Case Presentation

History: A 39-year-old male with a history of hepatitis C and polysubstance abuse presents with acute onset lower extremity paralysis and paresthesia, bilateral upper extremity weakness, and diffuse neck pain. He admits to falling from a standing height about 1 week prior, but states he was seen at another facility and discharged in good condition except for persistent neck pain. Review of systems is otherwise negative, and the patient has no previous history of similar episodes.

Physical Exam: Afebrile, well appearing, with normal vital signs. Physical examination is normal except for the following abnormal neurological findings: exquisite tenderness to palpation at C6 spinous process, bilateral upper extremity weakness (2/5) with normal deep tendon reflexes, bilateral lower extremity paralysis (0/5) with absent deep tendon reflexes, weakness of grip strength bilaterally, normal tone, and Babinski negative bilaterally. Ambulation and gait cannot be tested. Finger-to-nose testing is normal. Proprioception is intact bilaterally. There is absent perineal sensation. Weak contracture of the anal sphincter noted, but no bulbocavernosus reflex could be elicited.

Management: Laboratory studies and chest x-ray are normal. CT scan of head and cervical spine demonstrate no intracerebral abnormality but do show degenerative changes of the spine, most prominent at the C4-C7 levels; the canal diameter, however, is normal.

Neurosurgical consultation is requested for persistent lower extremity paralysis. An MRI is ordered, and high-dose methylprednisolone intravenous infusion started. The MRI reveals pre-vertebral soft tissue swelling from C2-C7 and increased T2-signal extending from C5-C6 within the epidural space and extending posteriorly 5 mm. There is associated cervical cord compression suggesting early abscess formation. The patient is taken for emergent neurosurgical decompression and drainage. Cultures were positive for Staphylococcus aureus. Patient is discharged home 15 days later able to ambulate but with residual lower extremity weakness.

Introduction

Back pain is second only to respiratory complaints as a reason for primary care visits, with 90%-95% having a non-life–threatening condition^1,2 and 85% recovering in 4-6 weeks without intervention.^1-3 The other 5%-10% of cases, however, may harbor a more serious pathology and warrant further diagnostic evaluation in the emergency department.

A history of recent or remote trauma often may mask the diagnosis of rare causes of back pain such as spinal epidural abscess (SEA).⁴ Of the epidural spinal cord compressive syndromes, defined as radiologic indentation of the thecal sac,^5,6 SEA composes approximately 0.2-2 cases per 10,000 hospital admissions⁷ or less than 1 case per million residents, thereby limiting many physicians’ experience with the diagnosis of this potentially debilitating cause of back pain.

Pathophysiology

SEA is a suppurative process confined within the epidural space, lying between the dura mater and the vertebral periosteum. The incidence of SEA is increasing in developed countries^8-11 likely because of an aging population, greater numbers of spinal procedures, drug abuse, and increased use of immunosuppressive agents and antibiotics, all of which contribute to an altered immune state.¹²

SEA affects patients of all ages, though the majority are between 30 years and 60 years old, with a predominance of males.⁷ SEA most often results from hematogenous dissemination from many sources, including skin or soft tissue infection (most common), respiratory tract infection (especially in pulmonary tuberculous), urinary tract infection, or bacteremia. In some cases, it is not possible to identify the origin.¹³ Hematogenous spread usually results in an abscess located posteriorly (80% of cases), whereas direct extension from retropharyngeal and/or retroperitoneal infection typically results in a more anterior spinal location (20% of cases).

The most common organism isolated is Staphylococcus aureus (60%-90%),^14,15 although Gram-negative bacteria are more common in intravenous drug users.^7,16 Interestingly, individuals who use intravenous drugs have been found to have higher carrier rates of S. aureus than the general population. Thus, the source of SEA pathogen in IVDU patients may be their chronic carrier state rather than the paraphernalia itself.^10,17-19

SEA more commonly affects the thoracic and lumbar spine, where the epidural space is wider. There is a more extensive extradural venous plexus, with an average abscess extension of 3-5 spinal cord segments.²⁰ SEA may present with symptoms measured in hours to days (acute) or weeks to months (chronic), or a combination of both.¹³ Neurologic symptoms are generally thought to result from mechanical compression, but the exact mechanism of spinal cord necrosis is still unclear. Some authors suggest vasculitis, thrombosis, and/or compression of the spinal vessels with resultant hypoxia as either a contributing factor or primary mechanism.^21-24

