Lateral Epicondylitis (Tennis Elbow) Arthroscopic Treatment

DEFINITION

Lateral epicondylitis (LE) is a common musculoskeletal disorder that is characterized by lateral epicondylar pain and tenderness over the origin of the extensor carpi radialis brevis (ECRB) slightly distal and anterior to lateral epicondyle with exacerbated pain at the resisted extension of the wrist.

The term epicondylitis is a misnomer due to the paucity of inflammatory changes implied by the suffix “-itis.”

Other known synonyms are traumatic enthesopathy of the ECRB, tendinopathy of ECRB, lateral epicondylalgia, lateral epicondylosis, tendinosis of ECRB, lawn tennis elbow, and so forth.

LE was first described in 1873 by F. Runge from Germany and was called a writer’s cramp attributed to a periostitis of lateral humeral epicondyle. The term tennis elbow was coined by H.P. Major in 1883 in relation to 1882 publication in the Lancet by H. Morris describing the condition as “the lawn tennis arm”

resulting from frequent back stroke.35

 

 

INCIDENCE

 

LE has an average prevalence of 3% in the general population, ranging from 0.7% to 4.0% and peaking in

patients aged between 45 and 54 years, with almost equal gender distribution.19,36 It is less common in black individuals. LE affects more often the dominant arm; bilateral or nondominant arm involvement is rare.

 

LE is a known work-related disorder with up to 14.5% prevalence in manual labor intensive industries such as foodprocessing industry or automobile manufacturing where repetitive “turn and screw” movements may be identified as a risk factor.23

 

The prevalence of LE among tennis players was reported at 1.3% to 14.1% with no gender difference. Risk factors such as heavy racquets, inappropriate grip size, high string tension, and so forth were suggested; however, the studies revealed that the use of string vibration dampers and grip size modifications did not have an effect on the development of the condition. It is more likely that LE is rather related to the improper

technique that is more common in inexperienced players.1

 

ANATOMY

 

The main anatomic structures associated with LE are lateral epicondyle of the humerus and the tendon of ECRB.

 

Anatomic position of the ECRB tendon makes its undersurface vulnerable to contact and abrasion against the lateral edge of the capitellum during elbow motion, especially in extension and pronation.

 

ECRB originates mainly from the lateral epicondyle by the common extensor tendon and inserts distally into dorsal surface on the base of the third metacarpal bone, thus acting as a prime dorsiflexor of the hand.

 

The proximal portion of ECRB is covered by the extensor carpi radialis longus (ECRL) so that the latter must be elevated to visualize the former.

 

The origin of ECRB is entirely tendinous and diamond shaped, whereas the ECRL origin is muscular and has a triangular shape.

 

It is crucial to identify the full length of the pathologic tissue of ECRB to perform an adequate resection that includes approximately 13 to 15 mm of tendon. For easier identification of the ECRB origin from the extensor digitorum communis (EDC), it is recommended to follow orientation of the fibers from distal to proximal end of

the forearm, and also, it could be easier distinguished from undersurface of the extensor.13

 

Among the other anatomic structures that possibly can be involved in the development of the condition are synovial fold (SF), capitellum, radial head, and joint capsule.

 

SF, also known as synovial plica or a synovial fringe, is a thickening of the synovium on the proximal edge of the annular ligament but distinct from the latter. SF prevents excessive movements in the radiohumeral joint.

 

Inflammation and thickening of SF (termed as SF syndrome) as the result of repetitive trauma can cause its impingement between the capitellum and radial head especially with elbow extension and forearm pronation. Subsequent focal synovitis may develop most often in the posterolateral quadrants of SF and is manifested by

painful snapping in the elbow joint.12,37

 

PATHOGENESIS

 

The attachment of the tendons and ligaments to bones is termed as enthesis (meaning insertion in Greek).

 

Entheses are sites of high mechanical stress, and with aging, normal entheses are subject of wear and tear with consequent degenerative changes.

 

ECRB enthesis is fibrocartilaginous and helps to create a more gradual change in mechanical properties between soft and hard tissues. Enthesis ensures that any bending of the tendon/ligament fibers during joint movements is spread away from the bone—thus dissipating stress concentration.

 

Stress concentration at an insertion site involves not only enthesis itself but neighboring tissues as well. Many entheses have bursa and fat near the insertion site and in some cases deep fascia.

 

The concept of “functional synovio-entheseal complex” implies that one component (the enthesis) is prone to microinjury and the other (the synovium) to inflammation.

