Spinal epidural abscess (SEA) following SCS implantation is a rare but life-threatening complication that will require surgical explantation of the device, evacuation of the abscess, and parenteral antibiotic therapy. Early diagnosis is essential to limit the neurologic compromise that can occur in these cases. In 1948, Heusner et al. classically described four distinct stages of SEA: Stage 1, which includes back pain and tenderness to spine palpation; Stage 2, in which spinal nerve root findings, radicular pain, nuchal rigidity, and hyperreflexia are seen; Stage 3, in which sensory findings, motor weakness, and bladder or bowel dysfunction are found; and finally Stage 4, paralysis [1]. In reality, the progression of symptoms may not be so linear and concrete. Recent studies have shown that the classic triad of “back pain, fever, and neurological deficit” is actually present in only 10% cases of SEA, but when present, it predicts poor outcomes [2].

In the case presented here, the diagnosis is straightforward, but in cases of spontaneous SEA in the absence of a recent spinal procedure or recent surgery, severe back pain with leukocytosis is the most common presenting scenario. A chief complaint of back pain is present in 70–95% of patients with SEA [2–4]. Fever was seen in about 20% of cases in one 10-year retrospective study [2] of patients with SEA and in 54% of cases in another [3]. Motor deficits may be present in 30% of cases of SEA, and bladder dysfunction or frank paresis is seen in about 25% of cases [5]. The mortality rate from SEA is less than 10% and is usually related to overwhelming sepsis or meningitis as a result of the abscess [3, 5, 6]. Approximately 50% of those who are treated for SEA are left with permanent neurologic deficits, including 15% with paresis or complete paralysis [7]. Motor deficits at the time of diagnosis highly correlate with permanent residual motor deficits after treatment [3].

The most common pathogens found in blood and wound cultures are Staphylococcus aureus and Streptococcus species [4]. MRSA was found in 20% of cases in a recent meta-analysis of SEA [4]. Cost of treatment is high. In one recent analysis, the mean total charges incurred for SEA inpatient treatment was $160,000 [5]. Risk factors for rapid clinical deterioration and poor outcomes include a history of diabetes mellitus, C-reactive protein >115, WBC > 12, age > 65, positive blood cultures, and the presence of MRSA [4].

The causes of SEA include hematogenous spread, direct inoculation, or contiguous spread of bacteria from a primary source. Skin and soft tissue infections are common sources of hematogenous spread of bacteria, in addition to urinary tract and respiratory tract infections. The vertebral column is highly vascularized, so hematogenous spread to this region is not unlikely. In this case, dehiscence of the surgical incision from a wound infection may have allowed spread of bacteria into the deeper tissue layers or contiguous spread of bacteria from a wound infection into the epidural space. Optimally, a wound check within 1 week after surgery and better patient vigilance could have mitigated this case, as a superficial wound infection after SCS can usually be treated successfully with antibiotics and not require explantation of the entire SCS system. Alternatively, poor aseptic technique or contamination of the introducer needle or electrode at the time of trial or permanent implantation may have been causes, but direct inoculation would likely cause abscess formation and clinical symptoms more immediately after implantation. In patients with diabetes and a history of smoking, it may be best to stage the percutaneous trial and allow complete healing of the skin prior to proceeding with the permanent implantation of an SCS system in the same region. In one case report, a patient developed back pain and an epidural abscess 3 days following a percutaneous SCS trial [8] and required surgical drainage. In most spontaneous cases of SEA, the bacterial infection is unimicrobial.

The incidence of SEA with SCS implantation is not well studied and is limited to case reports [8, 9]. In a recent retrospective analysis of 131 patients with 142 SCS or programmable pumps at a single institution by Engle et al., the overall infection rate was 2.8% in the first 12 months following implantation. In two of the 59 SCS systems implanted (3.4%), a postoperative infection occurred. In all cases in this series, the infections were at the IPG or pump site, and there were no cases of epidural abscess [10]. Longer operative time was an independent risk factor for these infections. Kumar et al. reported an 8% incidence of infection or wound breakdown following SCS implantation [11]. Follett et al. reviewed medical device reports from 2000 to 2002 from a single SCS manufacturer and analyzed 114 cases of infections related to SCS implantation. In all cases, the indication for SCS implant was non-cancer pain, and 38% of the patients had a medical condition that was a risk factor for increased infection risk. The majority of the infections occurred at the IPG pocket site. Wound cultures were positive for a Staphylococcus species in 48% of cases; a Pseudomonas species was identified in 3%; wound cultures were negative for bacterial growth in 18% of cases [12]. Infections were most likely to occur within the first month following surgical implantation, and in 91% of cases, the infection resolved without complications after treatment [12]. In another large, 20-year literature review of SCS publications by Cameron et al., an infection rate of 3.4% in 2972 SCS procedures was seen [13]. One case of psoas abscess related to implantation of an epidural electrode has also been described [14].