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Acute IntrameduUary Spinal Cord Abscess: Case Report Jonathan H. Erlich, M.B., B.S., B. Med. Sci., Jeffery V. Rosenfeld, F.R.A.C.S., F.R.C.S. (Ed.), Andrew Fuller, M.B., B.S., Dip. R.A.C.O.G., Graham V. Brown, F.R.A.C.P., Ph.D., Jack Wodak, F.R.A.C.P., and Brian P. Tress, F.R.A.C.R., F.R.C.R., M.D. Departments of Neurosurgery, Microbiology, Internal Medicine, and Radiology, The Royal Melbourne Hospital, Parkville, Australia

Erlich JH, Rosenfeld JV, Fuller A, Brown GV, Wodak J, Tress BP. Acute intrameduUary spinal cord abscess: case report. Surg Neurol 1992;38:287-90.

We report the first case of an acute pyogenic intramedullary cervical spinal cord abscess, brain abscesses, and meningitis due to an unusual anerobe, Bacteroides disiens. The importance of spinal magnetic resonance imaging for establishing the diagnosis is emphasized. KEYWORDS: Bacteroidesdisiens; Cerebral abscess; Intramedullary spinal cord abscess; Meningitis

Intramedullary spinal cord abscess is a rare condition first reported in 1830 [16]. Sixty-five cases have been subsequently recorded [3,5,11,16]. Acute intramedullary spinal cord abscess may present as an acute cord lesion with back pain and fever. By contrast, chronic intramedullary spinal cord abscess may have no specific features to distinguish it from other intramedullary lesions. Before 1944, the outlook for acute spinal cord abscesses with symptoms of less than 7 days was poor, with no reported survivors. Since 1944, the outlook for patients with an acute presentation has been relatively good [3,11]. We report a patient with acute cervical intramedullary spinal cord abscess associated with brain abscesses and chronic suppurative lung disease. Case Report A 59-year-old man with a past history of bronchiectasis presented to the emergency room with a 1-day history of progressive back pain, weakness in the left leg, and painful urinary retention. At the time of presentation he was afebrile, with a blood pressure of 160/80 mm Hg

Address reprint requests to: Jeffrey V. Rosenfeld, F.R.A.C.S., 97 Clarence Street, South Caulfield, Victoria, Australia, 3162. Received September 27, 1991; accepted January 23, 1992.

© 1992 by Elsevier Science Publishing Co., Inc.

and a pulse rate of 110 per minute. Examination revealed profound weakness in the left leg but normal power in the right leg. Deep tendon reflexes were brisk in the lower limbs, and the plantar reflexes were up-going. There was impairment of temperature sensation to a level o f T 1 0 on the right side. A complete myelogram was normal. Cerebrospinal fluid (CSF) examination revealed 10 erythrocytes, 70 polmorphonuclear leukocytes, and 22 lymphocytes per cubic millimeter, protein 0.77 g/L (normal range 0.00 to 0.40 g/L), and glucose 3.6 mmol/L (normal range 2.8 to 5.30 mmol/L). Gram stain and culture were negative. A provisional diagnosis of transverse myelitis was made, and the patient commenced on prednisolone, 80 mg orally daily, and cefotaxime, I gram intravenously every 8 hours. On the third day of his illness, pain increased and he developed mild right leg weakness. The following day, he developed paraplegia with a sensory level at T8. The patient continued to deteriorate, with paresis of both arms and increasing pain. Prednisolone was changed to methylprednisolone, 1 gram intravenously daily. The patient had a respiratory arrest and was intubated and ventilated. He was afebrile, with a sensory level at C3 on the left and C5 on the right. Investigations revealed hemoglobin 9.6 g/L (normal range 13.0 to 18.0 g/L), leukocyte count 11.1 (normal range 4.0 to 11.0), platelet count 208 × 109/L (normal range 150 to 400/L), and erythrocyte sedimentation rate 23 mm/h (normal range 0 to 15 mm/h). Magnetic resonance imaging (MRI) was performed on the fifth day of the illness and revealed a mildly enlarged spinal cord, with a high signal on T2-weighted scans consistent with edema at the level of C4 to C6 (Figure 1). Paramagnetic contrast agents were not approved for use at this time. A computed tomographic (CT) scan of the head revealed moderate hydrocephalus with fluid levels in the occipital horns, but no abscesses were identified. A further lumbar puncture revealed a pressure: of 35 cm H20, 205 erythrocytes, 6400 polymorphonuclear leukocytes, 25 lymphocytes, and 20 monocytes per mm ~. Bacterial 0090-3019/92/S5.00