 

Enthesis is a relatively avascular structure with a limited capacity to accumulate fluid.7

 

 

 

Histopathology

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Repetitive ECRB microtrauma initiates a degenerative process with ingrowth of weakened reparative tissue that results in angiofibroblastic hyperplasia known as angiofibroblastic tendinosis.

 

Degenerative, noninflammatory changes are characterized by the presence of disorganized collagen and immature fibroblasts and vascular granulation. Corticosteroid injections into tendons may also result in similar appearance.

 

Due to the described contact between the ECRB and the radiocapitellar joint, the matching cartilage lesions of the capitellum and radial head were reported in up to 65% and 81%, respectively, in surgical patients with LE.33

NATURAL HISTORY

 

The onset of LE is usually insidious, resulting from repetitive overuse microtrauma and rarely could it be secondary to an acute event.

 

LE progression can be categorized by three phases: (1) acute phase (up to 3 months), (2) subacute or intermediate phase (3 to 6 months), and (3) chronic phase (more than 6 months).

 

During acute phase, icing, rest, and activity modifications are recommended in conjunction with other conservative treatment modalities such as nonsteroidal anti-inflammatory drugs (NSAIDs).

 

In 90% to 95% of the cases, the timely administration of conservative treatment combined with a daytime bracing of the forearm (to reduce stress) placed over ECRB, distal to the lateral epicondyle, should alleviate acute LE symptoms.

 

With continuous repetitive trauma, fraying of the tendon and microtears can progress to macroscopic tears and even to rupture or avulsion.

 

If the lateral joint capsule is involved in chronic LE, it can avulse along with ECRB tendon that may result in the development of a lateral synovial cyst and lateral joint instability.

 

Chronic refractory LE could extend from ECRB and involve the anterior portion of EDC that may ultimately lead to weakening of wrist extension and supination.

 

 

In rare cases does severe chronic LE may require tendon transfer surgery for extensor function restoration. Baker et al6 have published an arthroscopic classification of LE that was found to be reliable (Table 1).

Table 1 Arthroscopic Classification of Lateral Epicondylitis

Type

Description

I

Fraying of the undersurface of the ECRB without a definitive tear

II

Linear tears specifically in the undersurface of the ECRB and the lateral capsule

III

Partial or complete avulsions of the ECRB origin

ECRB, extensor carpi radialis brevis. From 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.

 

 

PATIENT HISTORY AND PHYSICAL FINDINGS

 

Comprehensive assessment of patient’s history is an important first step in diagnosis of LE that directs the following clinical evaluation and helps in choosing appropriate course of treatment sequence.

 

The review of patient’s history must reflect the onset, circumstances, and duration of pain and associated symptoms.

 

Hand dominance, particularities of sport activities, and occupational factors should be documented in detail.

 

All previously applied treatments and their effectiveness should be recorded and evaluated.

 

Patients who have had a good initial response to conservative treatment followed by reaggravation of symptoms may have resumed strenuous activities too soon 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 also contribute to the diagnosis. Furthermore, a previous ulnar nerve transposition could place the ulnar nerve at risk when establishing arthroscopic portals and may require an open approach.

 

When pain and tenderness during palpation is present in the area just distal to lateral epicondyle and it is exacerbated at the resisted extension of the wrist, then patient is diagnosed with LE.

 

Physical Examination

 

It is pertinent to perform a thorough physical examination of both the ipsilateral and contralateral upper extremity as well as of the cervical spine.

 

Palpation of the lateral epicondyle and common extensor area. The epicenter of pain and tenderness is located slightly anterior and distal (1 to 3 cm) to lateral epicondyle over the origin of the ECRB. Erythema, warmth, or swelling is absent.

 

Positive “Chair test.” Patient refuses or unable to lift a chair with a pronated hand due to elicited lateral elbow pain.

 

Positive Cozen test. Exacerbated pain at the lateral epicondyle at the resisted dorsiflexion of the wrist while the forearm is pronated and elbow is flexed at 90 degrees.

 

Positive Mill test. Pain in the area of lateral epicondyle at the resisted extension of the middle finger while elbow is flexed at 90 degrees and forearm is pronated with wrist flexed.

 

Grip strength and resisted supination. Grip strength is diminished in 78% of patients with LE. Resisted supination elicits pain in 51% of patients. Pain with turning a door knob is indicative of LE.

