|Year : 2015 | Volume
| Issue : 1 | Page : 46-51
Epidural abscesses following chronic pain injections
Hariharan Shankar1, Hossam Hamda2, Patrick Russell3, Stacy Peterson3
1 Department of Anesthesiology, Clement Zablocki VA Medical Center, Wisconsin, USA
2 Department of Radiology, Clement Zablocki VA Medical Center, Wisconsin, USA
3 Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
|Date of Web Publication||1-Dec-2014|
Department of Anesthesiology, Clement Zablocki VA Medical Center, Medical College of Wisconsin 5000, West National Avenue, Milwaukee, Wisconsin - 53295
Source of Support: None, Conflict of Interest: None
This report will present two cases of epidural abscesses following pain interventions and review available evidence and provide preventive strategies for its avoidance. A 54-year-old man having chronic low back and leg pain with past history significant for alcohol dependence and lumbar spine surgeries received a caudal epidural steroid injection following multiple intravascular injection of contrast. Eleven days following the procedure he developed symptoms suggestive of epidural abscess. It was subsequently confirmed by magnetic resonance imaging (MRI) and underwent nonsurgical management of the abscess without any neurological deficit. A 50-year-old homeless man with history of intravenous drug abuse, alcohol abuse, hepatitis C positive, squamous cell carcinoma of the neck, and degenerative lumbar disc disease received trigger point injections to his lumbar paraspinal muscles for management of his myofascial pain syndrome. Fifteen days following the injection, he reported to the emergency (ER) room with complaints of worsening pain. An MRI revealed epidural; abscesses tracking from the paraspinal muscles. He was subsequently managed with intravenous antibiotics and recovered uneventfully. Following review of the literature, it is possible to come up with preventive strategies to mitigate the occurrence of epidural abscesses. One of the key factors is the presence of comorbid conditions including diabetes mellitus and prior spine surgery which may dictate technique for the management of pain.
Keywords: Adverse effects, complications, spinal epidural abscess
|How to cite this article:|
Shankar H, Hamda H, Russell P, Peterson S. Epidural abscesses following chronic pain injections
. Indian J Pain 2015;29:46-51
| Introduction|| |
Spinal epidural abscess (SEA) is a rare but serious complication, which may occur spontaneously or following various interventions. The recent multistate breakout of meningitis following injection of contaminated steroids has drawn additional interest.* SEA has been reported spontaneously and following pain clinic interventions like intradiscal therapy, facet joint injections, epidural steroid injections, spinal cord stimulator trial, vertebroplasty, and acupuncture. ,,,,,, The reported incidence of SEA is 0.2-2.8 per 10,000 hospital admissions per year. , In an analysis of admissions to a university hospital secondary to bacterial meningitis, Gaul et al., identified eight patients with history of paravertebral injections prior to admissionfor meningitis estimating risk at 1/1,000.  We present two cases of SEA following pain clinic interventions, discuss available evidence for diagnosis and management, and suggest preventive strategiesthat may aid the establishment of guidelines to decrease the development of SEA.
| Case Repor|| |
A 54-year-old male presented to the pain management clinic for management of his chronic mid low back and left > right leg pain in L5-S1 distribution. The pain was rated as 8/10, worse with bending and twistingand better with lying flat. There was no associated sensory disturbance or motor weakness. He reported no bowel or bladder incontinence. The patient's past medical history was significant for alcohol dependence, ulcerative esophagitis and hypertension. He had undergonemultiple lumbar surgeries including a L4-S1 laminectomy and fusion. He had received facet steroid injections with minimal relief and caudal epidural steroid injections with approximately 4 weeks of pain relief. Sensory andmotor examinations and deep tendon reflexes were normal. Extension of his spine was limited due to pain. Straight leg raise was positive bilaterally at 40°. His most recent magnetic resonance imaging (MRI) revealed osseous fusion with laminectomies, arachnoiditis, facet arthropathy, multilevel degenerative disc disease, and a far lateral L3-4 disc herniation contacting the left L3 nerve root.
