Spinal Epidural Abscess
Neurologists may encounter a patient with a spinal epidural abscess when consulted for "weakness." Infectious or noninfectious compressive extramedullary mass lesions require urgent diagnosis and management.
A spinal epidural abscess develops in the space outside the dura but within the spinal canal. An epidural abscess may develop in the space anterior or posterior to the spinal cord.
Heusner described the classic presentation of a spinal epidural abscess in 1948. The initial symptom is back pain at the level of infection. Fever may be present, but does not always occur. The neurosurgical literature describes the progression of symptoms in stages, which assists in predicting prognosis. Solitary back pain is referred to as stage 1. In stage 2, back pain is followed by radicular pain in the extremities or pain in a cervical, thoracic, or lumbar dermatomal distribution. As the infection progresses to stage 3, there is paresis of appendicular musculature, loss of sensation below the level of the lesion, and loss of bowel and bladder control. Finally, in stage 4, there is complete paralysis of appendicular muscles and loss of sensation below the level of the lesion.
Pathogenesis and Etiological Organism
A spinal epidural abscess develops by one of the following mechanisms: (1) as a result of the hematogenous spread of infection during the course of bacteremia from a remote site of infection; (2) from a contiguous site of infection (vertebral osteomyelitis/discitis, soft tissue paravertebral abscesses) (Figure 2A, B); (3) direct extension of infection from decubitus ulcers, infected abdominal wounds, or psoas abscesses; (4) trauma causing a locus minoris resistentiae allowing for hematogenous seeding of infection; and (5) direct inoculation during spinal instrumentation or epidural analgesia. Staphylococcus aureus is the most common causative organism followed by gram-negative bacilli.
(A) Sagittal T2-weighted magnetic resonance imaging (MRI) demonstrating discitis/osteomyelitis cord edema with compression. (B) Sagittal T2-weighted MRI shows progression of abscess.
Several factors are critical to the development of a differential diagnosis: the extent and tempo of the development of back pain and appendicular weakness, the presence or absence of a sensory level, the presence or absence of bowel and bladder involvement, the presence or absence of deep tendon reflexes, and the presence or absence of pathological reflexes. Osteomyelitis and discitis should be considered when fever and back pain precede the development of radicular pain, and when the neurological examination does not demonstrate signs of spinal root or cord compression. Thoracic transverse myelitis (TM) classically presents with back pain followed by lower extremity weakness and bowel and bladder dysfunction. TM affecting the cervical cord presents with back pain and upper extremity weakness. Similar to those with a spinal epidural abscess, TM can cause appendicular weakness, a well-defined sensory level, and absent or decreased deep tendon reflexes. The Guillain–Barre syndrome (GBS) presents as an ascending weakness with loss of the deep tendon reflexes. Urinary retention may develop in the course of the illness as a symptom of autonomic dysfunction, but is not a typical feature of the acute presentation of GBS.
Back pain, fever, weakness, the presence of a sensory level, the absence of deep tendon reflexes, and the presence of pathological reflexes is a spinal epidural abscess until proven otherwise.
Routine studies for suspected spinal epidural abscess include complete blood count with differential, erythrocyte sedimentation rate, C-reactive protein, and blood cultures. The neurologic exam findings should help to localize the lesion. Imaging should be targeted at the predicted area of the spinal epidural abscess as well as a few levels above and below. MRI is the recommended imaging study (Figure 2A, B), but a CT scan with contrast will also demonstrate the abscess.
Initial empiric antibiotic therapy should include a combination of vancomycin and a third- or fourth-generation cephalosporin to cover the most common etiological organisms of spinal epidural abscess: Staphylococcus aureus and gram-negative bacilli.
The majority of patients with spinal epidural abscess requires an emergent decompressive laminectomy at one or more levels with drainage of the abscess. Gram's stain and culture of the purulent material obtained at the time of surgery allows for identification of the infecting organism and modification of the antimicrobial coverage based on the organism and antimicrobial sensitivity testing of the bacterial culture.
The neurological deficits from a spinal epidural abscess can be attributed to one or a combination of the following: (1) compression of the spinal cord, (2) compression of the arterial blood supply, (3) arterial or venous thrombosis, or (4) septic thrombophlebitis. The prognosis therefore is dependent on the mechanism of spinal cord injury.
Spinal cord compression is the pathophysiology of the patient's neurological deficits when the neurosurgeon sees pulsation of the spinal cord in the operative field postdecompression. When the mechanism of injury is spinal cord compression, the single most important predictor of the final neurologic outcome is the patient's neurologic status immediately before surgery. Patients who undergo surgery with back pain or back pain plus radicular pain are expected to have a good outcome without neurological deficits. Those that undergo surgery with paresis, are expected to have either no weakness or a lesser degree of weakness postoperatively. Patients who are plegic but operated on within 24 to 36 hours of the development of paralysis are expected to regain some strength in the paralyzed extremities.
Similarly, the neurosurgeon is able to visualize thrombosed arteries and/or veins intraoperatively. When vascular pathology is the mechanism of spinal cord injury in spinal epidural abscess, recovery postsurgery is not likely. The vascular pathology may be compression of the arterial blood supply, an arterial or venous thrombosis with spinal cord ischemia, or thrombophlebitis with hypoxia secondary to obstructed venous drainage of the cord. Both cord compression and vascular pathology may be the mechanism of spinal cord injury in any individual patient.
Semin Neurol. 2019;39(3):334-342. © 2019 Thieme Medical Publishers