Lumbar Epidural Injection

• Discogenic pain
• Sciatica
• Spinal stenosis
• Post surgical pain
• Failed back surgery syndrome

The mechanisms by which steroids exert their analgesic effects have been debated for many years. Corticosteroids inhibit the enzyme phospholipase A2, an inflammatory mediator present in elevated concentrations in herniated and degenerative intervertebral discs, but its main role is as the rate-limiting factor involved in the production of arachidonic acid, which is the principal substrate for the cyclo-oxygenase and lipo-oxygenase pathways. Metabolism by these pathways results in the formation of the four different classes of eicosanoids: prostaglandins, prostacyclins, thromboxanes, and leukotrienes. Prostaglandins, along with these other arachidonic acid byproducts, can cause or exacerbate pain via their inflammatory effects and ability to sensitize peripheral nociceptors. In addition to their anti inflammatory effects, steroids may inhibit pain via their ability to suppress ectopic discharges from injured nerve fibers and depress conduction in normal unmyelinated C fibers.

Several proposed mechanisms for the beneficial effects do not involve steroids. The injection of local anesthetic can increase blood flow to ischemic nerve roots and, similar to steroids, suppress ectopic discharges from injured neurons and slow or halt nociceptive transmission. Moreover, the administration of saline, local anesthetic, or any non-steroid solution can exert an analgesic effect via the washout of inflammatory cytokines and the adhesiolysis of scar tissue.

The efficacy of epidural steroid injections is difficult to determine because of the multiple and heterogeneous factors associated with the injection and their outcome assessment. Differences in injection route, region, control group, injectate characteristics and patient pathology contribute to variation in outcomes and present challenges in the interpretation of existing studies regarding epidural steroid injections. Yet, there is a widespread consensus across specialties that epidural injections provide at least short-term benefit in well-selected patients. What is less clear is which patients are likely to benefit from the intervention, and whether they provide long-term pain relief.

The conceptual appeal of epidural steroid injection is that the pain relief from the procedure will allow the body time to heal itself, without the long-term sequelae associated with central sensitization.

Another rationale for the use of epidural steroid injection is fact that the evidence in support of the procedure is more robust, and the risk-benefit ratio more favorable, compared with other treatments. Among randomized clinical trials evaluating surgery for neuropathic low back pain and neck pain irrespective of etiology, most demonstrate temporary (i.e. 6 months) but not long-term benefit.

Epidural steroid injections may be administered via different routes including transforaminal (TF), interlaminar (IL), and caudal routes. The route is chosen by the physician on the basis of the type of spinal pathology and the level of the spine that is affected by the pathology.

There are no clinical trials examining the ideal number of epidural injections. Numerous guidelines have determined that the number of injections should be individually tailored to clinical response.

Complications associated with the epidural administration of corticosteroids are uncommon. Nevertheless complications can occur, as with any invasive procedure, and steps should be taken to minimize this.

Infection following epidural injections is rare. Epidural abscess is a condition that can occur spontaneously, in the absence of injection or instrumentation of the spinal canal. Spontaneous epidural abscesses are commoner in diabetic patients as shown by Tang et al in their review of 46 cases of spontaneous epidural abscess and found that 46% occurred in diabetic patients. Common presenting symptoms include paralysis, localized spinal pain, radicular pain, and chills and fever. ESR is generally raised.

Rapid recognition of illness and prompt initiation of therapy are the cornerstones of management for infectious complications. Most cases of epidural abscess require surgical drainage. Surgical decompression is urgently indicated if there is any neurologic compromise. While waiting for cultures, treatment with antibiotics that cover Staphylococcus aureus and Staphylococcus epidermidis is appropriate, as these are the most commonly isolated organisms.

Meticulous sterile technique with attention to skin preparation should prevent the large majority of infectious complications. Steroid injections should be avoided if there is any active infection. The incidence of infection following epidural steroid injections is too low to justify routine prophylactic antibiotic use, and there are no data to support the benefit of prophylaxis in immune compromised patients. Routine pre procedure antibiotic administration can lead to the development of resistant strains of pathogens.