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Figure 1, (A) Sagittal Tl-weighted MRI scan (TR 500, TE 30). The cervicalspinal cordat C4-6 is diffusely swollen, with normalsignal intensity. (B) Sagittal T2-weighted MRI scan (TR 2200, TE 85). There is an abnormally high signal intensity in the cervicalspinal cordat C4-6.

antigens (Pneumococcus, Haemophilus, and Neisseria) were negative. The CSF glucose level was 0.1 mmol/L and protein concentration was greater than 3.0 g/L. The provisional diagnosis was cervical spinal cord abscess, and surgical drainage was performed via a C3 to C5 laminectomy. A purulent exudate was noted around the cord, and aspiration of the swollen cord produced turbid fluid followed by frank green pus. The spinal cord was incised dorsally and a central abscess was found at the level of C4, with a syrinx at the level of C3. A right occipital burr hole was made, with insertion of a ventricular drain to treat the hydrocephalus. Gramnegative bacilli in the pus were identified as Bacteroidies disiens (Figure 2). Postoperatively, the antibiotics were changed to chloramphenicol, i g intravenously 6 hourly, and ceftazidime, 2 g intravenously 8 hourly. Initially, there was some improvement, with increased power on the right side and a decreased polymorphonuclear leukocyte count in the CSF. When the anaerobe was identified, metronidazole was added, 500 mg intravenously 8 hourly. Ceftazidime was ceased after 8 days due to ab-

normal liver function tests, and cefotaxime, 2 g intravenously 8 hourly, was substituted. The intraventricular drain was removed on day 11. On day 13, his conscious state deteriorated and a CT scan revealed worsening hydrocephalus. On day 27, a further deterioration in conscious state was noted. CT scan revealed left occipital and frontal cerebral abscesses (Figure 3). Imipenem was substituted for cefotaxime; however, the patient continued to deteriorate and death occurred on day 31. Permission for postmortem examination was refused.

Discussion The most common cause of intramedullary spinal cord abscess is hematogenous spread from another septic focus, usually chronic respiratory disease or bacterial endocarditis [1,3,4,11,13]. Congenital dermal sinus, spinal trauma from stab wound or lumbar puncture, and bacterial meningitis have also been implicated [1,3,4]. Organisms isolated from spinal cord abscess are Staphylococcus, Streptococcus pneumoniae,

Haemophilus,

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Figure 2. PhotomicrographshowsBacteroidies disiens and leukocytes (gram stain, original magnification x I000).

Proteus, Listeria monocytogenes, and Pseudomonas cepacia [ 1,3,4,9,11,13]. The tapeworm sparganum [5], the yeast Histoplasma capsulatum [ 15 ], Toxoplasma [ 10], and Mycobacterium [17] are more unusual organisms that have been reported to cause intramedullary infection, and the latter two patients also had human immunodeficiency virus infection [10,17]. In about one third of reported cases no organism was isolated [3,13]. The organism found in this case, Bacteroidies disiens, is unusual, but it has been isolated from normal human gingiva and from one patient with pneumonia [8]. In our case, it is presumed to have spread via the blood from a pulmonary focus. It was/3-1actamase positive and resistant to penicillin but sensitive to chloramphenicol, metronidazole, and clindamycin. Intramedullary spinal cord abscess from a primary pulmonary focus has been reported predominantly in the cervical and upper thoracic cord, as in our case [11,13]. The presence of acute neurological signs suggesting a spinal cord lesion and imaging studies revealing an enlarged spinal cord with or without abnormal CSF findings raises the possibility of intramedullary cord abscess [3,11]. The CSF findings in intramedullary cord abscess are variable, with normal to high CSF protein and variable leukocyte and erythrocyte counts. In only one case of intramedullary cervical cord abscess was the CSF found to grow an organism. In other cases, the CSF was sterile despite variable cell counts [3]. The MRI of our patient demonstrated an enlarged cervical spinal cord with increased signal on T2-weighted images, consistent with cord edema. We believe that the reason the syrinx was not identified on the MRI study