 

IMAGING AND OTHER DIAGNOSTIC STUDIES

 

Radiographic evaluation is required to exclude coexisting pathology, especially in recalcitrant cases and is limited to anteroposterior (AP) view in full extension and lateral view at 90-degree flexion of the elbow.

 

 

Calcification in the area of ECRB origin can be detected in up to 25% of patients (FIG 1A).28

 

Magnetic resonance imaging (MRI) has 90% to 100% sensitivity and 83% to 100% specificity for detecting epicondylitis.27

 

MRI reveals increased signal intensity on T1- and T2-weighted images and thickened extensor tendon (FIG 1B).

 

Coronal or axial T2-weighted images show fluid signal intensity in the areas of partial- or full-thickness tendon tears of ECRB. Adjacent soft tissue edema may be seen on T2-weighted sequences.

 

 

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FIG 1 • A. Standard AP radiograph of the elbow showing calcification of the 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 epicondyle. C. US image of 42-year-old man with severe unilateral chronic LE of the dominant hand. Long-axis view of the right lateral epicondylar region demonstrates thickening and a hypoechoic area (asterisk) within the ECRB with loss of normal fibrillar pattern at its insertion into the right epicondyle and cortical irregularity (arrow) consistent with lateral epicondylosis. D. US image. Long-axis view. Normal appearance of the left ECRB at its insertion (asterisk) at the left lateral epicondyle in the same patient.

Normal appearance of a cortical layer (arrow head) of the left epicondyle. E. US image of 42-year-old man with severe chronic LE. Short-axis view. Small region of calcification (red circle) within the ECRB tendon near its insertion into the right lateral epicondyle.

 

 

Magnetic resonance arthrography with gadolinium contrast agent may help in detection of intra-articular and periarticular lesions such as collateral ligament tears, capsular disruptions, loose bodies, and so forth.

Intravenous gadolinium contrast administration helps to demonstrate bone perfusion and viability.16

 

Thickening of SF beyond 3 mm and abnormal signal intensity with irregular margins on MRI may be associated with SF syndrome.

 

Histologic and surgical findings correlate with MRI findings of tendon damage and degeneration.38

 

Ultrasound (US) is a noninvasive method for LE evaluation that also allows immediate dynamic measurements in flexion and extension.

 

US evaluation of LE has a reported sensitivity of 80% and specificity of 50%. US, however, has a high false-positive rate and is most useful in the evaluation of the extent of the tendon lesion in symptomatic patients.

 

Tendinosis is manifested as a tendon thickening and hypoechoic heterogeneous echo texture with loss of normal longitudinally oriented fibrillar pattern (FIG 1C,D). Tendon tears are seen as anechoic areas.

 

The degree of hyperemia on Doppler imaging reflects the extent of the increased vascularity, and

depending on the stage of the process, it may indicate pathologic changes or can reflect the healing progression.

 

Surrounding fluid and calcification may also be seen (FIG 1E).

 

A convex boundary of the extensor tendons, an erosive lateral epicondylar cortex, internal calcifications, and tendon tears on a gray-scale US combined with color Doppler findings of neovascularity have a high diagnostic accuracy.22,30,38

 

Multiple steroid injections can affect the echo texture of the tendon.

 

Normal SF is identified by US as a hyperechoic triangular silhouette and pathologic SF exhibits thickening and irregular echogenicity.12

Other Evaluation Methods

 

Self-reported measures include a number of validated patientbased questionnaires.

 

 

Patient-Related Tennis Elbow Evaluation (PRTEE) questionnaire assesses both elbow function and pain and is considered as a standard and reliable outcome measure for LE.

 

Visual Analog Scale (VAS) is commonly used for pain intensity evaluation.

 

Disability of the Arm, Shoulder, and Hand (DASH) questionnaire quantifies pain and disability related to upper extremity.

 

Andrew-Carson Elbow Scores (ACES) and Mayo Elbow Performance Score (MEPS) are also used for evaluation of patients with LE before and after treatment.

 

 

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Biomechanical assessment includes pain-free grip (PFG) strength and rate of force development measured with Jamar dynamometer. Maximal grip strength can be adversely affected in LE patients.

 

Grip strength of dominant versus nondominant arm should be measured using dynamometer before and after treatment. As the dominant side is usually stronger, equal strength may signify the loss of strength on the affected dominant side.

 

Surface electromyography (EMG) is also an established method to quantify changes in patients with LE.