This can occur from direct injury to the spinal cord or the nerve roots. Another mechanism of injury is the injection of steroid suspension into a spinal medullary artery with embolization of end arterioles supplying the spinal cord, but this appears to be less common that direct needle trauma to the spinal cord. Direct injury to the spinal cord or dorsal nerve root could occur even without dural puncture, when narrowing or obliteration of the epidural space caused by a large disc herniation, displaces the spinal cord posteriorly. More severe neurologic injury occurs if material is injected into the spinal cord, which is more likely to occur in those who are deeply sedated and unresponsive during the procedure.

High-dose intravenous steroids administered in the hours immediately following traumatic spinal cord injury have been shown to result in a significant reduction in neuronal injury.

Both epidural and subdural hematomas have been reported following epidural steroid injections in patients without coagulopathy or concurrent use of anticoagulants. The most important risk factor for bleeding is coagulopathy, either primary or pharmacological. Anticoagulants like warfarin and antiplatelet drugs such as clopidogrel, rivaroxaban and digabatran are contraindications to epidural injections. On the other hand, NSAIDs, including aspirin, do not appear to appreciably increase the risk of epidural bleeding. The discontinuation of medications in patients receiving antithrombotic or thrombolytic therapies before epidural steroid injections is not devoid of risks and the decision must be made after careful consideration of the risks and benefits, in consultation with a specialist.

Because of its location at the distal end of the spinal column, its shallow depth (which enables compression) and the fact that it can easily be accessed with a small gauge needle, the caudal approach might be considered when an epidural steroid injection is strongly indicated and the risk of discontinuing warfarin or antiplatelet therapy is high.

Accidental dural puncture during attempted epidural injection is associated with a headache incidence of greater than 50%. Introduction of air into the subdural or subarachnoid space during attempted epidural needle placement can produce pneumocephalus and an immediate headache that can last up to several days. Conservative management of postdural puncture headache includes bed rest, hydration, caffeine, and mild analgesics. Following known dural puncture, an epidural blood patch can quickly and effectively reduce or eliminate the ensuing spinal headache.

Glucocorticoid administration reduces the hypoglycemic effect of insulin and interferes with blood glucose control in diabetic patients. Following injection of depo-steroids, diabetic patients can experience significant increases in blood glucose levels and insulin requirements for 1 to 2 days after injection. Glucose levels in diabetic patients should be monitored closely during the first 2 days following any type of steroid injection. Patients need to be informed that adjustment of their insulin dose may be required.

Exogenous administration of glucocorticoids can result in a clinical pattern called ‘cushingoid’ syndrome. On the other hand steroid injections can cause suppression of plasma cortisol levels. The most prudent guiding principle is to use repeated steroid injections only in those who experience significant benefit and to space the injections at long-enough intervals to allow complete recovery of adrenal function.

Direct neurotoxicity caused by the unintentional intrathecal injection of corticosteroid suspensions has been hypothesized to result in arachnoiditis and aseptic meningitis in some individuals. However, the link between intrathecal corticosteroid administration and these neurotoxic syndromes is not clear. Arachnoiditis is an inflammatory condition involving the leptomeninges and the underlying neural structures. Commonly encountered symptoms include constant burning pain in the lower back and legs, urinary frequency, incontinence, muscle spasms in the back and legs, variable sensory loss and motor dysfunction. Adhesive arachnoiditis is a severe and often progressive form that is associated with neuropathic pain and neurologic dysfunction. The intrathecal injection of neurotoxic substances can result in arachnoiditis if there is sufficient chemical irritation or inflammation. Aseptic meningitis is a generally benign condition that produces signs of neurological irritation, including burning pain in the legs, headache, meningismus, and in severe cases, seizures. Fever and nausea are often present.