 28, 1987, without neurologic deficit. To date he is asymptomatic and neurologically normal. 713
ACUTE SPINAL EPIDURAL ABSCESS
Figure 2. Myelography showing complete block.
Figure 1. X-ray of cervical spine. Case 2 A 22-year old male intravenous drug user was admitted with excruciating lower back pain, urinary frequency, and constipation duning the week prior to admission. Examination revealed a 3/4 systolic murmur, bilateral weakness of the thigh flexors, and tenderness over L-4 and L-5 vertebrae. His temperature was 1020F. Blood cultures revealed Staphylococcus aureus. Spine radiographs and myelography revealed changes of osteomyelitis and an epidural mass at L-4 and L-5. He was treated with penicillin; the weakness resolved and pain subsided. He was discharged symptom-free after 47 days of intravenous antibiotic therapy. He has been symptom-free since discharge on December 20, 1987.
Case 3 A 47-year-old man with a history of alcohol abuse was admitted with fever, chills, and neck and right shoulder pain. Examination revealed mastoid tenderness and neck pain on palpation and movement. There was also a decrease in the neck range of motion. Radiographs 714
revealed a narrowing of C-6 and C-7 disc space. Leukocytosis was present (39 000 mm3). Spinal fluid revealed a glucose of 90 ,ugm%, protein 83 ,ugm%, and 2 lymphocytes/cc. The patient was initially diagnosed with mastoiditis, but on the second hospital day a computerized scan revealed an anteriorly placed epidural mass displacing the cord posteriorly. The patient's pain increased, and antibiotics were increased. His neurologic status was carefully monitored, as the patient had right shoulder bursitis. After 6 weeks of antibiotic therapy, a second computerized scan revealed complete abscess resolution. He was discharged on oral antibiotic therapy on January 16, 1988. There has been no recurrence of signs or symptoms to date.
DISCUSSION Although the clinical picture and diagnostic correlates are well established, diagnosis of acute spinal epidural abscess is often difficult (Table 1). Usually evidence of infection distinguishes inflammatory from noninflammatory entities, but prior partial antibiotic therapy may initially mask fever and leukocytosis. Meningitis is the most difficult to differentiate in phase 1, during which fever, neck stiffness, headache, and movement discomfort are common findings. Localized tenderness may be the only clue helpful in differentiating the two. The clinical picture has been well described by Heusner,13 who delineated the phases as noted in Table 2. The duration of phases varies. In phase 1, a careful history, examination, and sensitivity to patients at risk for acute spinal epidural abscess are important (Table JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 82, NO. 10
ACUTE SPINAL EPIDURAL ABSCESS
TABLE 1. DIFFERENTIAL DIAGNOSIS OF ACUTE SPINAL EPIDURAL ABSCESS Meningitis Acute subdural abscess Spinal epidural hematoma Vascular lesions Osteomyelitis Acute transverse myelitis Disc protrusion Tumor
TABLE 2. PHASES OF ACUTE EPIDURAL ABSCESS Midline back pain, fever, focal tenderness Phase 1 Phase 2 Radicular pain, abnormal reflexes, leukocytosis, nuchal rigidity Phase 3 Weakness of voluntary muscles and sphincters, sensory abnormalities Phase 4 Paralysis
3). In phase 2, diagnosis should be made based on focal neurologic findings and adequate history. This is the phase during which treatment should be administered to avoid risk of irreversible neurologic deficit. The sources of infection are the bloodstream, osteomyelitis, and other contiguous spread-psoas abscess, decubiti, operative wounds, and epidural catheters. The cases described illustrate three of the four phases of acute spinal epidural abscess and suggest that there may be options other than surgical management. In the case that required surgery, medical management was not used correctly, as the correct diagnosis was not initially made. If osteomyelitis is diagnosed, early routine radiographs may be deceiving as the disease may not yet be visible. In case 1, spinal fluid failed to reveal typical findings because antibiotics masked the diagnosis. The patient in case 1 was in phase 3 when the diagnosis was made. The presence of neurologic deficit and the cervical location indicated that laminectomy was the management of choice. The patient in case 2 had a lumbar spinal epidural abscess associated with osteomyelitis. Conservative therapy was instituted. The patient in case 3 was in phase 2 and was managed medically. Bursitis caused a problem in differential diagnosis, but frequent neurologic evaluations permitted conservative therapy.
