Kevin P. Murphy, Jeffrey R. Giuliani, and Brett A. Freedman
DEFINITION
Epicondylitis is overuse tendinosis at the elbow, with pain localized to the origin of the lateral common extensor mass or, much less commonly, the origin of the medial common flexor mass.
Lateral epicondylitis (LE), also known as tennis elbow, is the most common overuse injury of the elbow, resulting from repetitive microtrauma at the origin of the extensor carpi radialis brevis (ECRB).
The hallmark clinical finding is pain localized to the lateral aspect of the elbow reproducible with resisted wrist extension and forearm supination.
Medial epicondylitis results from repetitive valgus forces at the elbow, with tendinosis commonly localized to the origins of the flexor carpi radialis and pronator teres, with tenderness slightly anterior and distal to the medial epicondyle.
Nonoperative management is the initial treatment of choice for epicondylitis. It is successful in 90% to 95% of patients.3,10
Nonetheless, for the 5% to 10% of LE patients who fail to respond to nonoperative management and develop chronic recalcitrant symptoms, the senior author's (KPM) treatment of choice since 1995 has been arthroscopic release.
Cadaveric and anatomic studies have shown that elbow arthroscopy and ECRB release is safe, reliable, and reproducible.7,11
The treatment of choice for recalcitrant medial epicondylitis is open débridement of pathologic tissue of the flexor pronator origin. This will not be discussed in this chapter.
ANATOMY
The common extensor tendon origin represents the confluence of four tendons: ECRB, extensor digitorum communis, extensor digit minimi, and extensor carpi ulnaris.
The ECRB origin is on the distal anterolateral aspect of the lateral epicondyle. It covers an area of about 1.5 cm and lies deep to the other three muscles of the extensor mass.
Arthroscopically, the ECRB is the muscle belly and tendon that can be seen lying just superficial to a thinned-out portion of the lateral joint capsule.
The extensor carpi radialis longus actually originates from the lateral humeral supracondylar ridge, 2 to 3 cm superior to the common extensor tendon, and then passes distally, anterior, and superficial to the ECRB.
The lateral ulnar collateral ligament is deep to the extensor tendons and originates from the lateral epicondyle, reinforcing the lateral joint capsule as well as inserting onto the annular ligament and supinator ridge of the ulna.
PATHOGENESIS
The actual pathophysiology of LE is still not completely understood, and minimal advances in our knowledge of the disease process have occurred in the past 2 years.
Proposed causes include bursitis, synovitis, ligament inflammation, periostitis, tendinitis, tendinosis, and extensor tendon tears.
It is widely accepted that LE is not an “itis” or inflammatory condition but rather a tendinosis.6
The most commonly accepted cause today is tendinosis as a result of microscopic tearing of the ECRB muscle with repetitive trauma that causes ingrowth of weakened reparative tissue known as angiofibroblastic hyperplasia or angiofibroblastic tendinosis.
The process of repetitive microand macrotearing can ultimately lead to a spectrum of ECRB tendinosis ranging from fraying to complete tendon failure if the condition is not addressed early.6
NATURAL HISTORY
Epicondylitis responds to conservative management in 90% to 95% of cases.
If treated in the acute setting with activity modification, in conjunction with other conservative modalities, nonsteroidal anti-inflammatory medication may contribute to the alleviation of symptoms experienced with acute LE.
With progressive repetitive trauma, fraying of the tendon and microtears can progress to macroscopic tears and fibrillations of the ECRB, which ultimately could lead to complete tendon rupture or avulsion.
If the lateral joint capsule is involved in chronic LE, it can avulse along with the ECRB tendon and create a lateral synovial cyst or a sense of lateral joint instability.
Chronic refractory LE originates in the ECRB tendon, but it could extend to involve the anterior portion of the extensor digitorum communis, which may ultimately lead to weakness with wrist extension and supination.