Risk Factors

Although injection drug use is the most common hematogenous source of SEA, accounting for 52% of cases in some populations, diabetes mellitus is the most common risk factor overall,⁷ followed by trauma, intravenous drug use, and alcoholism. These patient groups are thought to possess cellular and humoral immune system dysfunction.⁷ Less common risk factors are malignancy, end-stage renal disease, epidural anesthetics, vascular access, spinal trauma, and degenerative joint disease, most of which facilitate entry of pathogens by disruption of normal anatomic barriers.⁷

Signs and Symptoms

SEA is a great imitator, making early diagnosis difficult. It is estimated that 51% of patients have more than two emergency department visits prior to diagnosis,²⁵ even though 98% had at least one known risk factor.²⁵ Patients generally seek medical attention at a median of 7 days.²⁶

Back pain is the most common symptom.²⁵ The “classic” triad of SEA (fever, back pain, and neurologic deficits) is uncommon and present in fewer than 20% of patients. Absence of fever is not reassuring, as only a third of patients with SEA report a history of fever. Unrelenting pain, which is exacerbated at night, is very worrisome both for malignancy and infection.²⁷

A history of minor trauma is often offered as an explanation for the pain in 19% of patients, while 14% report a history of chronic back pain.²⁵ This trauma may distract the emergency physician from considering SEA in the differential diagnosis. Symptoms typically progress from back pain and localized tenderness to muscle weakness, sphincter incontinence, sensory deficits, and finally paralysis if untreated.⁷

Physical Exam

The physical exam alone is not sensitive for detecting SEA, and neurologic examination has been documented as normal in more than two-thirds of patients during the initial emergency department visit.²⁵ Either cursory neurological examinations or poor charting is demonstrated by the lack of documentation of a digital rectal examination for roughly half of all patients with SEA.²⁵ Usually some minimal notation as to a “nonfocal” neurologic examination is often documented, but specific details regarding sensation, strength, reflexes, and cerebellar function are often absent.²⁵

Back pain is usually localized to the midline, with marked tenderness to percussion of the spinous process.²⁷ Radicular pain or neurological deficits are found in 62% and 41% of patients, respectively.²⁵

When assessing for cord compression, it is important to note that the physical examination is less sensitive than a history of urinary retention. Several features of the examination can be helpful. For example, sensory and motor deficits, as well as a positive straight leg raising test, occur in about 80% of cases.²⁷ More specific findings include saddle anesthesia, which has a sensitivity of about 75%, and diminished anal sphincter tone with a slightly higher sensitivity.²⁷ In addition, it is important that during the physical exam, particular attention is given to the entire integumentary and musculoskeletal system to assess all potential sources of infection.

Diagnostic Studies

Recommended laboratory studies include blood cultures (which have excellent correlation with pathogenic abscess organisms and are helpful in guiding antibiotic therapy),^14,15 complete blood count, and erythrocyte sedimentation rate (ESR).

A normal white blood cell count (WBC) is insufficient to rule out the diagnosis. In fact, in Davis et al., the WBC count was elevated in only 60% of patients. However, the ESR was elevated above 20 mm/h in 98% of patients, although it was frequently obtained after admission and in patients in whom the diagnosis was already suspected.²⁵ The ESR may also be used to guide therapy, because it has been shown to correlate with disease resolution.^14,15

Conventional radiographic investigations are not helpful,^10,14,16,21 as sclerotic changes are present only after the SEA has developed into a chronic condition.²⁸ Gadolinium-enhanced MRI is the imaging modality of choice, as it is accurate in defining the extent of the abscess along with the degree of thecal sac compression.²⁹ MRI also aids in the differentiation of SEA from spinal tumors, hematomas, transverse myelitis, spinal cord infarction, or intervertebral disk prolapse.²⁹

If MRI is unavailable, CT myelography is an equally sensitive diagnostic option^{10,14,15,21,24,30} and is the most commonly used diagnostic method worldwide,⁷ despite possessing an inherent increased risk of infection.^31,32 CT without myelography is noninvasive but can make delineation of the spinal cord from the epidural space difficult.³²

Lumbar puncture is contraindicated, as it carries the risk of spreading bacteria into the subarachnoid space with resultant meningitis, and should not be performed.^7,26

Management

Surgical drainage and associated laminectomy within 24 hours of presentation are the mainstay of therapy.^4,14 Laminotomy also has been performed in an attempt to preserve the integrity of the spine following operative drainage^33-35 and is especially advantageous for children by allowing for attempted closure of the posterior covering of the spinal canal.⁷ Interventional radiology is an alternative for cases in which the SEA is small and therefore suitable for attempted CT-guided aspiration and drainage.⁴

Although these infections are usually monomicrobial,^17,29,36,37 broad-spectrum antibiotic therapy covering S. aureus, E. coli, and P. aeruginosa should be initiated early after blood cultures are obtained,^38,39 and urgent infectious disease consultation should be sought.