 

DIFFERENTIAL DIAGNOSIS

 

There are approximately 30 etiologies associated with lateral elbow pain syndrome. The differential diagnosis of lateral elbow pain includes (but is not limited to) the conditions listed below:

 

Posterolateral elbow plica impingement may also cause refractory lateral elbow pain syndrome. When pain is located posterolaterally and mainly in the radiohumeral joint (but not along the lateral epicondyle or ECRB) and is exacerbated by flexion-extension of the pronated forearm, then the intra-articular synovial plica involvement is suspected (SF syndrome). This condition also may be manifested by painful clicking, snapping, and locking of the elbow joint. Intra-articular arthroscopic resection of the SF should be considered in cases of the SF syndrome.

 

Radial tunnel syndrome (RTS). Maximal tenderness in RTS is typically noted 3 to 4 cm distal and anterior to the epicondyle (more distal than in LE) due to compression of the posterior interosseous nerve (PIN) within the supinator muscle. PIN is the continuation of the deep branch of the radial nerve. RTS is usually manifested with motor deficit without pain. Electrodiagnostics (nerve conduction and EMG) can help to

confirm the diagnosis. LE and RTS may coexist in up to 5% of the patients.

 

Posterolateral rotatory instability (PLRI) is caused by an injury to the lateral ulnar collateral ligament (LUCL) that provides varus stability. Although PLRI can be associated with lateral elbow pain, the positive lateral pivot shift test, posterolateral rotatory drawer test, and push-up test can clinically differentiate

instability from epicondylitis.26,29 Milder forms of instability may lead to secondary LE. Conversely, patients with chronic LE may occasionally sustain an acute injury and develop instability.17

 

Osteoarthritis, particularly in the radiocapitellar joint. The physical examination usually reveals mechanical symptoms and decreased range of motion (ROM). Radiographs confirm sclerosis, osteophyte formation, loose bodies, and narrowing of the radiocapitellar joint.

 

NONOPERATIVE MANAGEMENT

 

 

More than 40 different treatment modalities were implemented for LE therapy. Nonoperative management of LE is successful in 90% to 95% of the cases.9,29

 

Treatment modalities and algorithms are extensive and include myriad combinations ranging from rest and

activity/equipment modifications to acupuncture and botulinum toxin injections and further extending into the vast field of electrophysical methods and even exotic alternatives.

 

Realizing that the natural history of LE appears to include spontaneous resolution, the rest and removal of the repetitive overuse activities is a logical and biomechanically necessary component in any initial treatment.

Prevention of nighttime wrist flexion by cock-up wrist brace to reduce extensor tension, combined with a physical therapy program that includes strengthening and stretching exercises, are recommended elements of conservative management.

 

Local steroid injections. There is a moderate evidence of short-term pain relief due to suppression of inflammation and analgesic effect of the neuropeptides after corticosteroid injections. However, high recurrence rates (72%) and possible deleterious effect on tendon integrity is increasingly discouraging the

use of local corticosteroid injections.14,34

 

Platelet-rich plasma (PRP) injection for treatment of chronic LE. Platelet α-granules release various growth factors and cytokines that promote angiogenesis, tissue remodeling, and wound healing. PRP application is a safe, easy to implement, and relatively low-cost technique that involves the preparation of platelet-rich concentrate from autologous blood (3 to 10 times that of whole blood). Preparation systems, optimal formulation, and application regimen continues to evolve. It was reported (including randomized trials) that

significant pain reduction and functional improvement was continued.18,20

 

Extracorporeal shock wave therapy was approved by U.S. Food and Drug Administration for LE treatment in 2003. Shockwaves are generated by electrohydraulic, electromagnetic, or piezoelectric technique. The produced pulse energy is concentrated at the target point and induces neovascularization and blood supply of the tendon-bone junction, thus alleviating pain and initiating regeneration. The reported success rate

ranged from 68% to 91%; however, significant placebo effect was also noticed.39

 

Graston technique is a form of strong massage that is enhanced with the use of hard edged tools to perform an instrument-assisted augmented soft tissue mobilization. There are limited data supporting the effectiveness of the controlled microtrauma and scar breakdown resulting in stimulation of tendon healing

and functional improvements in patients with LE.8

 

Prolotherapy is a complementary treatment for LE that involves the iatrogenic stimulation of tissue repair by

injection of irritant/sclerosant solution into damaged tendons. The proposed mechanism of action includes the induction of inflammatory response with consequent collagen synthesis that leads to a stronger fibrous tissue at the lateral epicondyle. It may be considered as a less expensive alternative for patients who are

opposing corticosteroid injections.10

 

An example of nontraditional therapeutic approach includes leech therapy. Randomized trial showed significantly stronger short-term pain reduction due to blood flow augmentation by histamine-like vasodilators and analgesia by proteinase inhibitors contained in leech saliva. A strong placebo effect was

also suspected.5

 

 

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The other nonoperative modalities include autologous blood injections, laser light therapy, low-intensity ultrasound physiotherapy, ionophoretic dexamethasone administration, transcutaneous electrical nerve stimulation, topical nitric oxide, and so forth.