Baker et al2 have published an arthroscopic classification system for LE that we have found to be reliable (Table 1).
Rarely, in the chronic setting, treatment may require tendon transfer surgery to restore long extensor function.
PATIENT HISTORY AND PHYSICAL FINDINGS
The pain associated with LE can be secondary to an acute event, but most commonly it is insidious in onset—the result of repetitive microtrauma.
Patients typically report pain with resisted wrist extension and supination with the elbow extended.
It is important to ask the patient about length and type of conservative treatment, history of corticosteroid injections, and response to prior therapy.
Patients who have had a good or excellent initial response to steroids, followed by reaggravation of symptoms, may have resumed strenuous activities too soon or too abruptly and may respond to an additional trial of nonoperative management.
A prior surgical history of the involved elbow is extremely important for operative planning and can contribute to the diagnosis. Furthermore, a history of a prior ulnar nerve transposition could place the ulnar nerve at risk when establishing arthroscopic portals and may require an open approach.
The physical examination should include.
Palpation of the lateral epicondyle–common extensor mass; the surgeon should document the exact location of tenderness to palpation, which is critical for differential diagnosis. This is the most predictive examination for LE.
Resisted wrist extension: Pain with resisted middle finger extension is commonly present in patients with LE but can also be diagnostic for posterior interosseous nerve (PIN) syndrome.
Resisted supination and grip strength: Grip strength is diminished in 78% of patients with LE. Resisted supination elicits pain in 51% of patients. The differential includes bicep tendinitis. Pain with turning a doorknob can also indicate LE.
Chair test: The test is positive when a patient refuses or is unable to lift a chair with the arms forward flexed, elbows and wrists in extension, and forearms in pronation.
The differential diagnosis for lateral elbow pain is long, so it is pertinent to perform a thorough physical examination of both the ipsilateral and contralateral upper extremity, as well as the cervical spine.
The differential diagnosis of lateral elbow pain includes (but is not limited to) the following:
Compressive neuropathy of the radial nerve–radial tunnel syndrome or PIN. The point of maximal tenderness in both radial tunnel syndrome and PIN syndrome is more distal than in LE. PIN syndrome presents with a motor palsy, whereas LE is a diagnosis of pain. Radial tunnel syndrome can be tested for specifically with the resisted middle finger extension test. Selective injections and electrodiagnostics can confirm the diagnosis.
Posterolateral rotatory instability is caused by an injury to the lateral ulnar collateral ligament. Although posterolateral rotatory instability can be associated with mechanical symptoms, the lateral pivot shift test can clinically differentiate instability from epicondylitis.8,10
Osteoarthritis, particularly in the radiocapitellar join.
The physical examination usually causes mechanical symptoms and decreased range of motion.
Radiographs confirm sclerosis, osteophyte formation, loose bodies, and joint space narrowing of the radiocapitellar joint.
IMAGING AND OTHER DIAGNOSTIC STUDIES
Radiographs have been of limited benefit in the diagnosis of LE but should be obtained to rule out other causes of pain or coexisting pathology, especially in recalcitrant cases.
Radiographic evaluation of the elbow in a patient with lateral elbow pain should be limited to an anteroposterior view in full extension and a lateral view with the elbow flexed at 90 degrees.
One study reports an incidence of calcification about the ECRB origin from chronic tendinosis in up to 25% of patients (FIG 1A).9
Historically, magnetic resonance imaging (MRI) has had limited utility in the diagnosis of LE.
MRI can demonstrate ECRB tendon thickening, increased signal on T1 and T2 images, and in advanced disease high T2-signal cystic areas that correspond to partial or complete ECRB avulsions or large areas of mucoid degeneration, which are nonspecific findings for LE (FIG 1B).
Despite its limited specificity for LE, MRI can be a useful, noninvasive technique to visualize concomitant intra-articular elbow pathology and soft tissue pathology.
