Medial epicondylitis primarily affects the pronator teres and flexor carpi radialis, which attach to the anterior aspect of the medial epicondyle. These muscles are subject to repeated trauma and micro‐tearing either because of repetitive overuse or less often because of a direct blow or sudden extreme contraction.2
Repetitive forearm pronation and wrist flexion is thought to be the most likely culprit. The term epicondylitis was used to describe this condition as early theories postulated an inflammatory process involving the bursa, periosteum, synovium and annular ligament.9,10
However, the preferred term now is tendinoses, as there are many pathological studies which have shown that there is micro‐tearing with disruption of the collagen bundles, vascular and fibroblast proliferation, focal hyaline degeneration and an incomplete reparative process with no evidence of any inflammatory process.11
Histological analysis by Nirschl and Pettrone has shown that there is disruption of normal architecture with later stages demonstrating micro‐tearing, tendon degeneration and aborted, incomplete neurovascular response.11
They have called these changes “angiofibroblastic hyperplasia”. Macroscopically, the pathologic tissue appears grey and friable. A chronic cycle of tendon micro‐tearing, degeneration and repair ensues with weakening of the common flexor origin and potential for rupture.
Nirschl has proposed four descriptive stages of epicondylar tendinosis.12
Stages 1 and 2 represent pathologic tissue alteration with angiofibroblastic degeneration. Structural failure is the hallmark of stage 3. Stage 4 shows fibrosis or calcification.
Diagnosis is usually based on clinical findings. Ultrasound or MR imaging is useful for diagnosing other conditions such as ulnar neuritis and ulnar collateral ligament instability as these may co‐exist. Very few studies describe the imaging findings in medial epicondylitis, probably because of the relatively low prevalence of this condition compared to lateral epicondylitis. A study by Kijowski and de Smet evaluating the MR findings in medial epicondylitis concluded that intermediate to high T2 signal intensity within the common flexor tendon and the presence of paratendinous soft tissue oedema were the most specific findings.13
Three out of the 15 patients in their study had tears of the ulnar collateral ligament and one had an abnormal ulnar nerve. No studies discuss the sonographic features of medial epicondylitis, but two reports describe the sonographic features of lateral epicondylitis4,8
and a third examines dynamic ultrasound in the evaluation of the ulnar collateral ligament.14
Non‐surgical treatment has been the mainstay of treatment for epicondylitis2
and includes RICE (rest, ice, compression and elevation), topical medications such as dimethylsulfoxide, oral non‐steroidal anti‐inflammatory analgesics, counter‐force braces and physiotherapy. Although conservative treatment is described as being the most successful, one study has shown that 26% of such patients have recurrence of symptoms and 40% have prolonged minor discomfort.15
Surgical treatment is recommended in patients who fail to respond to conservative treatment. Again there are few reports on the surgical treatment of medial epicondylitis. However, one study reported an 87% success rate in patients (n
26) after an average follow‐up of 7 years,16
while another reported good results in 14 of 17 patients.17
The use of local steroid injection for tendinosis is well documented. The mechanism of short‐term relief following steroid injection or needling is not understood. However, it is postulated that fenestration of an area of tendinosis with needling may promote beneficial bleeding into new channels created through mucoid degeneration. The mechanical disruption may initiate a healing response in the tendon.4,18
One study showed a significant decrease in pain after 6 weeks, but there was recurrence of the pre‐injection pain after 3 months and 1 year.19
Another study showed pain relief in up to 89% of patients, but again there was recurrence of symptoms in 54%.20
Autologous blood injection is a novel treatment for tendinosis. No studies have investigated the efficacy of this treatment for medial epicondylitis, although two studies have evaluated its use in lateral epicondylitis. One report by Edwards and Calandruccio showed that 22/28 patients responded to autologous blood injections, with average Nirschl scores decreasing from 6.5 to 2.0 with a mean follow‐up of 9.5 months.4
Another study by Connell et al
showed good response, with decreased modified Nirschl scores from a median pre‐procedure score of 6 (6–7) to 0 (0–1) at 6 months and significant reductions in VAS scores in 33/35 patients with refractory lateral epicondylitis.5
In our study, local anaesthesia was achieved by injecting all patients with 0.25% bupivacaine along the superficial surface of the tendon. Rigorous dry needling was followed by injection under guidance of autologous blood into the areas of tendinosis. Dry needling fenestrates the tendon causing further fibril disruption and local bleeding before the blood injection. All patients had a second injection after 4 weeks which we postulate is the optimal time interval. Two patients returned for a third injection.
In our group of 20 patients, there were three clear treatment failures with recurrence of the pain to the pre‐injection level. Two of these patients have had a successful tendon repair and one is still awaiting surgery. There were no identifiable features at baseline ultrasound to suggest a poor outcome in this group. We excluded patients with intra‐articular pathology or substantive tears of the tendon. As in most procedures, we believe that patient selection is critical to the success of treatment. All patients with partial or full‐thickness tears of the common flexor tendons or involvement of the ulnar collateral ligament are referred directly to surgery.
There are a number of limitations to our study. The most obvious one is that all sonographic observations were made by a single radiologist and hence we have no measure of either intra‐ or inter‐observer variability. There is no control group and the subject bias inherent in our study was unavoidable. At study outset, we opted to use colour Doppler, although it could be argued that power Doppler may be more sensitive and less susceptible to flow direction. Although we believe that dry needling and autologous blood injected into a area of tendinosis induces a healing response with the formation of scar tissue, we have no histopathological correlation and the exact mechanism is not completely understood.
What is already known on this topic
- Medial epicondylitis or golfer's elbow represents an incomplete healing response to repetitive micro‐trauma and interstitial tearing of the common flexor tendon.
- Non‐surgical treatment is the established method of treatment for medial epicondylitis.
- Autologous blood injection is described as a novel method of treatment for tennis elbow.
- The hypothesis for the mechanism is that the transforming growth factor‐β and basic fibroblast growth factor carried in the blood act as humoral mediators to induce the healing cascade.
What this study adds
- Our study demonstrates that the combined action of dry needling and autologous blood injection under ultrasound guidance is an effective way to treat patients with refractory medial epicondylitis.
- We have also demonstrated a significant decrease in pain scores and the modified Nirschl scores.
- Although autologous blood injection has been described as a novel method of treatment for tennis elbow, this method of treatment has not been previously reported in the medical literature for refractory medial epicondylitis.
In summary, we feel that the combined action of dry needling and autologous blood injection under ultrasound guidance is an effective treatment for patients with refractory medial epicondylitis as demonstrated by a significant decrease in VAS pain and a fall in the modified Nirschl scores. However, further research to explain the exact mechanism of healing by this technique and analysis of the various studies regarding the use of this technique in other tendinopathies is essential.