Printer Friendly

Treatment of holocord spinal epidural abscess via alternating side unilateral approach for bilateral laminectomy.


A particular treatment dilemma is encountered when an epidural abscess extends along the entire length of the spinal canal with a progressing neurological deficit. While decompressing the entire length of the cord is often required, minimizing the invasiveness of any required surgical intervention improves both the short and long term outcome of the patient. To date, this is the first reported case of the surgical management of a holocord epidural abscess (extending 20 vertebral levels) through level-skipping laminectomies. It is also the first reported case of these laminectomies being performed via an alternating-side unilateral approach for this condition.

Case Presentation

A 51-year-old white male presented with a 2-month history of back pain, intermittent fevers, bilateral lower extremity paresthesias, and lower extremity weakness. He had fallen 6 weeks prior to admission and sustained rib and clavicle fractures, but had been recovering well over the past few weeks. However one week prior to admission he started developing progressive weakness to the point that the patient was non-ambulatory with only antigravity strength in the legs. He had a significant past medical history of poorly controlled diabetes mellitus and right foot cellulitis. Workup at a referring institution revealed a right lung mass (Figure 1) and "air in the spinal canal" (Figure 2). This pneumorachis was present prior to lumbar puncture at the outside facility, and no lung biopsy was performed at the referring institution. Magnetic resonance imaging (MRI) demonstrated severe stenosis at C7-T1, T5-T7, T11-T12, and L4-S1, with significant contrast enhancement, consistent with an epidural abscess (Figures 3-4). At the cephalic end, the abscess began at the level of C4-5 and extended caudally to the level of the sacrum at S1.

The patient was initially started on broad-spectrum triple antibiotic therapy, which consisted of vancomycin, metronidazole and ceftazidime. He underwent bilateral laminectomies using a unilateral approach at T1-T2, T6-T7, and T11-T12 alternating from the left side, right side and left-side respectively, for evacuation of the epidural abscess and decompression of the spinal cord. Laminectomies were performed at levels that were at or within one level of imaging evidence of severe canal stenosis including the cervical and thoracic spine. All purulent material was evacuated from C4 to S1. This was accomplished via placement of a pediatric feeding tube under direct vision through the laminectomy defects up and down along the spinal canal, through which irrigation was gently passed. These tubes were then left in place for 72 hours as drains along all aspects of the spinal canal. Of note, the procedure resulted in minimal blood loss and only three 5cm incisions.

The surgery was uncomplicated and post-operatively the patient demonstrated significant improvement in lower extremity strength. Imaging demonstrated good decompression of the spinal cord (Figure 5). Intraoperative cultures were remarkable for methicillin-resistant staphylococcus aureus (MRSA). Regarding his lung lesion, thoracic surgery had been consulted. They felt that this lesion represented a hematoma from his rib fracture, since it was directly contiguous to the rib fracture. Therefore no treatment was performed on the lesion.


Spinal epidural abscess (SEA) is diagnosed in approximately 1 in 20,000 hospital admissions. Unfortunately, the diagnosis has doubled in the past few decades owing to an increase in the aging population, spinal instrumentation, intravenous drug use, and vascular access.12 Patients who present with an epidural abscess are generally predisposed to this condition due to concomitant immunodeficiency, diabetes, or alcoholism. (1-4) In general, bacteria gain access through contiguous spread of infection. (5) The pathophysiology of neurologic decline has been postulated to be due to direct spinal cord compression; however in animal models septic thromboses have been noted. (6) Improvement after decompressive surgery has been well documented, leading to the belief that direct compression appears to be the predominant mechanism. (1-4)

SEAs are often recognized by the clinical triad of fever, back pain, and neurologic deficit; however, only a minority of patients present with this constellation of signs and symptoms. (2,7,8) Clinical presentation does generally progress through four distinct stages. (2,7) Stage one presents with focal back pain in the affected area (predominant symptom); stage two presents as radiculopathy at the level of the affected area; stage three presents as motor weakness, sensory deficit, and loss of bowel and bladder control; finally stage four presents with paralysis. (7) The exception to this typical progression is a spinal abscess in the thoracic area where stage 2 can be occult. The typical pathogen responsible is coagulase positive staphylococcus or staphylococcus aureus with a reported incidence of 70%. (1-4,9-13) Pathogens are typically attracted to fat tissues, therefore abscesses will characteristically present along the posterior rather than the anterior canal. (1,14)