DIFFERENTIAL DIAGNOSIS
Lateral
Radiocapitellar chondromalacia
Osteochondral loose bodies
Radial head fracture
Osteochondritis dissecans lesion
PIN entrapment
Medial
Inferior cruciate ligament strains or tears
Medial epicondyle avulsion fracture
Ulnar neuritis
Ulnar subluxation
Medial epicondylitis
Osteochondral loose bodies
Olecranon stress fracture
Valgus extension overload syndrome
Pronator teres syndrome
FIG 1 • A. Standard AP radiograph of the elbow showing calcification of the extensor carpi radialis brevis (ECRB) tendon. B. T1-weighted MRI of the elbow. Arrows show intermediate or high signal intensity of the ECRB tendon at its insertion site on the lateral epicondylitis.
Anterior
Anterior capsular strain
Distal biceps tendon strain
Brachialis strain
Distal biceps tendon rupture
Coronoid osteophyte
Posterior
Valgus extension overload syndrome
Triceps tendinitis
Triceps tendon avulsion
Pronator teres syndrome
Olecranon stress fracture
Osteochondral loose bodies
Olecranon bursitis
NONOPERATIVE MANAGEMENT
LE responds to conservative management in 90% to 95% of cases.
Treatment algorithms and modalities are extensive and include rest, activity modification, anti-inflammatory medication, phonophoresis, iontophoresis, massage, stretching, strengthening, counterforce bracing (tennis elbow wraps), sporting equipment modification, acupuncture, extracorporeal shock wave therapy, and corticosteroid injections.
No single nonoperative protocol has proved to be the best, and there is a severe paucity in empiric support for any modality.
Realizing that the natural history of LE appears to be one of spontaneous resolution for most patients within 6 to 12 months, rest and removal of the offending overuse activity is probably the most important component in the initial treatment of LE.
While steroid injections and nonsteroidal anti-inflammatories have been recommended in the treatment of LE, there is little to no empiric evidence to support their use.
A three-stage rehabilitation program with the most widespread acceptance entails rest to reduce pain, counterforce bracing followed by progressive wrist extensor strengthening, and a delayed resumption of inciting activities.
Extracorporeal shock wave therapy has been the most clinically studied nonoperative modality in the past 2 years.
It is difficult to clearly define its role in the treatment of LE given the conflicting results in several studies, along with the relatively short-term follow-up data currently available.
We believe extracorporeal shock wave therapy should be considered a possible alternative to surgery for refractory cases only. It is not a first-line therapy at this point.
SURGICAL MANAGEMENT
Despite 3 to 6 months of nonoperative management, approximately 5% to 10% of patients develop recalcitrant symptoms that may require surgical intervention.
The surgical options include open, percutaneous, and arthroscopic surgical techniques, with success rates that vary from less to 65% to 95% good or excellent outcomes.
The pervasive move toward minimally invasive surgical techniques and the desire for a quick return to full activity have resulted in research and development of safe and effective means for performing arthroscopic releases for LE.
In comparison with open procedures, arthroscopy has several distinct advantages, including the ability to address intra articular pathology, preservation of the superficial common extensor origin and therefore grip strength, faster return to work and sports-related activities, and lower morbidity.
Arthroscopy appears to combine the best attributes of the earlier return to activity seen with percutaneous procedures and the decreased recurrence rates commonly reported with open procedures.
Preoperative Planning
The surgeon must review radiographs and imaging studies for concomitant pathology such as osteochondral loose bodies, radiocapitellar arthrosis, fracture, and injury to surrounding soft tissue structures like the lateral collateral ligament complex.
Under general anesthesia
The lateral pivot shift test, described by O'Driscoll, tests the elbow for a lateral ulnar collateral ligament injury by stressing the elbow in supination, and valgus and axial compression as the elbow is moved from full extension over the patient's head to 20 to 40 degrees of flexion.10
Posterolateral rotatory instability is diagnosed when the radiocapitellar joint subluxes, creating a sulcus proximal to the radial head.
