Corticosteroids are believed to provide long-term pain relief because of their ability to inhibit the production of phospholipase A2 (PLA2) and through membrane-stabilising effects - hence their utility for epidural steroid injections (ESIs).
Radicular pain is described as a sharp, lancinating and radiating pain, often shooting from the low back down into the lower extremity in a radicular distribution. Radicular pain is the result of a nerve root lesion or inflammation. ESIs have been recommended to deliver steroids in a more localised fashion to the area of affected nerve roots, thereby decreasing the systemic effect of the administered steroid. Studies have indicated that ESIs are most effective in the presence of acute nerve root inflammation.
Clinical manifestations of nerve root inflammation include some or all of the following: radicular pain, dermatomal hypesthesia, weakness of muscle groups innervated by the involved nerve roots, diminished deep tendon reflexes and positive straight leg-raising tests.
ESIs can provide both diagnostic and therapeutic benefits. Diagnostically, ESIs may help to identify the region and spinal column of potential pain generation through pain relief after local anesthetic injection to the site of presumed anatomical pathology. In addition, if the patient receives several weeks or more of pain relief, then it may be reasonable to assume that an element of inflammation was involved in his or her pathophysiology. This last element of diagnostic information is also the therapeutic element. Since prolonged pain relief is presumed to be due to a reduction in an inflammatory process, it is also reasonable to assume that during the prolonged pain relief, the afflicted nerve roots are also relatively protected from the deleterious effects of inflammation.
Historical evidence of nerve root inflammation has been demonstrated during surgery in patients with radicular low back pain (LBP) from lumbar disc herniation. Animal research in dogs and rats also has revealed severe inflammation locally at the epidural space and nerve root after injection of autologous nuclear material into the epidural space. High levels of PLA2, an enzyme that controls the initial inflammatory cascade, has been demonstrated in herniated disc material from surgical samples in humans. Leukotriene B4, thromboxane B2 and inflammatory products also have been discovered within herniated human discs after surgery. Animal models have demonstrated that injection of PLA2 into the epidural space induced locally demyelinated nerve roots with ectopic discharges, which is considered to be the primary pathophysiological mechanism of sciatica (radicular pain).
Since lumbar radicular pain may originate from inflammation of the epidural space and the nerve root, the analgesic effects of corticosteroids most likely are related to the following mechanisms:
Inhibition of PLA2 and inflammation
Inhibition of neural transmission in nociceptive C fibres
Reduction of capillary permeability
Recent studies have demonstrated positive efficacy of lumbar ESIs when proper placement is confirmed by using fluoroscopic guidance and radiographic confirmation through the use of contrast. Approximately 60-75% of patients receive some relief after ESIs. Benefits include relief of radicular pain and lower back pain, improvement of quality of life, reduction of analgesic consumption and improved maintenance of work status.
Most patients take several days to respond to ESIs. This is generally due to the delayed effects of the corticosteroid. The commonly used compounds with prominent glucocorticoid action include betamethasone sodium phosphate and betamethasone acetate (Celestone Soluspan), methylprednisolone acetate (Depo-Medrol) and triamcinolone hexacetonide (Aristospan). Each milliliter of Celestone Soluspan contains 3 mg of highly soluble betamethasone sodium and 3 mg of the relatively insoluble acetate salt. Thus, Celestone Soluspan provides both rapid onset and extended anti-inflammatory activity.
Depo-Medrol and Aristospan, being relatively insoluble, provide a sustained anti-inflammatory effect. However, the multidose vials of Depo-Medrol contain benzyl alcohol, which is potentially toxic when administered locally to neural tissue and may increase the risk of arachnoiditis or meningitis. Thus, for epidural injections, many physicians prefer to use only steroid preparations without such preservatives. One option is to use only single-dose vials of the corticosteroids because these generally do not contain benzyl alcohol. However, for some steroid products, even the single-dose vials may contain at least some preservatives or antimicrobial additives, so physicians should be aware of all of these factors when deciding on the steroid of choice for injection into the epidural space.
The volume of the injection is dictated mainly by the approach used. In cervical and thoracic epidural injections, a total of 3-5 ml may be used for ESIs using the interlaminar approach. However, in transforaminal ESIs, clinicians generally use a total volume of only about 1.5-2 ml. The volume used for lumbar ESIs is slightly greater, generally using 6-10 ml for interlaminar ESIs, up to 20 ml for caudal ESIs and 3-4 ml for transforaminal ESIs. For interlaminar ESIs, 13 typical corticosteroid doses are 12-18 mg for Celestone and 80-120 mg for methylprednisolone. Half of these steroid doses are generally used when performing transforaminal ESIs. The epidural steroid is injected in a diluent, such as lidocaine (1-2%) and/or normal saline.
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