 

No single nonoperative protocol has proved to be the best, and there is paucity in evidence-based support for each modality.

 

SURGICAL MANAGEMENT

 

There are more than 15 surgical techniques described for LE treatment ranging from regular ECRB release to tendon reconstruction and denervation of lateral humeral epicondyle. The three major surgical options for treatment of LE include (1) open surgical techniques, (2) percutaneous release, and (3) arthroscopic treatment.

 

Indications for surgery are (1) pain that constrains daily life activities and work performance and (2) recalcitrant symptoms after 6 months of adequate nonoperative treatment.

 

The arthroscopy of the elbow was first reported in 1931 by Burman MS in a cadaveric study.

 

In comparison with other surgical options, arthroscopy has several distinct advantages, including the ability to address intra-articular pathology, preservation of the superficial common extensor origin and therefore grip strength, lower postoperative morbidity, and faster return to work and sports-related activities.

 

The distinct ability of arthroscopy to address concurrent intra-articular pathology, unlike in open and percutaneous procedures, may be particularly important due to the high rates of associated intra-articular lesions.

 

Contraindications for arthroscopic surgery are (1) active infection, (2) extended postsurgical, posttraumatic, or arthritic changes of elbow anatomy (eg, severe ankylosis, previous ulnar nerve transposition), (3) insufficient experience with arthroscopic technique and instrumentation, and (4) neurologic deficit.

 

Evidence-Based Indications for Arthroscopic Treatment of Lateral Epicondylitis

 

There is fair-quality evidence (level II or III studies with consistent findings) for recommendation of elbow arthroscopy for the treatment of LE (grade of recommendation, B).40

Preoperative Planning

 

The surgeon must review all imaging data for concomitant pathology such as osteochondral loose bodies, radiocapitellar arthrosis, fracture, and injury to surrounding soft tissue structures such as the lateral collateral ligament complex.

 

Under general anesthesia

 

The lateral pivot shift test, described by O’Driscoll,29 evaluates the elbow for an LUCL 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.

 

PLRI is diagnosed when the radiocapitellar joint subluxes, creating a sulcus proximal to the radial head.

 

In addition, the surgeon must examine the ROM of the elbow under anesthesia in full flexion and extension, pronation, and supination.

 

Examination under anesthesia should always include comparison 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

 

Techniques include partial epicondylectomies, partial resection of the annular ligament, and lengthening (slides) of the extensor tendons.

 

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.

 

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.2

 

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 the untransposed ulnar nerve, and 22 mm from the median nerve.24

 

 

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TECHNIQUES

• Diagnostic Elbow Arthroscopy

Once the patient is positioned, draped, and the surgical landmarks are drawn, the joint is distended by

 

injection of 20 mL of saline via the direct lateral approach into the joint using an 18-gauge needle (TECH FIG 1).

 

The proximal medial portal is established first. This is the viewing portal that 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.

 

 

 

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 mL of saline via the direct lateral portal.

 

 

Alternatively, the arthroscope light can be used to transilluminate 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 saline that was previously injected to distend 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 injury.

 

Next, a trocar is introduced bluntly into the joint, followed by the 4-mm, 30-degree arthroscope.

 

The anterior compartment of the elbow should be inspected first for pathology (osteoarthritis, loose bodies, capsuloligamentous flaps or plicae); 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.

 

The proximal lateral portal is made under direct arthroscopic visualization using techniques for skin and soft tissue management similar to those described for the proximal medial portal placement.

 

The radial nerve is the structure that is most at risk with this portal.

• Arthroscopic Lateral Elbow (Extensor Carpi Radialis Brevis) 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, presented 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 through the proximal lateral portal (the working portal) in order to gain exposure to the ECRB attachment site on the lateral epicondyle.

 

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).

 

Next, the arthroscope is advanced proximally to the ECRB origin on the lateral epicondyle.

 

At this stage, care must be taken to avoid injury to the articular surface of the capitellum or radial head (TECH FIG 2E).

