Orthopaedic Surgery/Lateral Epicondylitis
| Lateral Epicondylitis | ||
| <<Repetitive Strain Sydromes | Medial Epicondylitis>> |
Tendinopathy of the common extensor origin also referred to as tendinosis, has replaced the previous moniker, tennis elbow and lateral epicondylitis. In what seems to be a trend to make our nomenclature less assertive as to our professed understanding of the workings of this condition we hope to take a step back and give a broader more fundamental look at the issue. In light of the lack of histologic evidence implicating inflammation it seems appropriate to defenestrate the term epicondylitis from our working clinical vocabulary.
Steroid injections work frequently enough that they are commonly perceived as useful and certainly something to try at least a time or two before any surgical intervention. Histology usually does not include evidence for acute or chronic inflammation. Why then do we use steroid injection? Two reasons seem likely, first it has been the traditional recommendation and secondly, it seems to work by golly, not always but pretty often.
How is this possible in view of the science which tells us there is no inflammation. Recent efforts attempt to tease out an answer. It seems that needling alone, or needling with injection of blood can also meet with success in alleviating symptoms. While this seems to have merit, it has yet to be adopted widely. This may be that the process of drawing blood is inconvenient in the clinic setting, or it may be that it does not work so well. Lidocaine injection takes place from time to time to verify relief of symptoms when considering whether a patient can be predicted to improve with a surgery. The usual scenario is the patient referred having had umpteen cortisone injections and unwilling to have another. I don't believe I have ever seen lidocaine alone, with needling of the tendon origing to affect a lasting benefit.
Is it in fact the needling rather than the steroid. Are we rebooting the healing computer by micotrauma to the tendinous origin, seems doubtful but maybe at some point in the subacute phase this could play a role.
Alternatively, does the steroid in fact cause the partially ruptured fibers which are the source of the symptoms to rupture thus relieving the symptoms. I am reminded of the chymopapain era though, or the clostridial enzyme era (has that passed?) how does it know when to stop dissolving tissue?
Surgery often seems ultimately successful and accomplishes in essence the completion of a tear with variable degrees of removal of grossly abnormal appearing tissue on the assumption that the tissue in situ is a potential source for the pain. Studies seem to indicate that release whether arthroscopic or percutaneous or open seem about equivalent. In view of this success, it seems reasonable to conclude that when steroid injection works it is in essence accomplishing the same thing. When it does not work it may be that while completing some tear it may be setting the ground work for the adjacent tissue to fail and herein lies the concern.
Steroids are often used very early within days or weeks of symptom onset and indeed sometimes a quick cure is achieved. How efficient. What we do not know is whether the early injection of steroid might in some cases interfere with normal healing processes and prevent the successful resolution of the problem in a time frame like 3 to 4 months. Instead with injection at 3 weeks we have a period of relief and then relapse and eventually a chronic problem, perhaps one requiring surgery.