Introduction

Since its first description in G.B. Morgagni´s landmark work De sedibus et causis morborum per anatomen indigatis libri quinque, ¹ published in 1761, spinal epidural abscess (SEA) has been a rare entity of infectious disease associated with mortality rates as high as 80 to 100%. High morbidity and mortality rates have been steadily lowered with the advent of surgical decompressive techniques, namely laminectomy, since the early 20th century, and antimicrobial agents since the 1940s, but SEA remains a potentially life-threatening condition; recent publications have cited mortality rates ranging from 2 to 31%. ² , ³ Moreover, the incidence of SEA seems to be on the rise: Baker et al ⁴ reported an annual incidence of 0.2 to 1.2 per 10,000 hospital admissions in 1975, but more recent publications reported remarkably higher rates, reaching 2.5 to 3 per 10,000 hospital admissions. ² More patients with known risk factors (see below) for the development of SEA are among the reasons for the observed increase in SEA incidence rates.

Etiology

Spinal epidural abscess is an infectious process located in the epidural space of the spine (cervical 15%, thoracic 50%, lumbar 35% ⁵ ), which is initiated by microorganisms that cause an inflammatory response. Typically, Staphylococcus aureus is found in specimens from SEA, accounting for 60 to 90% of cases. ⁶ , ⁷ Methicillin-resistant S. aureus (MRSA) is also reported with increasing frequency. ⁷ Other bacterial organisms causing SEA include: Streptococcus, Escherichia coli, Pseudomonas aeruginosa, Diplococcus pneumoniae, Serratia marcescens, and Enterobacter. In chronic SEA, Mycobacterium tuberculosis is found in at least 25% of cases worldwide. Fungal and parasitic infections are seen less frequently. These include Cryptococcus, Aspergillus, Brucella, and Echinococcus.

There are three patterns of infection of the spinal epidural space:

1. 
   

   Direct inoculation of microorganisms via spinal procedures (lumbar puncture, dorsal epidural injections, spinal surgery, stab wounds, other types of wounds)

   
   
2. 
   

   Extension of inflammation per continuitatem from neighboring infection sites, such as spontaneous spondylodiskitis, psoas abscess, urinary tract infection including pyelonephritis and paranephritic abscess, pharyngeal abscess, mediastinitis, vertebral osteomyelitis, and decubital ulcers

   
   
3. 
   

   Hematogenous spread from other organ systems: among these patterns, skin infections such as furuncles are most common, followed by intravenous (IV) injections (especially with drug abuse), bacterial endocarditis, urinary tract infections, respiratory tract infections, and dental and pharyngeal infections

Following the diagnosis of SEA, diagnostic tests to determine the specific site(s) of primary focus of infection are obligatory. Physicians should be aware of the various entry sites and initiate ear, nose and throat (ENT), cardiology, dental, urological, pneumological, abdominal, or dermatological consultations, whenever the cause of infection remains vague.

Patients with one or more of the following conditions are prone to develop SEA due to decreased immunocompetency: diabetes mellitus (15%), chronic renal failure (2%), IV drug abuse (9%), HIV infection (1%), immunosuppressive therapy including long-term corticosteroids (7–16%), and alcoholism (5%). These risk factors are well known, ² , ⁶ and their presence should help to enhance the diagnosis of SEA in patients with precarious symptoms.

Symptomatology

According to Heusner, ⁸ the initial symptomatology of SEA classically includes back pain, spine tenderness, and fever. In the second stage, spinal irritational signs such as Lasègue’s, Kernig’s, Lhermitte’s, or Brudzinski’s signs are encountered, sometimes along with pain radiating into the arms or legs, followed by motor weakness, bowel or bladder dysfunction, and sensory deficits, which can rapidly (< 24 hours) advance into the last stage of paralysis. Unfortunately, the classic triad of early symptoms of SEA is not always present, leaving the physician with a single nonspecific symptom that can be seen in a large number of other spinal and extraspinal conditions. Thus, postoperative SEA may be associated with very few symptoms in the early stages. Additional encephalopathy may draw the attention away from the spine as a source of symptoms. ⁹ Meticulous attention to the patient’s description of symptoms and short-term follow-up combined with diagnostic tests should prevent the physician from making a misdiagnosis or a late diagnosis.

Diagnostic Tests

Laboratory tests, although not specific, can enhance the diagnostic process. Usually, the erythrocyte sedimentation rate is increased by more than 30%, and elevated serum C-reactive protein levels and leukocyte counts are seen especially in patients with acute SEA.

Although elevated leukocyte counts of cerebrospinal fluid (CSF) specimens are often found as a sign of inflammation, we do not encourage the use of lumbar or cervical epidural or CSF puncture close to abscesses as a diagnostic tool for verification of SEA, as these procedures carry a risk of promoting the infection to the intrathecal space.

Radiographic tools are used to confirm the clinical diagnosis. Magnetic resonance imaging (MRI) is the imaging modality of choice. Lesions can be best detected on sagittal and axial images, with a T1-weighted hypointense and T2-weighted hyperintense epidural mass, which typically enhances with gadolinium contrast. Enhancement can include the complete mass, or only patches, or have a ring-like appearance as a result of different stages of the abscess formation.