 

Consequently just superficial to the ECRB, the ECRL 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).

 

It was shown that using this technique, an average of 23 mm of ECRB tendon and 22 mm of lateral epicondyle can be safely resected.24

 

In addition, limitations of the 30-degree scope field of visualization precludes the excessive resection, thus preventing the injury to the LUCL, which is posterior to an intra-articular line bisecting the head of

the radius.31

 

If needed, a direct lateral portal can be added when the elbow is flexed 90 degrees for access to the posterior compartment.

 

This portal enters the soft tissue triangle between the radial head, the lateral humeral epicondyle, and the olecranon.

 

The medial antebrachial cutaneous nerve injury is of concern 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.

 

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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 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 healthyappearing ECRL superficially.

G. The final step to decorticate the lateral epicondyle. A 4.0-mm abrader. The ECRB release is complete.

 

 

Finally, the joint is freed of all arthroscopic fluid, portals are closed with figure-of-eight 3-0 nylon sutures, and a soft tissue dressing is applied.

 

In cases of cartilage lesions (eg, microfractures in lateral quadrants of radial head or capitellum), it is advised to débride the unstable articular cartilage using a motorized shaver or curette.33

 

Addition of arthroscopic decortication to a simple ECRB release is an option; however, it may result in increased postoperative pain and wound bleeding and decreased ROM in early postoperative period. The long-term results nevertheless are similar.21,32

 

Application of 70-degree arthroscope may offer a better visualization and a chance to “see around the corner.” It shows ECRB insertion and radial collateral ligament (RCL) frontally and centered in the optical field in comparison to a standard 30-degree camera that shows ECRB and RCL at the side of the optical

field that can make the distinction of the dissection plane between them more difficult.4 Although more

aggressive resection may be possible with the 70-degree arthroscope, this could potentially injure the

lateral collateral ligament complex. Resection to the limit of the visualization provided by the 30-degree arthroscope produces adequate release while protecting the lateral collateral ligament.31

In our experience, the standard 30-degree scope was always satisfactory and it also prevents the too posterior advancement with 70-degree lenses and possible injury of RCL and potential destabilization of the joint. In addition, 70-degree instrumentation requires longer learning curve, more equipment, and increase in operating time and cost.

 

 

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PEARLS AND PITFALLS
	Indications ▪ Indication for arthroscopic release is pain that lasts longer than 6 months despite a trial of nonoperative methods (rest, counterforce bracing, stretching, and strengthening).   Absolute ▪ Distortion of normal bony or soft tissue anatomy that precludes safe portal contraindications placement Previous ulnar nerve transposition or implanted hardware that interferes with medial portal placement Osteomyelitis or local cellulitis   Avoiding ▪ Neurovascular injury is avoided by using the “nick and spread” technique: neurovascular injury   An 11-mm arthroscopic blade placed through the skin and is used to pull skin distally for small incision. A hemostat is used to bluntly dissect the capsule.   A 2.7-mm arthroscope is used rather than a 4.0-mm arthroscope. If a 4.0-mm scope is desired, the joint is entered over a switching stick. A postoperative intra-articular injection of 10 mL of Marcaine provides 24 hours of pain relief but may preclude immediate postoperative neurologic evaluation due to transient radial nerve palsy from extravasation of fluid.   Complete lateral ▪ The ECRB insertion site spans 1.5 cm of lateral epicondyle. release ▪ Débridement of the ECRB tendon is carried up the lateral flare of the epicondyle. Lateral epicondyle decortication is best done with an abrader and ensures that the entire ECRB tendon is released.   Access to ▪ Direct lateral portal for visualization. posterior ▪ Direct posterior portal as the working portal. compartment ▪ Surgeon is seated with arthroscope draping across the thighs. The patient’s wrist should be flexed and the dorsum of the hand should be on the surgeon’s

 

 

thigh. Raising or lowering the bed allows for the elbow to be extended and flexed, respectively.

 

Iatrogenic lateral collateral ligament complex injury

• The surgeon should not decorticate posterior to the lateral epicondyle.

• A 30-degree scope prevents injury to the lateral collateral ligament as it limits posterior visualization, thus precluding excessive resection.

 

POSTOPERATIVE CARE

 

 

Postoperatively, soft dressing is applied, and for 2 days, the arm is placed in a sling. The active and passive ROM exercises are initiated immediately.

 

Edema control is achieved with regular icing during the first 72 hours postoperatively.