is, first, because the scan was performed 3 days prior to surgery, when the syrinx may have been small or nonexistent, and second, because proteinaceous fluid and leukocytes within the syrinx would tend to produce a high signal on the T2-weighted scaris, which would render it difficult to distinguish between the syrinx and surrounding cord edema. In other reports, MRI without paramagnetic contrast showed an increased signal [ 10,15 ] and an enlarged spinal cord [5 ]. However, MRI scans without paramagnetic contrast media lack the tissue specificity to determine the cause of the edema. Had gadolinium diethylenetriaminepentaacetic acid been available, it is likely that it would have shown the classic "ring" enhancement of an abscess [14]. This is the 21st case of acute cervical intrameduUary spinal cord abscess in which the symptoms have been present for less than 7 days. Prior to the antibiotic era, acute presentations invariably led to a fatal outcome [1]. Morbidity and mortality have improved with modern antibiotics and surgery [3,11]. In case reports of spinal cord abscess since 1944, the only reported deaths have been associated with brain abscess [7,13]. The improved outlook probably reflects the prevention of death due to uncontrolled sepsis rather than differences in etiology. Our case is the only report of an acute presentation with an associated brain abscess to undergo surgery and emphasizes that, even with surgery and antibiotics, this complication indicates a poor prognosis. Our case illustrates the rapidly progressive nature of intramedullary spinal cord abscess and the need for a high index of suspicion when accompanied by suggestive history, physical signs, and CSF findings, even though

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Figure 3. (A) Contrast-enhanced C T scan shows a left occipital lobe abscess (arrow). (B) Contrast-enhanced C T scan shows a right frontal lobe abscess (arrow).

myelography may be negative. If early diagnosis and effective intervention are to lead to more favorable results, early MRI scanning with paramagnetic contrast is advised.

References 1. Artz PK. Abscess within the spinal cord. Review of the literature and report of three cases. Arch Neurol Psychiatry1944; 51:533-43. 2. Bean JR, Walsh JW, Blacker HM. Cervical dermal sinus and intramedullary spinal cord abscess: case report. Neurosurgery 1979;5:60-2. 3. Blacklock JB, Hood TW, Maxwell RE. Intramedullary cervical spinal cord abscess. J Neurosurg 1982;57:270-3. 4. DiTullio MV. Intramedullary spinal abscess: a case report with a review of 53 previously described cases. Surg Neurol 1977;7:351-4. 5. Fung CF, Thomas HKN, Wong WT. Sparganosis of the spinal cord. J Neurosurg 1989;71;290-2. 6. EL Gindi S, Fairburn B. Intramedullary spinal abscess as a complication of a congenital dermal sinus. J Neurosurg 1969;30:494-7.

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7. Keener EB. Abscess formation in the spinal cord. Brain 1955;78:394-400. 8. Kirby BD, George W, Sul~er V, Citron D, Finegold S. Gramnegative anaerobic bacilli: their role in infection and patterns of susceptibility to antimicrobial agents. 1. Little-known Bacteroides species. Rev Infect Dis 1980;2:914-51. 9. Koppel BS, Daras M, Duffy KR. Intramedullary spinal cord abscess. Neurosurgery 1990;26:145-6. 10. Mehren M, Burns PJ, Mamani F, Levy CS, Laureno R. Toxoplasmic myelitis mimicking intramedullary spinal cord tumor. Neurology 1988;38:1648-50. 11. Menezes AH, Graf CJ, Perret GE. Spinal cord abscess: a review. Surg Neurol 1977;8:461-7. 12. Morrison RE, Brown J, Goodin RS. Spinal cord abscess caused by Listeria monocytogenes. Arch Neurol 1980;37:243-4. 13. Parker RL, Collins GH. Intramedullary abscess of the brain stem and spinal cord. South Med J 1970;63:495-7. 14. Runge VM, Clanton JA, Price AL, et al. Evaluation of contrastenhanced MR imaging in a brain abscess model. AJNR 1985;6:139-47. 15. Voelker JL, Muller J, Worth RM. Intramedullary spinal Histoplasma granuloma. J Neurosurg 1989;70:959-61. 16. Woltan HW, Adson AW. Abscess of the spinal cord: report of a case with functional recovery after operation. Brain 1926; 49:193-206. 17. Woolsey RM, Thomas JC, Chung HD, McGarryJD. Mycobacterial meningornyelitis associated with human immunodeficiency virus infection. Arch Neurol 1988;45:691-3.

Acute intramedullary spinal cord abscess: case report.

We report the first case of an acute pyogenic intramedullary cervical spinal cord abscess, brain abscesses and meningitis due to an unusual anerobe, B...
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