In addition, the surgeon must examine the range of motion of the elbow under anesthesia in full flexion and extension, pronation and supination.
Examination findings under anesthesia should always be compared with the contralateral extremity.
Positioning
The patient is placed in the prone position on the operating table in the standard fashion.
The operative elbow is flexed at 90 degrees and hangs over the bed to gravity. A sandbag may be placed under the operative extremity to maintain elbow flexion.
The surgeon is seated for the procedure.
Approach
As stated previously, LE can be treated with a multitude of well-described open or percutaneous procedures with the goal to débride diseased tissue.
Techniques include partial epicondylectomies, partial resection of the annular ligament, and lengthening (slides) of the extensor tendons.
Our bias is toward arthroscopic treatment.
Numerous arthroscopic portals have been described for elbow arthroscopy, but nine are most commonly used: two medial, four lateral, and three posterior.
When addressing LE, the surgeon must be able to perform a diagnostic arthroscopy of the anterior compartment of the elbow and be able to visualize, evaluate, and address pathology of the lateral capsule and the undersurface of the ECRB tendon.
Absolute contraindications to elbow arthroscopy are distortion of normal bony or soft tissue anatomy that precludes safe portal placement, previous ulnar nerve transposition or hardware that interferes with medial portal placement, or local cellulitis.
Although LE could be addressed through a combination of the different medial and lateral portals, we have had the most success avoiding injury to neurovascular structures and improving visualization with the proximal anteromedial portal as the standard viewing portal and the proximal lateral portal as the working portal.
The proximal anterolateral portal pierces the brachioradialis, brachialis, and lateral capsule before entering the anterior compartment with the elbow flexed to 90 degrees.
This approach places the radial nerve on average 13.7 mm from the cannula versus 7.2 mm when using the standard anterolateral portal.1
The proximal anteromedial portal passes just anterior to the medial intermuscular septum and stays deep to the brachialis muscle, avoiding injury to the brachial artery and median nerve.
On average this portal remains 6 mm proximal to the medial antebrachial cutaneous nerve, 3 to 4 mm anterior to an untransposed ulnar nerve, and 22 mm from the median nerve.7
DIAGNOSTIC ELBOW ARTHROSCOPY
Once the patient is positioned, prepared, and draped and the surgical landmarks are drawn, the joint is distended using an 18-gauge needle to inject 20 mL of saline via the direct lateral approach into the joint (TECH FIG 1).
The proximal medial portal is established first. This is the viewing portal and allows for the proximal lateral portal to be created under direct arthroscopic visualization.
The surgeon makes a 2-mm longitudinal skin incision using a no. 11 scalpel blade, 2 cm proximal and 2 cm anterior to the medial epicondyle.
This incision should go no deeper than the skin to protect the cutaneous nerves and veins.
Alternatively, the arthroscope light can be used to transluminate the skin and identify these structures so that they can be avoided before making the skin incision.
A hemostat is inserted through the subcutaneous tissue, onto the medial humeral condylar ridge, and down to the medial capsule, using blunt dissection.
The capsule is robust and a pop should be felt as it is entered.
Some of the normal saline that was previously injected to inflate the joint will now be released through the portal site, further confirming entry into the joint.
Staying anterior to the medial intermuscular septum protects the ulnar nerve from danger.
Next, a blunt trocar is introduced into the joint, followed by the 4-mm, 30-degree arthroscope.
The anterior compartment of the elbow should be diagnostically inspected for pathology (osteoarthritis, loose bodies, capsuloligamentous flaps or redundancies); these will be addressed once the proximal lateral portal is established.
After the anterior compartment has been inspected, attention is directed toward the lateral capsule and ECRB tendon.
An 18-gauge spinal needle is inserted 2 cm proximal and 2 cm anterior to the lateral epicondyle.
