Lumbar epidural steroid injections (LESI) are commonly used for lumbar radicular complaints as a therapeutic and diagnostic modality. LESI have increased exponentially in the Medicare population since the 2000s (1-3). These procedures are typically used as a treatment option for lumbar radiculopathy prior to surgical intervention. Failure of improvement in symptoms or deteriorating neurological function following epidural injections usually warrants surgical consideration.
Post-operative infections following lumbar decompression without the use of instrumentation are thought to be low with rates ranging from 0.7% to 2.4% (4,5). There have been conflicting studies on risk of epidural injections to post-operative infections in lumbar decompression (6,7). There are also no studies to our knowledge that evaluate the association of LESI and readmission following lumbar decompression.
The purpose of this study was to determine if a recent history of spinal epidural injections predisposed patients to post-operative infections following non-instrumented lumbar decompression. We also sought to determine if there are certain time intervals that can be established as being at higher risk so that practitioners can appropriately counsel patients regarding the risks of injections and subsequent decompressions.
A thorough evaluation of the PearlDiver database (PearlDiver Technologies, West Conshohocken, PA, USA) was performed for patients undergoing lumbar decompression for spinal stenosis or disc herniation without instrumentation from 2005–2014. PearlDriver is a privately owned dataset containing a full sample of Medicare data. This data set contains various interventions and conditions based on current procedure terminology (CPT) codes and International Classification of Diseases 9th Revision Clinical Modification Diagnoses and Procedures (ICD-9-CM). All of the data is anonymous and de-identified, therefore no institutional review board is required. Medicare was the nationwide insurance provider for our patient selection.
Inclusion parameters were those having undergone primary lumbar decompression for spinal stenosis or disc herniation without instrumentation (CPT: 63030, 63047). Patients undergoing lumbar fusion procedures (CPT: 22612, 22614, 22633, 22630, 22830), and revision lumbar procedures (CPT: 22830, 63042, 63044) were excluded. Data for patients who underwent LESI was also queried (CPT: 64483, 62311). Ninety-day postoperative infection was assessed using ICD-9 codes (998.5, 998.51, 998.59, 996.67) and CPT codes (20005, 22015) (Table S1).
Utilizing Boolean operations, a control group was created for comparison purposes, which included all patients meeting the above procedural criteria without a previous documented LESI. This control group was matched to the 3 study cohorts by using the maximum number of available patients with a similar distribution of variables: age, gender, race, region and comorbidities such as hypertension, auto immune deficiency, body mass index, chronic kidney disease, diabetes, chronic liver disease, chronic obstructive pulmonary disease, hyperlipidemia, cardiac disease, and tobacco use. Matching was performed strictly on a one-to-one basis, where for every patient in the cohort study, one patient in the control group was selected. The matched cohorts were then assessed by the average Charlson-Comorbidity Index (CCI) to ensure adequate matching. Matching with the CCI allowed for a more accurate comparison between the two groups.
Statistical comparisons of cohort demographics and postoperative infection rates between the study and control groups were performed using Pearson chi-square analysis. Odds ratios and their 95% confidence intervals were calculated. For all statistical comparisons, P<0.05 was considered significant. SPSS software (version 22 for Macintosh, IBM) was used for all statistical calculations.
The database was queried for patients undergoing primary decompression without fusion, identifying 4 groups: (I) lumbar decompression with no 6-month LESI history (n=8,090); (II) lumbar decompression performed within 0–1 month after LESI (n=755); (III) lumbar decompression between 1 and 3 months after LESI (n=3,209); (IV) lumbar decompression performed between 3 and 6 months after LESI (n=4,126). The study groups each had a P value of 1.00 compared to the control group (n=8,090), indicating no difference was found between the study and control groups (Table 1).
The rate of post-operative infection was low in all time periods, ranging from 1.98% to 1.40%. Patients having LDC within a month after their LESI had greater odds of infections (OR =1.37; 95% CI, 0.62–3.00; P=0.43), but no statistical significance was found in this group compared to the matched control group. In the LDC 1 to 3 months following a LESI, there was a statistically significant higher incidence of 90-day postoperative infection compared to the matched control group (OR =4.69; P<0.001). Similarly, patients who had a LDC 3 to 6 months following LESI had a statistically significant higher incidence of infection compared to the matched control group (OR =5.33; 95% CI, 2.79–10.17; P<0.001) (Table 2).