He requested another caudal epidural steroid injection for pain relief. Following informed consent, with the patient prone, the area was prepped twice with isopropyl alcohol, followed, after drying, with 2% chlorhexidine gluconate and 70% isopropyl alcohol formulation twice (ChloraPrep, CareFusion Corporation, San Diego, CA) as is the normal protocol at our center. Fivemilliliter of 1% lidocaine was used for anesthetizing the skin at the point of entry. A 16 gauge R.K. epidural needle (Epimed, Farmers Branch, TX) was introduced with intermittent fluoroscopic guidance through the sacral hiatus into the caudal epidural space. A 19-gauge Brevi-XL catheter (Epimed, Farmers Branch, TX) was subsequently advanced to the L5-S1 level through the epidural needle. Digital subtraction angiography (DSA) revealed epidural as well as vascular spread ofiopamidol 300. DSA was repeated after withdrawing the catheter approximately 1cm. As there continued to be vascular spread despite repeated withdrawing of the catheter until the needle hub [Figure 1], the epidural needle was repositioned and a new 19-gauge catheter was advanced to the L5-S1 level. Following DSA,10 ml of injectate containing 80 mg methylprednisolone, 2 ml of 1% lidocaine, and 6 ml of preservative free normal saline were injected. The needle and catheter were removed after flushing with sterile preservative free normal saline. There were no apparent immediate complications.
|Figure 1: Fluoroscopic AP image of the sacrum following contrast injection through a caudally placed catheter showing linear spread and subsequent lateral spread (broad arrows) of contrast from the catheter tip (long arrow)|
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Eleven days following the procedure, during a mental health visit, the patient complained of persistent pressure and pain in the low back. He reported to us that he had increased pain and pressure in the buttocks and posterior thighs along with urinary dribbling. Despite our advice to seek immediate medical attention, he decided to visit the emergency room (ER)only the following day. On physical examination, neurological examination was intact. His complete blood count including differential, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and urine analysis were within normal limits. An MRI of the lumbar spine initially was reported as having no significant changes since the prior MRI. The following weekday, 2 days later, the neuroradiologist reviewed the MRI and noticed two small epidural abscesses anterior to the thecal sac at L4-5 and L5-S1 (largest 10 mm × 4 mm). The patient was immediatelyadmitted to the hospital. Neurosurgery opined that the abscesses were too small for surgical intervention. Infectious disease consultants recommended 6 weeks of meropenem (2 g Q8h) and daptomycin (600 mg daily) intravenously to provide broad spectrum coverage as culture was not feasible. He was neurologically intactduring his hospital stay. His pain was managed withmorphine sustained release 15mg twice daily with oxycodone 5 mg every 4 hprn. Inflammatory markers including ESR and CRP remained within normal limits for the duration of his hospital stay. Post-antibiotic MRI of the lumbar spine at 6 months showed resolution of the epidural abscess with persistent enhancing epidural soft tissue at L5-S1, suggestive of unchanged postsurgical fibrosis. He recovered uneventfully, except for his low back pain which was subsequently managed with hydrocodone prn.
A 50-year-old homeless veteran living at the dormitorywas referred by neurosurgeon for conservative management of low back pain following a fall 12 years prior. His past medical history was significant for spinal stenosis, degenerative disc disease, facet arthropathy, hepatitis C with elevated liver enzymes, intravenous drug abuse, and cocaine and alcohol abuse. His pain was constant, burning with occasional shooting down the legs to the feet with no specific dermatomal pattern. He rated his background pain as 7/10, made worse by prolonged sitting, standing, or any activity. He had tried nonsteroidal anti-inflammatory drugs (NSAIDs) with limited benefit. He had previously been on oxycodone and was switched to propoxyphene with moderate control. He had stopped physical therapy due to pain. His MRI revealed degenerative disc disease at L4-5 and L5-S1 with multilevel facet arthropathy, severely narrowed foramina at L4-5 and L5-S1 with likely compromise of the bilateral L4 and L5 nerve roots, respectively. Neurological examination was normal including FABERs and straight leg raise. A diagnosis of myofascial pain with possible facet arthropathy was considered. He was started on cyclobenzaprine 10 mg prn and encouraged to participate in physical therapy including the use of transcutaneous electrical nerve stimulation (TENS). As he reported no benefit, a diagnostic medial branch block was performed which provided no pain relief. He was subsequently found to have squamous cell carcinoma of the neck with metastasis to the cervical nodes for which he received chemotherapy and radiation. His pain complaints were subsequently managed with opioids given the new diagnosis by his oncology team. When he complained ofintolerable back and leg pain, a caudal epidural steroid injection was performed as there were no spinal metastases. This provided him only a week of pain relief. Given the multiple comorbid conditions, with predominantly low back pain, we elected to perform trigger point injections. He receiveda total of six trigger point injections to his lumbar paraspinal musclesafter wiping the area with alcohol wipe with a 25 g 1.5-inch needle using 1% lidocaine. Patient reported immediate improvement of his pain.