Surgical intervention when indicated greatly improves the long-term neurological outcome. In a study by Lohr et al., ambulatory status of patients with SEA upon admission was 57.7% and improved to 80.8% in the long-term with surgical decompression. (1) Therefore in symptomatic patients, surgical intervention is clearly indicated in medically stable patients. (1-4,8,14-16) This intervention should be urgent since patients with thoracic SEA that have progressed to profound plegia have a poor long-term prognosis. (4,16) Patients that are neurologically stable without imaging evidence of severe canal stenosis may be managed conservatively (15,17,18) with the goal of pathogen identification and initiation of appropriate antibiotic therapy. The standard surgical approach is a posterior decompression, unless there is evidence of vertebral body compromise (i.e. osteomyelitis/diskitis). In this case an anterior stabilization procedure may be required. (3,19-21)

A particular treatment dilemma is presented when SEA extends along the entire length of the spinal canal, as in this patient, since traditional surgical decompression would involve extensive disruption of soft tissue and removal of bone via laminectomy. In addition to the morbidity of the large surgical incision itself, both clinical data and biomechanical studies have demonstrated that bilateral disruption and damage to paraspinal muscles and ligaments, together with removal of the spinous process, are significant risk factors for postoperative instability and/or kyphosis. (22)

The use of strategically placed laminectomies with decompression using irrigation of additional levels is a useful alternative to more extensive surgery. Additionally, performing these laminectomies via a unilateral approach preserves the majority of the posterior musculature and their bony attachments. Alternating approach sides of these 'skip' laminectomies potentially balances any weakness between sides resulting from the stripping, dissection, and denervation of the posterior paraspinal muscle complex. Previously reported literature supports the efficacy of a minimally invasive technique of abscess evacuation via interlaminar fenestration/laminotomy; the technique described in this report is likewise useful for larger and more tenacious SEAs. (3,9)


The patient was discharged on intravenous vancomycin for a total of 8 weeks of antibiotic therapy. On two-week outpatient follow-up the patient was doing well with completely healed surgical incisions. He reported a significant improvement in lower extremity paresthesias, strength, pain, and was once again ambulatory. At six months, he demonstrated no signs of instability. This case illustrates the efficacy of skip laminectomies via an alternating side unilateral approach for holocord epidural abscesses. This strategy minimizes incision size, tissue disruption, and the amount of muscular weakness/ imbalance postoperatively.


(1.) Lohr M, Reithmeier T, Ernestus RI, Ebel H, Klug N. Spinal epidural abscess: prognostic factors and comparison of different surgical treatment strategies. Acta neurochirurgica. Feb 2005;147(2):159-166; discussion 166.

(2.) Rigamonti D, Metellus P. Spinal epidural abscess. NEJM. Feb 8 2007;356(6):638; author reply 638-639.

(3.) Kim SH, Lee JK, Jang JW, Seo BR, Kim TS, Kim SH. Laminotomy with continuous irrigation in patients with pyogenic spondylitis in thoracic and lumbar spine. J Korean Neuro Soc. Oct 2011;50(4):332-340.

(4.) Rigamonti D, Liem L, Sampath P, et al. Spinal epidural abscess: contemporary trends in etiology, evaluation, and management. Surg Neur. Aug 1999;52(2):189-196; discussion 197.

(5.) Grewal S, Hocking G, Wildsmith JA. Epidural abscesses. Brit J Anaes. Mar 2006;96(3):292-302.

(6.) Feldenzer JA, McKeever PE, Schaberg DR, Campbell JA, Hoff JT. The pathogenesis of spinal epidural abscess: microangiographic studies in an experimental model. J Neuro. Jul 1988;69(1):110-114.

(7.) Davis DP, Wold RM, Patel RJ, et al. The clinical presentation and impact of diagnostic delays on emergency department patients with spinal epidural abscess. J Emerg Med. Apr 2004;26(3):285-291.

(8.) Reihsaus E, Waldbaur H, Seeling W. Spinal epidural abscess: a meta-analysis of 915 patients. Neuro Rev. Dec 2000;23(4):175-204; discussion 205.