 

The dressing is removed in 2 days by patients and portals are treated with Betadine and bandages.

 

The first office follow-up visit is scheduled within 10 days for wound inspection, suture removal, and ROM evaluation.

 

If arthroscopic procedure was extended with repair of radial or humeral collateral ligaments, then splinting will be required for 3 weeks followed by hinged bracing for the next 6 weeks.

 

Forceful grip is avoided for 4 weeks.

 

 

Gradual strengthening program is initiated 4 weeks after surgery. Heavy or repetitive manual work is discouraged for 4 to 6 weeks.

 

Patients usually return to activities of daily living within 2 weeks and return to sport-dependent activities not sooner than 6 weeks.

 

OUTCOMES

Success rate with good or excellent results was reported in up to 92% of the LE cases treated arthroscopically.3,40

In our experience with more than 250 arthroscopic procedures performed for the LE treatment during last decade, the intra-articular pathology such as loose bodies, synovitis, posteriorly spurs, cartilage radiohumeral lesions, and so forth was observed in almost 85% of patients. The SF was identified in 80% of the cases with at least one-third of which had some degree of SF abnormality (thickening, inflammation, etc.).

Our results of arthroscopic lateral elbow release had shown that 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.6

The arthroscopic treatment of LE is a safe, reliable, and reproducible treatment that provides a lasting effect.

 

 

 

COMPLICATIONS

Minor complications of elbow arthroscopies were reported in 11% and included prolonged drainage at a portal side, persistent minor contractures of less than 20 degrees, and transient nerve palsies.

Rheumatoid arthritis and a flexion contracture of the elbow were identified as risk factors for the development of transient nerve palsies. Incidence of neurapraxia was reported at 2.5% and incidence of joint infection at 0.8%. Other iatrogenic injuries may include damage to articular cartilage, synovial fistula

formation, and tourniquet-related complications.3

The most common complications of elbow arthroscopy are related to nerve injuries that may be caused by portal placement, trocar misdirection, débridement with shaver, thermal damage from cautery, and so forth.

Specific nerve injuries described after arthroscopic treatment of LE include the PIN transection and neuroma involving median nerve and anterior interosseous nerve (branch of

P.257

median nerve). PIN is at risk during lateral portal placement (proximal anterolateral portal) and during capsulectomy. It is recommended that during portal placement, the trocar is directed toward the center of the joint avoiding passing through the soft tissues anterior to the joint where the neurovascular structures

are positioned.11

Our rate of postoperative transient radial nerve palsy is in accordance with the reported incidence of transient paresthesias of less than 3%.25

Certain poor outcomes after arthroscopic débridement could be attributed to the residual microscopic tendinopathy, resulting from inadequate tendon resection.15

PLRI may result from the excessive débridement and iatrogenic LUCL injury. To prevent this complication, the tendon débridement must be limited to the anterior aspect of the lateral epicondyle.

Hematoma formation is rare as well as persistent weakness in the grip strength.

 

REFERENCES

1. Abrams GD, Renstrom PA, Safran M. Epidemiology of musculoskeletal injury in the tennis player. Br J Sports Med 2012;46:492-498.

    

    

2. Adolfsson L. Arthroscopy of the elbow joint: a cadaveric study of portal placement. J Shoulder Elbow Surg 1994;3:53-61.

    

    

3. Ahmad CS, Vitale MA. Elbow arthroscopy: setup, portal placement, and simple procedures. Instr Course Lect 2011;60:171-180.

    

    

4. Arrigoni P, Zottarelli L, Spennacchio P, et al. Advantages of 70° arthroscope in management of ECRB tendinopathy. Musculoskelet Surg 2011; 95:S7-S11.

    

    

5. Bäcker M, Lüdtke R, Afra D, et al. Effectiveness of leech therapy in chronic lateral epicondylitis. A randomized controlled trial. Clin J Pain 2011;27:442-447.

6. 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.

    

    

7. Benjamin M., McGonagle D. The enthesis organ concept and its relevance to the spondyloarthropathies. Adv Exp Med Biol 2009;649: 57-70.

    

    

8. Blanchette MA, Normand MC. Augmented soft tissue mobilization vs. natural history in the treatment of lateral epicondylitis: a pilot study. J Manipulative Physiol Ther 2011;34:123-130.