Fifteen days after the trigger point injections, he reported to the emergency room complaining of exacerbation of his low back pain and tingling in his right lower extremity. Despite limited examination due to pain, overall weakness was noticed. When pain was not controlled with intravenous opioids, given the history of malignancy, alumbar spine MRI was performed which revealed, newright-sided multiloculated epidural abscesses starting at the L4-5 level with extension into the right facet joint and right paraspinal muscles [Figure 2]. His CRP was 165 mg/l and ESR rose to 90 mm/h. Gram-positive cocci were found in blood. After consultation with infectious disease and neurosurgery, a nonoperative treatment was planned. He was started on intravenous vancomycin and later switched to cefazolin when blood culture revealed methicillin-sensitive Staphylococcus aureus. Patient was discharged approximately 2 months later in a stable condition. Follow-up MRIshowed resolution of abscesses. His pain wassubsequently managed with tramadol and hydrocodone under close supervision.
|Figure 2: (a) Sagittal T2-weighted STIR image demonstrates multiple posterior epidural collections at L4-5, and L5 levels (arrows) worrisome for multiple posterior epidural abscesses. (b) GAD-enhanced fat saturated axial T1-weighted image demonstrates right posterior epidural collection with marginal enhancement (long arrow) worrisome for posterior epidural abscess. Abnormal enhancement of the right and left facet joints (arrow head) and multiple paraspinal ring enhancing collections (short arrows) are worrisome for facet septic arthritis and multiple paraspinal abscesses. (c) Sagittal T2-weighted STIR follow up image demonstrates complete resolution of the multiple posterior epidural abscesses. (d) GAD-enhanced fat saturated axial T1-weighted MRI follow up image demonstrates complete resolution of the multiple posterior epidural and the paraspinal abscesses. The persistent bilateral facet enhancement (arrows) is due to hypertrophic|
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| Discussion|| |
This report discusses the presentation and nonsurgical management of SEA in two different types of pain clinic interventions with varied comorbid conditions. These two cases of SEA are out of approximately 16,000 procedures performed at our center between 2005 and 2013 giving an incidence of 1.25 per 10,000 which is similar to the incidence reported in prior publications. , Reasons for the development of SEA in our patients could be postulated based on existing reports.  Prior spine surgery and history of alcohol dependence, preexisting conditions common in those who go on to develop SEA, was present in our first patient. Perineum is an arearife with organisms. After prepping the area with alcohol, followed by ChlorPrep and waiting for the manufacturer recommended time for its efficacy, it would be expected that the area of needle entry would be sterile. Hematoma, however small, could have provided a nutrient-rich medium for organisms from the needle tract. The injectate used was not compounded and was obtained from a reputed manufacturer. Unlike prior reports, our first patient did not have elevated white blood cell (WBC), ESR, or CRP at presentation. Report of persistent postprocedural pain to the mental health provider was immediately relayed to our clinic for appropriate workup. Our neuroradiologist notified us immediately following the detection of an incorrect MRI read by the covering resident stressing the importance of effective communication in patient management.
History of intravenous drug abuse, carcinoma, and hepatitis C were present in oursecond patient; which have been reported in those who developed SEA.  Of note, he had received an uncomplicated steroid injection in the past. The only possible source may have been incomplete sterilization of the skin, with alcohol, prior to trigger point injection. As he was homeless, it is quite likely that he may not have had facilities for a shower prior to the procedure.
Both our patients' time to reporting symptoms of SEA falls within the previously reported range.  Despite conservative management, both our patients recovered completely without neurological deficits.
Review of all the reports of SEA available in the literature poses some interesting common threads in their occurrence, diagnosis, and management. The following summarizes our present knowledge about the features and management of SEA in the pain clinic:
Patients who developed SEA were more likely to have Diabetes mellitus, prior spine surgery, immunocompromised states or prior history of intravenous drug use. Other reported risk factors include local or systemic infection, alcohol abuse, trauma, invasive procedures, malignancy, hemodialysis and smoking [Table 1]. ,,, By affecting the neutrophil and macrophage responses to inflammation and infection, these factors including smoking impair the body's ability to fight invasion by organisms. 
Sources of infection
The following are possible sources of infection: Skin (the most common source), local infection, systemic infection with hematogenous spread, unsterile technique, unsterile needles, and contaminated injectates including diluents, local anesthetics, and steroid.  Several studies have compared topical disinfectants prior to invasive procedures and have shown chlorhexidine to be the more efficacious agent with a relative risk of 0.2 compared to povidone iodine. ,, Most earlier reports of SEA following interventional pain procedures were in cases where povidoneiodine was used for skin disinfection.
Staphylococcus aureus is the most commonly cultured organism in SEA (70%).  In the case of SEA following spinal interventions, Staphylococcus species are the most common pathogen with methicillin-resistant Staphylococcus aureus (MRSA) topping the list. , Other reported organisms include, Streptococcus viridans, Klebsiella pneumonia, Escherichia More Details coli, and some fungal species. 