Using techniques for skin and soft tissue management similar to those described for the proximal medial portal placement, the proximal lateral portal is made under direct arthroscopic visualization.
The radial nerve is the structure most at risk with this portal.
TECH FIG 1 • Lateral intraoperative photograph showing the surgical landmarks with the standard proximal anterolateral working portal (1) and the direct lateral portal (2). Joint is initially distended with 20 cc of normal saline via the direct lateral portal.
ARTHROSCOPIC LATERAL ELBOW (ECRB) RELEASE
With the proximal medial portal as the standard viewing portal, the 30-degree scope is advanced just past the radial head to visualize the lateral joint capsule and undersurface of the ECRB origin (TECH FIG 2A).
The capsule often adheres to the undersurface of the ECRB and can have varying degrees of degeneration, presenting as linear tears (type II lesion), fraying, or yellowish fatty infiltration, or it can have a thin, translucent appearance (TECH FIG 2B).
If the capsule is intact, it is débrided using a 4.5-mm synovial shaver inserted in the working portal—the proximal lateral portal.
The capsule and tendon may be completely avulsed and retracted; this is classified as a type III lesion (TECH FIG 2C).
The undersurface of the ECRB is in plain view once the capsule is débrided.
The release of the muscle should begin at the site of degeneration or tear using a 4.5-mm incisor (TECH FIG 2D).
TECH FIG 2 • A. Type I lesion showing synovitis and fraying of the lateral joint capsule. B. Type II lesion showing linear tear of the joint capsule and the extensor carpi radialis brevis (ECRB) tendon near its insertion site. C. Type III lesion showing complete avulsion and retraction of the lateral capsule and ECRB tendon. D. Fatty degeneration of the ECRB tendon (arrow), which is overlying the ECRL muscle–tendon. E. A 4.5-mm shaver is used for the initial débridement of the ECRB, which is in close proximity to the capitellum (C) and radial head (R). F. Débridement of the pathologic ECRB tendon and capsule with healthy-appearing extensor carpi radialis longus superficial. G. A 4.0-mm abrader is the final step to decorticate the lateral epicondyle. The ECRB release is complete.
Next, the surgeon progresses proximally to the ECRB origin on the lateral epicondyle.
Care must be taken to avoid injury to the articular surface of the capitellum or radial head during this process (TECH FIG 2E).
Just superficial to the ECRB the extensor carpi radialis longus will come into view (TECH FIG 2F).
A 4.0-mm abrader is placed in the proximal lateral portal to débride the remaining origin of the ECRB and to decorticate the lateral epicondyle and distal lateral condylar ridge to promote healing (TECH FIG 2G).
The cadaveric model by Kuklo et al7 showed that using this technique, an average of 23 mm of ECRB tendon and 22 mm of lateral epicondyle can be safely resected.
In addition, the 30-degree scope field of visualization avoids injury to the lateral ulnar collateral ligament, which is posterior to an intra-articular line bisecting the head of the radius.11
If needed, a direct lateral portal can be made when the elbow is flexed 90 degrees for access to the posterior compartment.
This portal enters the soft tissue triangle created by the radial head, the lateral humeral epicondyle, and the olecranon.
The medial antebrachial cutaneous nerve is the structure at risk with this portal.
Once the arthroscope is introduced into the joint, the elbow is extended and the scope is advanced into the posterior compartment.
If a working portal is needed, a direct posterior portal can be placed midline between the medial and lateral epicondyles about 3 cm proximal to the olecranon tip.
The joint is expressed free of all arthroscopic fluid, portals are closed with figure 8 3-0 nylon sutures, and a soft tissue dressing is applied.
POSTOPERATIVE CARE
Postoperatively the patient is placed into a sling for comfort.
Range of motion is begun immediately with the assistance of a physical therapist.
Rehabilitation goals include edema control with icing, full active range of motion, gradual strengthening, hand exercises, and ergonomic education.
Patients return to full activity as tolerated.