In most instances, vancomycin combined with a cephalosporin having antipseudomonal activity (ceftazidime or cefepime) or meropenem is indicated until culture results can provide information to tailor therapy.⁴⁰ In selected cases in which the patient does not have risk factors for nosocomial drug-resistant organisms, empiric therapy with nafcillin (or oxacillin), combined with a third-generation cephalosporin (ceftriaxone or cefotaxime) may be appropriate.⁴⁰ Regardless of antibiotic selection, the duration of treatment is usually a minimum of 4-6 weeks.^7,40

Trial Therapies

Nonsurgical treatment is a viable option for selected patients, including poor surgical candidates, those with bleeding tendencies, lack of neurological deficits, or complete paralysis for more than 3 days.⁷ Those patients with large abscesses extending from the cervical to the lumbar segments may also be candidates for conservative treatment.^13,41

In general, the most important prerequisite for nonsurgical treatment is that the diagnosis must be made before the initial onset of neurological deficits.¹² Close, continued monitoring is essential to ensure immediate surgical intervention at the first sign of deterioration.⁴² The rarity of SEA overall precludes a prospective randomized trial that would elucidate the role of medical versus surgical treatment of SEA.⁴²

Specific treatment options, however, are not determined by the emergency physician, who should consider all cases of SEA neurosurgical emergencies.²⁹

Hyperbaric oxygen (HBO) has been used to treat a variety of infected and hypoperfused wounds.⁴³ Although the mechanism by which HBO acts as a beneficial adjunct in treating SEA is not completely understood, it is thought to enhance the direct bactericidal or bacteriostatic effect of antibiotics.⁴³ There is anecdotal evidence of a cervical epidural abscess managed conservatively with HBO and antibiotics after initial treatment failure from antibiotics alone.⁴³ HBO has also been used in conjunction with laminectomy.⁴⁴

Prognosis

Prior to the 1930s, most patients with SEA died. The mortality of SEA dropped from 34% in the period of 1954-1960 to about 15%^7,45,46 in 1991-1997. Complete recovery can be expected in about 45% of patients,⁷ but permanent neurologic sequelae remain common.

The duration of neurologic impairment has a significant influence on outcome. Not surprisingly, the longer the duration of symptoms such as bowel/bladder dysfunction or paralysis, the poorer the prognosis.⁴⁷ The most significant factor contributing to duration of symptoms is delay in diagnosis, with the most common misdiagnosis being meningitis, followed by intervertebral disk prolapse, urinary tract infection, and vertebral osteomyelitis.⁷

In a study by Davis et al., residual weakness remained in 37% of SEA patients (91% of whom had suffered a diagnostic delay).25 SEA patients without paralysis preoperatively or whose paralysis had developed less than 36 hours before the operation had better prognoses with respect to survival and recovery of function.²² In contrast, no patients with paralysis developing 48 hours or more before surgical decompression showed recovery of neurologic function.²²

Better outcomes are found in younger patients or those with thecal sac compression less than 50%. The prognosis is also better if the abscess is located in the lumbosacral region, likely because of less nerve root compression in this location compared to the direct cord compression that occurs in the cervical or thoracic spine.⁴⁷ Patients with anteriorly located SEA have an increased risk of osteomyelitis, with a resulting worse prognosis.⁴⁷

Conclusion

Nearly every publication on spinal epidural abscess emphasizes timely treatment to avoid or reduce permanent neurological disability. Risk factor assessment along with a thorough physical examination may afford a better screening strategy than simply using the presence of the “classic triad” for identification of SEA patients. This underscores the importance of considering SEA in high-risk patients and initiating a workup in the emergency department to avoid potentially catastrophic delays.

In summary, “The problem with spinal epidural abscesses is not the treatment, but its early diagnosis.”⁴⁸

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