Other imaging modalities are far less specific: computed tomography (CT) in conjunction with myelography can show epidural mass extensions in patients not amenable for MRI scanning. However, the intrathecal injection of contrast media close to SEA holds a significant risk of distributing the inflammatory process leading to meningitis or myelitis.

Treatment Options

Historically, decompressive laminectomy was the first treatment for SEA. When antibiotics became available in the 1940s, with sulfonamides among the first substances used, nonsurgical therapy became another option in patients without neurocompression.

Nowadays, treatment is unequivocally surgical in most cases of SEA, especially in the presence of a neurologic deficit, followed by antibiotic treatment (initially empirical, secondarily specific to the causative microorganism) as soon as specimens for microbiological examination have been collected.

There is good evidence in the literature that surgery plus antibiotic treatment is superior to antibiotic treatment alone, even if no neurologic deficit is noted upon presentation, and that early surgery is superior to late surgery. ⁵ , ¹⁰ – ¹⁵

Patients considered unable to undergo surgical therapy, or those with persisting complete neurologic deficit lasting longer than 48 hours, with little concern about an ascending lesion, or those who are neurologically stable and lack risk factors that portend the failure of medical treatment may be initially treated with antibiotics alone and close clinical monitoring. ⁵

Surgical evacuation of pus is generally achieved by laminectomy, which enables a wide posterior decompression of the thecal sac and spinal cord. Posterior decompression is viable for anteriorly, posteriorly, and circumferentially located SEA, because all these locations can be reached without significant distortion of the thecal sac or spinal cord. If an anterior SEA is associated with spondylodiskitis or vertebral osteomyelitis, which by itself is recommended to be treated with anterior or lateral diskectomy or corpectomy together with anterior/lateral instrumentation, anterior decompression may be considered through the opening of the epidural space. However, this procedure carries a risk of disseminating the infectious process to the retropharyngeal, mediastinal, pleural, or retroabdominal space. Surgical principles for treatment of vertebral osteomyelitis and spondylodiskitis should be followed (see Chapter 6).

The exact extent of surgical decompression is tailored to the lesion as depicted by MRI, with multiple levels of involvement requiring longer decompressions. But multilevel decompressions can lead to instability and thus require a simultaneous stabilization of the vertebral column. Attempts to reduce the size of the decompression, and thereby potentially reduce the chances for postoperative instabil ity by choosing minimally invasive techniques, have been reported only in small case series with comparable results of recurrence and residual abscess. ¹⁶ , ¹⁷ Laminotomy and laminoplasty have been used, together with open surgical irrigation of the epidural space from one or more entry points, in multilevel SEA. CT- or fluoroscope-guided percutaneous catheter insertion with irrigation has been used predominantly in children, but the case numbers remain small. ⁵ In light of these studies, percutaneous CT-guided aspiration is discouraged due to the risk of intrathecal dissemination and the possibility of inadequate decompression due to the remaining solid fragments of the abscess formation.

Following laminectomy, the abscess wall is opened using microhooks. Pus or inflammatory tissue available from the lesion is harvested for microbiological cultures. Greater manipulations to resect the abscess wall must be avoided, as this might lead to (new) neurologic deficits. Irrigation with Ringer’s solution decreases the concentration of microorganisms and inflammatory substances and should be used extensively. Antibiotic additions (e.g., gentamicin) can be used at the discretion of the surgeon, but no evidence citing any advantages exists. Ultrasound may guide the surgeon to remnants of granulation tissue that may still compress the thecal sac. A subfascial extraspinal suction drain can be inserted for evacuation of pus or blood. Continuous postoperative irrigation and suction should be reserved for recurrent cases, as irrigation may lead to dural compression.

Instrumented stabilization is warranted in all cases, where postoperative instability is deemed possible, especially in cases of simultaneous spondylodiskitis and vertebral osteomyelitis.

Antibiotic therapy is the second mainstay of SEA treatment. Selection of an appropriate agent depends on the microorganism found in the SEA specimen. The yield of the surgical specimen is fairly low (~ 40%), especially in chronic lesions. In these cases, blood cultures taken preoperatively may increase the likelihood of finding the causal microorganism. Because S. aureus is the most likely microorganism, third-generation cephalosporins are used as the empirical antibiotic, and vancomycin is used in cases where MRSA is not ruled out. If SEA is combined with spondylodiskitis or vertebral osteomyelitis, bone-penetrating agents should be considered, such as clindamycin. The selection of the appropriate antibiotic agents should also be based on the microorganisms that are typically the underlying cause, whether the cause is diverticulitis or a urinary tract infection. If in doubt, consult a microbiologist.

Antibiotic therapy should be continued for at least 3 to 4 weeks. Bioavailability should be considered in the choice of the antibiotic agent, when switching from IV to peroral administration. Most authors suggest a period of 6 to 8 weeks for treatment. Discontinuation is possible when clinical symptoms and signs have subsided and laboratory findings (erythrocyte sedimentation rate, C-reactive protein) have returned to normal levels. However, follow-up laboratory tests should be performed for a couple of weeks to rule out recurrences. Follow-up MRI is only helpful in patient who do not respond adequately to antibiotic therapy and in whom recurrence is known or suspected, as MRI reliably depicts reduction of the abscess size. ¹⁸