(9.) Rath SA, Neff U, Schneider O, Richter HP. Neurosurgical management of thoracic and lumbar vertebral osteomyelitis and discitis in adults: a review of 43 consecutive surgically treated patients. Neurosurgery. May 1996;38(5):926-933.

(10.) Khanna RK, Malik GM, Rock JP, Rosenblum ML. Spinal epidural abscess: evaluation of factors influencing outcome. Neurosurgery. Nov 1996;39(5):958-964.

(11.) Hlavin ML, Kaminski HJ, Ross JS, Ganz E. Spinal epidural abscess: a ten-year perspective. Neurosurgery. Aug 1990;27(2):177-184.

(12.) Del Curling O, Jr., Gower DJ, McWhorter JM. Changing concepts in spinal epidural abscess: a report of 29 cases. Neurosurgery. Aug 1990;27(2):185-192.

(13.) Hadjipavlou AG, Mader JT, Necessary JT, Muffoletto AJ. Hematogenous pyogenic spinal infections and their surgical management. Spine. Jul 1 2000;25(13):1668-1679.

(14.) Danner RL, Hartman BJ. Update on spinal epidural abscess: 35 cases and review of the literature. Rev Infect Dis. Mar-Apr 1987;9(2):265-274.

(15.) Nussbaum ES, Rigamonti D, Standiford H, Numaguchi Y, Wolf AL, Robinson WL. Spinal epidural abscess: a report of 40 cases and review. Surg Neuro. Sep 1992;38(3):225-231.

(16.) Wang LP, Hauerberg J, Schmidt JF. Long-term outcome after neurosurgically treated spinal epidural abscess following epidural analgesia. Acta Anaesthesiologica Scandinavica. Feb 2001;45(2):233-239.

(17.) Mampalam TJ, Rosegay H, Andrews BT, Rosenblum ML, Pitts LH. Nonoperative treatment of spinal epidural infections. J Neuro. Aug 1989;71(2):208-210.

(18.) Messer HD, Lenchner GS, Brust JC, Resor S. Lumbar spinal abscess managed conservatively. Case report. J Neuro. Jun 1977;46(6):825-829.

(19.) Pee YH, Park JD, Choi YG, Lee SH. Anterior debridement and fusion followed by posterior pedicle screw fixation in pyogenic spondylodiscitis: autologous iliac bone strut versus cage. J Neuro. May 2008;8(5):405-412.

(20.) McGee-Collett M, Johnston IH. Spinal epidural abscess: presentation and treatment. A report of 21 cases. Med J Australia. Jul 1 1991;155(1):14-17.

(21.) Fayazi AH, Ludwig SC, Dabbah M, Bryan Butler R, Gelb DE. Preliminary results of staged anterior debridement and reconstruction using titanium mesh cages in the treatment of thoracolumbar vertebral osteomyelitis. The Spine Journal: Official Journal of the North American Spine Society. Jul-Aug 2004;4(4):388-395.

(22.) Okawa A, Shinomiya K, Takakuda K, Nakai O. A cadaveric study on the stability of lumbar segment after partial laminotomy and facetectomy with intact posterior ligaments. J Spinal Dis. Dec 1996;9(6):518-526.

Roy Hwang, MD

West Virginia University, Dept of Neurosurgery, RCBHSC, Morgantown

Brian H. Yung, MD

West Virginia University, Dept. of Neurosurgery, RCBHSC, Morgantown

Cara Sedney, MD

West Virginia University, Dept. of Neurosurgery, RCBHSC, Morgantown

Vincent J. Miele, MD

University of Pittsburgh Medical Center, Dept. of Neurosurgery, Pittsburgh, PA

Corresponding Author: Roy S. Hwang, MD, WVU Dept. of Neurosurgery, Morgantown, WV 26506-9000. Email:
COPYRIGHT 2015 West Virginia State Medical Association
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2015 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Title Annotation:Case Report
Author:Hwang, Roy; Yung, Brian H.; Sedney, Cara; Miele, Vincent J.
Publication:West Virginia Medical Journal
Article Type:Clinical report
Geographic Code:1U5WV
Date:May 1, 2015
Previous Article:Re: passage of SB 335--creating access to Opioid Antagonist Act.
Next Article:Benign mesothelial mesenteric cyst: case report and literature review.

Terms of use | Privacy policy | Copyright © 2018 Farlex, Inc. | Feedback | For webmasters