Soldiers undergoing this technique were able to return to full, unrestricted active duty within an average of 6 days (less than 28 days).11
OUTCOMES
Cadaveric and anatomic studies have shown that elbow arthroscopy and ECRB release is safe, reliable, and reproducible.7,11
Two clinical series confirm the long-term subjective and functional improvement, as well as faster return to activity, with arthroscopic treatment.
In 16 patients who underwent an arthroscopic release, the average return time to unrestricted work was 6 days, with no complications or need for further surgery.11
In 2000, we evaluated the clinical results of arthroscopic lateral elbow release. Patients rated 95% of the elbows to be “much better” or “better.” Sixty-two percent of the patients were completely pain-free at an average of 2.8 years of follow-up.2
Results from open releases have shown time to return to activity as long as 3 to 6 months, with one study reporting that 60% of patients could not return to high-demand sports participation postoperatively.
Arthroscopy, unlike open and percutaneous procedures, gives the surgeon the distinct ability to address concurrent intra-articular pathology.
This may be particularly important because we have found rates of intra-articular pathology from 11% to 18% in our series, and some have reported rates as high as 40%.9
COMPLICATIONS
Transient nerve palsy versus direct nerve injury14
Superficial infection
Iatrogenic lateral collateral ligament injury with posterolateral instability7
Hematoma
REFERENCES
1. Adolfsson L. Arthroscopy of the elbow joint: a cadaveric study of portal placement. J Shoulder Elbow Surg 1994;3:53–61.
2. Baker CL Jr, Murphy KP, Gottlob CA. Arthroscopic classification and treatment of lateral epicondylitis: two-year clinical results. J Shoulder Elbow Surg 2000;9:475–482.
3. Boyd HB, McLeod AC. Tennis elbow. J Bone Joint Surg Am 1973; 55A:1183–1187.
4. Field LD, Altchek DW, Warren RF, et al. Arthroscopic anatomy of the lateral elbow: a comparison of three portals. Arthroscopy 1994; 10:602–607.
5. Jerosch J, Schunck J. Arthroscopic treatment of lateral epicondylitis: indication, technique and early results. Knee Surg Sports Traumatol Arthrosc 2006;14:379–382.
6. Kraushaar BS, Nirschl RP. Current concepts review: tendinosis of the elbow (tennis elbow). J Bone Joint Surg Am 1999;81A:259–278.
7. Kuklo TR, Taylor KF, Murphy KP, et al. Arthroscopic release for lateral epicondylitis: a cadaveric model. Arthroscopy 1999;15:259–264.
8. Mehta JA, Bain GI. Posterolateral rotatory instability of the elbow. J Am Acad Orthop Surg 2004;12:405–415.
9. Nirschl RP, Pettrone FA. Tennis elbow: the surgical treatment of lateral epicondylitis. J Bone Joint Surg Am 1979;61A:832–839.
10. O'Driscoll SW, Bell DF, Morrey BF. Posterolateral rotatory instability of the elbow. J Bone Joint Surg Am 1991;73A:440–446.
11. Owens BD, Murphy KP, Kuklo TR. Arthroscopic release for lateral epicondylitis. Arthroscopy 2001;17:582–587.
12. Peart RE, Strickler SS, Schweitzer KM. Lateral epicondylitis: a comparative study of open and arthroscopic lateral release. Am J Orthop 2004;33:565–567.
13. Plancher KD, Halbrecht J, Lourie GM. Medial and lateral epicondylitis in the athlete. Clin Sports Med 1996;15:283–305.
14. Thomas MA, Fast A, Shapiro D. Radial nerve damage as a complication of elbow arthroscopy. Clin Orthop 1987;215:130–131.
15. Verhaar J, Walenkamp G, Kester A, et al. Lateral extensor release for tennis elbow: a prospective long-term follow-up study. J Bone Joint Surg Am 1993;75A:1034–1043.