CONCLUSION Acute spinal epidural abscess may not be as uncommon as reported. Suspicion should be raised JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 82, NO. 10
TABLE 3. INCREASED RISK FACTORS FOR ACUTE SPINAL EPIDURAL ABSCESS Intravenous drug abuse Septicemia, especially associated with spine trauma Operative wounds in close proximity to the spine Decubiti over spinal area Epidural mechanical entry Acquired immunodeficiency syndrome
when a patient presents with any of the signs and symptoms listed in Table 2, especially patients with increased risk factors. The recommended diagnostic aids are magnetic resonance imaging, computerized tomography, and myelography. Magnetic resonance imaging is believed to be the most effective technique in demonstrating early osteomyelitis. We find that computerized tomography and myelography demonstrate both the lesion and the block degree. The suspicion of spinal epidural abscess should not be abandoned until all diagnostic tests have been evaluated. Laboratory data may be altered by prior therapy. Once the diagnosis is confirmed, there are management choices other than surgery. 14,15 Although surgery is indicated in a patient with rapidly progressing phase 3 disease, in phases 1 or 2, conservative management with neurologic monitoring is recommended. Epidural abscesses in the lumbar area are, by location, more amenable to conservative management compared with those in the cervical area. There are fewer risks of irreversible neurologic deficit in acute spinal epidural abscess located in the lumbar area because of anatomic relationships between the epidural space and vital neural elements. In the cervical spinal canal, the spinal cord occupies a greater percentage of space, whereas the spinal cord is present for only a small percentage of the longitudinal lumbar spinal canal. The nerve roots are more resistant to compression and less likely to suffer from infarction and functional compression associated with spinal epidural abscess, allowing for a more conservative approach in managing acute spinal epidural lumbar abscesses. Acknowledgement The authors thank Kenneth Roistacher, MD (Infectious Diseases), Fred Schialaba, MD (Neurosurgery), and the Radiology service for assistance in diagnosis and management.
Literature Cited 1. Baker AS, Ojemann RG, Swartz NM, Richardson EP, Jr. Spinal epidural abscess. N Engl J Med. 1976;293:463-468.
715
ACUTE SPINAL EPIDURAL ABSCESS
2. Hancock DO. A study of 48 patients with acute extradural abscess. Paraplegia. 1973;10:285-288. 3. Lasker JR, Wharter DH. Cervical epidural abscess. Neurology. 1987;37:1747-1753. 4. Yerner EP, Musher PM. Spinal epidural abscess. Med Clin North Am. 1985;69(2):375-384. 5. Feldenzer JA, Waters DC, Knake JE, Hoff JT. Anterior cervical epidural abscess: the use of intraoperative spinal sonography. Surg Neurol. 1986;25:105-108. 6. Peterson JA, Paris P, Williams AC. Acute epidural abscess. Am J Emerg Med. 1987;5:287-290. 7. Morgagni JB. 1762. Desedibus et Causis Morobum Per Anatomic Indagatis. Naples: Typographia Simoniana 5 vols. The Seats and Causes of Diseases Investigated by Anatomy. Naples, Italy: Typographia Simoniana; 1962. 8. Browder J, Meyers R. Pyogenic infections of the spinal epidural space: a consideration of the anatomic and physiologic pathology. Surgery. 1941 ;10:296-308.
716
9. Yerner EF, Musher DM. Spinal epidural abscess. Med Clin North Am. 1985;69(2):375-384. 10. Schmutzhard E, Alchner F, Dierckx RA, Gerstenbrand F, Willeit J. New perspectives in acute spinal epidural abscess. Acta Neurochir (Wein). 1 986;80(3-4):1 05-108. 11. Firsching R, Frowein RA, Niltner K. Acute spinal epidural empyema. Acta Neurochir (Wein). 1985;74(1-2):68-71. 12. Peterson JA, Paris P, Williams AC. Acute epidural abscess. Am J Emerg Med. 1987;5(4):287-290. 13. Heusner AP. Nontuberculous spinal epidural infections. N Engl J Med. 1948;239:845-854. 14. Leys D, Lesoin F, Vaud C, et al. Decreased morbidity from acute bacterial spinal epidural abscesses using computered tomography and non-surgical treatment in selected patients. Ann Neurol. 1 985;1 7:350-355. 15. Bouchez B, Arnoj J, Delfosse JM. Acute spinal epidural abscess. J Neurol. 1985;281 :343-344.
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 82, NO. 10