Pain clinic interventions reported to have caused epidural abscess include: Trigger point injections, epidural catheterization for analgesia, epidural steroid injections, facet steroid injections, intradiscal interventions, and vertebroplasty. ,
Common presenting symptoms in those with SEA include constitutional symptoms like fever (60%), chills and headache, besidesworsening back pain (70%), neurological deficits (30%)with or without paralysis, and bowel/bladder incontinence.  Physical exam findings may include inflammatory signs in the overlying skin, tenderness to palpation, muscle weakness, sensory disturbance, and if delayed severe neurological deficits [Table 2].
Diagnosis can be challenging secondary to the nonspecific nature of most complaints in those with SEA leading to a delayed diagnosis (up to 70%).  The average reported time to initial complaints is variously reported as 7-14 days.  Diagnostic delays could be avoided with suitable decision trees and appropriate cost effective use of resources. Using an algorithmic approach, almost a 70% reduction in delays and 60% reduction in the incidence of neurological deficits has been demonstrated. 
Patients with SEA often have leukocytosis and elevated inflammatory markers. In those with spinal pain having risk factors for SEA, increased ESR has a high degree of sensitivity (100%) and less specificity (67%) in identifying SEA. ,, MRI with gadolinium contrast is presently the most commonly used imaging modality due to lack of radiation although computed tomography (CT) myelogram, a more invasive diagnostic procedure, is equally sensitive and had been used extensively in the past. ,, Patients with spinal metal hardware or any other contraindication to MRI are offered CT myelogram.
Preoperative neurologic status dictates the risk of permanent neurological consequences. Among patients with SEA, those with shorter duration of neurological symptoms, abscesses in the lumbar area, <50% thecal sac compression, and younger patients appear to have a better prognosis.  A prompt neurosurgical consultation to minimize neurological sequelae is suggested, though percutaneous drainage has also been reported in the literature. , Reported management options include surgical drainage, percutaneous drainage, or medical management with antibiotics in those with either surgical risk factors or without neurological deficits. , Medical management is usually preceded by image-guided biopsy and blood cultures prior to initiating antibiotics. Blood and abscess cultures have high concordance. The duration of antibiotic therapy has not been definitively determined, but 6-8 weeks of intravenous antibiotics are usually an accepted duration by infectious disease consultants.
Review of available literature shows some common features in those who go on to develop SEA. Although most reports allude to preventive strategies, no clear outlines exist. This may be because of the low incidence, the large sample size required and ethical dilemmas in conducting a randomized controlled trail. The following is an attempt, based on the available evidence, to establish strategies to prevent the occurrence of SEA.
- Patient selection: Patients having an immunosuppressive state including diabetes mellitus and with prior history of spine surgery may be considered for noninterventional management or at the very least not involving steroid injection. This is one of the most important preventive strategies as many reports have documented higher incidence of SEA in those with diabetes mellitus and prior spine surgery. But at present other options are limited for interventional pain management. As the duration of pain relief following epidural steroid injections has been demonstrated to be only short term, a consideration may be given for neuromodulation in this select population.
- Site of entry: When the target may be reached by an alternate route, the route with the least amount of background organisms prior to skin preparation should be chosen, for example, caudal versus interlaminar approach.
- Sterile precautions: All interventional procedures in those with preexisting immunosuppression, diabetes mellitus, and prior spine surgery should be performed by adopting universal sterile precautions including cap, mask, and sterile gloves. In addition, during time out, product verification including examination of contents and expiration date should be included. It may be suggested to the patient to have a shower prior to arrival for the procedure.
- Skin prep: Chlorhexidine should be utilized for all interventions including strict adherence to time to drying of the agent.
- Needle in needle technique: A strong consideration should be given for using the needle in needle technique especially where the skin flora is likely to be high at the needle entry site.
- Early detection: Better outcomes have been reported in those whose diagnosis was established earlier. To facilitate this, a follow-up phone call in 2-5 days to specifically enquire about worsening back pain should be encouraged.
Although one could argue for prophylactic antibiotic administration in those with risk factors, it may potentially delay the occurrence of SEA and most importantly may lead to antibiotic resistant organisms.
| Conclusion|| |
SEA is one of the most distressing complications of pain clinic interventions with significant morbidity. These cases of SEAillustrate the importance ofhigh degree of suspicion, early detection, and treatment to avoid more deleterious sequelae. Following some of the suggested preventive strategies, based on a synthesis of information from published literature, may help prevent the occurrence of SEA.
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[Figure 1], [Figure 2]
[Table 1], [Table 2]