The association of intra-articular corticosteroid injections and surgical site infection has been well documented in other orthopaedic subspecialties (8-11). While there are some existing studies evaluating LESI and infection rates following spine surgery, these studies have shown conflicting results regarding the correlation between LESI and risk of post-operative infection with various spine procedures (6,7,12). Eismont et al. used a canine model undergoing serial epidural steroid injections to compare the impact of corticosteroids on dural tissue (13). In this study they demonstrated a 27% decrease in dural tensile strength as well as a 72% decrease in mitochondria volume in those canine given serial epidural injections compared to the control group. This current study illustrates a statistically significant increased risk of post-operative infection when LESI was placed 1–6 months prior to a primary single level lumbar decompression without fusion. Fortunately, the overall incidence of infection for this specific cohort remained low (1.4–1.98%).
The use of epidural injections for lumbar radiculopathy is relatively safe. A recent study of 52,935 patients who received LESI reported major complications in only 6 patients (0.011%), 4 of which developed infection, and 2 developed hematomas (14). Despite the low incidence of infection following epidural steroid injection, multiple case reports have shown possible devastating complications, including extensive spinal abscesses, discitis, and death (15-20). These infections are theorized to occur for various reasons. First, direct contamination or inoculation from skin flora may lead to infection. Secondly, glucocorticosteroids function by directly or indirectly reducing the inflammation process, which can limit the immunological response to indolent or early infection (21). Singla et al. suggests a critical time period may exist before the immunosuppressive properties of glucocorticoids resolve (12). The pharmacokinetics of these theories have not been further studied. It is reasonable to believe that these processes could be active for months when considering patients who receive these injections report relief of symptoms due to glucocorticoids for months, indicating the glucocorticoids may be active in this space (12). This group also suggests the glucocorticoids prevent the natural host response to tissue injury and pathogen exposure, which leads to increased susceptibility to infection (12). It is also proposed that epidural injections can lead to epidural scarring, increased vascularization and promotion of degenerative changes at the injection site, which can potentially complicate the surgical site also (22). These multifactorial concerns all may contribute to the increased risk of surgical site infection. Though the anti-inflammatory properties of steroids may be advantageous in the pre-operative period and relieve patients of their symptoms, in the post-operative period, the anti-inflammatory properties may be detrimental.
LESI as a risk factor may be confounded by the length of surgery due to severe stenosis (9,12). It can be postulated our cohort that required a LESI prior to a subsequent spinal decompression was more likely to have a more severe stenosis that was not able to be relieved with injections or postponed beyond 6 months. An explanation for the increased infection rates in the LESI 1–6 months cohort is that potentially these patients would require slightly more decompression and an increased length of surgery since operative time is another known risk factor for surgical site infection (23).
An inevitable limitation in this study is the use of an insurance database which requires accurate human input, and so there is the potential for missed and incorrect data. Additionally, we were unable to account for the amount of previous LESIs which may predispose the patient to additional infection risks or indicate more severe stenosis. This dataset also does not indicate the length of surgery or post-operative discharge disposition which also could indicate the complexity of the case or patient condition. It is also feasible that LESIs cause indwelling latent infections that are not included in a review of the 90-day post-operative course. Lastly, while a multivariate analysis of comorbidities was not possible, we accounted for this difference in comorbidities with the use a matched control group based on CCI (24,25).
While LESI is helpful for possibly delaying or avoid lumbar surgery, it may predispose patients to higher infection and readmission rates following lumbar decompressions without fusion. This study provides additional evidence for the increased risk of post-operative infection in lumbar decompression performed after LESI. It also proves evidence for an increased risk of readmission following lumbar decompression after LESI. Surgeons and pain management specialist should counsel patients on these risks and possibly modify the time to surgical intervention.
Conflicts of Interest: The authors have no conflicts of interest to declare.
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