Spinal epidural abscess is a suppurative infection of the central nervous system. Although classically patients with spinal epidural abscess present with midline back pain, fever, and neurologic deficits, presentations of this disease process can be variable. Spinal epidural abscess is difficult to diagnose if clinical suspicion is not high. When left untreated spinal epidural abscess can cause significant morbidity and mortality. Thus any clinical concern for this diagnosis requires prompt evaluation and treatment.
In patients presenting with spinal epidural abscess, bacteria enter the epidural space resulting in a suppurative infection. Most often, the bacteria enter the epidural space through hematogenous spread. Risk factors for spinal epidural abscess include immunosuppressed state (i.e., diabetes mellitus, alcoholism, cirrhosis, end-stage renal disease, HIV infection), intravenous drug abuse, direct instrumentation (i.e., acupuncture, paraspinal or epidural injection, lumbar puncture, CNS surgery), and bacteremia. Diabetes mellitus is the most common risk factor associated with spinal epidural abscess, although intravenous drug use and epidural catheter placement are becoming increasingly important risk factors in the development of this disease process.
Spinal epidural abscess is an uncommon diagnosis. The incidence of this disease process is 1.2 per 10,000 patients. Although spinal epidural abscess is uncommon, its incidence has been increasing in recent years. This increased diagnosis is thought to be because of expanded utilization of invasive spinal procedures, increasing age of the population, and increasing rates of intravenous drug use.
In one-third of cases of spinal epidural abscess, there is no identifiable nidus of infection. Diabetes mellitus is the greatest risk factor for a spinal epidural abscess. In total, 33% of patients presenting with spinal epidural abscess have diabetes mellitus. Other important risk factors for the development of spinal epidural abscess include intravenous drug use and instrumentation of the epidural space. In intravenous drug use, hematogenous seeding of the epidural space occurs which leads to spinal epidural abscess. Instrumentation of the epidural space occurring during lumbar puncture or epidural catheter placement can directly inoculate bacteria into the epidural space causing this infectious process. Of note, the incidence of a spinal epidural abscess after epidural catheter placement is approximately 0.5% to 3%.
Staphylococcus aureus accounts for 63% of spinal epidural abscess infections, followed by gram-negative bacilli (16%), streptococcal infections (9%), and other bacteria/mycobacteria/fungi accounting for ~10% of infections.
Bacteria enter the epidural space and seed the area between the dura mater and vertebral wall within the spinal canal. This introduction of bacteria into this normally sterile space results in a suppurative infection within this confined area. Most commonly this occurs via hematogenous seeding of the epidural space. Hematogenous spread can occur from soft tissue infections, infected catheters, endocarditis, urinary tract, or respiratory tract infections. Bacteria also can enter the epidural space through the direct extension of infected tissue. This occurs when psoas abscess, vertebral osteomyelitis, or discitis leads to spinal epidural abscess. Additionally, a spinal epidural abscess can be the result of direct inoculation of this tissue. Epidural injections, epidural catheter placements, lumbar punctures, and other central nervous system (CNS) procedures all can result in epidural abscess through direct inoculation.
Infection also can be the result of the contiguous spread of an infection such as vertebral osteomyelitis, discitis, retropharyngeal abscess, retroperitoneal abscess or through penetrating injury, epidural injection or catheter placement, lumbar puncture, or recent CNS surgery.
Once bacteria have gained entrance into the epidural space, a resulting pyogenic infection occurs which then results in abscess formation. Damage to the spinal cord may occur through a number of mechanisms including (1) direct compression from expanding abscess, (2) thrombosis and thrombophlebitis of adjacent veins, (3) interruption of arterial blood supply, and (4) bacterial toxins.
Typically spinal epidural abscess will involve 3 to 5 spinal cord segments. Given that spinal epidural abscesses most commonly are caused by hematogenous spread, 9% of patients presenting with this diagnosis will have two or more noncontiguous areas of pyogenic collections.
The classic triad of a spinal epidural abscess is back pain (75%), fever (48%), and neurologic deficits (33%) due to the direct compressive effects of the abscess. The classic triad presents in as few as 8% of patients, thus if clinical concern exists for this disease prompt diagnostic evaluation must be undertaken.
Pain may be elicited through palpation or percussion of spinous processes overlaying spinal epidural abscess. Pain also may be elicited through straight leg raise from compression of spinal nerve roots. As this disease process progresses patients will develop neurologic deficits consistent with spinal cord or cauda equina compression: urinary retention, bowel incontinence, anesthesia (perianal and saddle anesthesia), motor weakness, or paralysis.
Lab evaluation should include blood cultures, complete blood count, inflammatory markers, and coagulation studies. These studies often will reveal elevated white blood cell count and elevated inflammatory markers. Although the erythrocyte sedimentation rate is often elevated in these patients, it does not rule out the diagnosis of spinal epidural abscess (85% to 94% sensitivity).
Positive cultures by frequency in specimen type is (1) abscess aspirate: 90%, (2) blood: 62%, and (3) CSF: 19%.
If there is a concern for spinal epidural abscess, patients should undergo immediate MRI of the entire spine. If MRI is unavailable, CT with IV contrast is an alternative although less sensitive.
Lumbar puncture is unnecessary as it lends little diagnostic utility and has potential morbidity in the setting of spinal epidural abscess.
Emergent surgical Spineconsultation is the standard of care all patients with radiographic findings epidural abscess and abnormal neurological examinations due to mass effect from an epidural abscess. These patients usually require an emergent surgical evaluation to decompress the spinal cord and nerve roots.
Overall, the treatment of spinal epidural abscess focuses on elimination of the suppurative mass and eradication of the causative organism. This is accomplished through aspiration, surgical drainage, and antibiotic therapy. The assistance of interventional radiology or spine surgery (orthopedics or neurosurgery) will be required in the management of many if not all of these patients
Death and paralysis are the most feared complications of spinal epidural abscess. Death occurs in 5% of patients typically due to sepsis. Paralysis occurs in 4% to 22% of patients with a spinal epidural abscess. If paralysis occurs, surgery should be performed within 24 to 36 hours of the onset of paralysis. Recovery of neurologic function is unlikely if paralysis occurs greater than 24 hours prior to surgery.
Empiric antibiotic regimens should include vancomycin (30-60 mg/kg) plus a third or fourth generation cephalosporin (2g cefotaxime Q6H, 2g ceftriaxone Q12H, 2g ceftazidime Q8H, or 2g cefepime Q8H) until speciation and sensitivities of the infecting organism result for more targeted antibiotic therapy. Typically, patients will require a prolonged course of antibiotics (4 to 6 weeks) to treat this infection.
Repeat MRI should be obtained if the patient has worsening symptoms, deteriorating clinical exam, or at 4 to 6 weeks of therapy.