    

    

9. Boyd HB, McLeod AC. Tennis elbow. J Bone Joint Surg Am 1973;55A: 1183-1187.

    

    

10. Carayannopoulos A, Borg-Stein J, Sokolof J, et al. Prolotherapy versus corticosteroid injections for the treatment of lateral epicondylosis: a randomized controlled trial. PM R 2011;3:706-715.

     

     

11. Carofino BC, Bishop AT, Spinner RJ, et al. Nerve injuries resulting from arthroscopic treatment of lateral epicondylitis: report of 2 cases. J Hand Surg Am 2012;37(A):1208-1210.

     

     

12. Cerezal L, Rodriguez-Sammartino M, Canga A, et al. Elbow synovial fold syndrome. AJR Am J Roentgenol 2013;201:W88-W96.

     

     

13. Cohen MS, Romeo AA, Hennigan SP, et al. Lateral epicondylitis: anatomic relationships of the extensor tendon origins and implications for arthroscopic treatment. J Shoulder Elbow Surg 2008;17: 954-960.

     

     

14. Coombes BK, Bisset L, Brooks P, et al. Effect of corticosteroid injection, physiotherapy, or both on clinical outcomes in patients with unilateral lateral epicondylalgia: a randomized controlled trial. JAMA 2013;309:461-469.

     

     

15. Cummins CA. Lateral epicondylitis: in vivo assessment of arthroscopic debridement and correlation with patient outcomes. Am J Sports Med 2006;34:1486-1491.

     

     

16. Dewan AK, Chhabra B, Khanna AJ, et al. MRI of the elbow: techniques and spectrum of disease. J Bone Joint Surg Am 2013;95:e99(1)-e99(13).

     

     

17. Dzugan SS, Savoie FH III, Field LD, et al. Acute radial ulno-humeral ligament injury in patients with chronic lateral epicondylitis: an observational report. J Shoulder Elbow Surg 2012;21:1651-1655.

     

     

18. Halpern BC, Chaudhury S, Rodeo SA. The role of platelet-rich plasma in inducing musculoskeletal tissue healing. HSS J 2012;8:137-145.

     

     

19. Herquelot E, Gueguen A, Roquelaure Y, et al. Work-related risk factors for incidence of lateral epicondylitis in a large working population. Scand J Work Environ Health 2013;39:578-588.

     

     

20. Kaux JF, Crielaard JM. Platelet-rich plasma application in the management of chronic tendinopathies. Acta Orthop Belg 2013;79:10-15.

21. Kim JW, Chun CH, Shim DM, et al. Arthroscopic treatment of lateral epicondylitis: comparison of the outcome of ECRB release with and without decortication. Knee Surg Sports Traumatol Arthrosc 2011;19: 1178-1183.

     

     

22. Kotnis NA, Chiavaras MM, Harish S. Lateral epicondylitis and beyond: imaging of lateral elbow pain with clinical-radiologic correlation. Skeletal Radiol 2012;41:369-386.

     

     

23. Krogh TP, Bartels EM, Ellingsen T, et al. Comparative effectiveness of injection therapies in lateral epicondylitis: a systematic review and network meta-analysis of randomized controlled trials. Am J Sports Med 2013;41:1435-1446.

     

     

24. Kuklo TR, Taylor KF, Murphy KP, et al. Arthroscopic release for lateral epicondylitis: a cadaveric model. Arthroscopy 1999;15:259-264.

     

     

25. Lattermann C, Romeo AA, Anbari A. Arthroscopic debridement of the extensor carpi radialis brevis for recalcitrant lateral epicondylitis. J Shoulder Elbow Surg 2010;19:651-656.

     

     

26. Mehta JA, Bain GI. Posterolateral rotatory instability of the elbow. J Am Acad Orthop Surg 2004;12:405-415.

     

     

27. Miller TT, Shapiro MA, Schultz E, et al. Comparison of sonography and MRI for diagnosing epicondylitis. J Clin Ultrasound 2002;30:193-202.

     

     

28. Nirschl RP, Pettrone FA. Tennis elbow: the surgical treatment of lateral epicondylitis. J Bone Joint Surg Am 1979;61A:832-839.

     

     

29. O’Driscoll SW, Bell DF, Morrey BF. Posterolateral rotatory instability of the elbow. J Bone Joint Surg Am 1991;73A:440-446.

     

     

30. Obradov M, Anderson PG. Ultra sonographic findings for chronic lateral epicondylitis. JBR-BTR 2012;95:66-70.

     

     

31. Owens BD, Murphy KP, Kuklo TR. Arthroscopic release for lateral epicondylitis. Arthroscopy 2001;17:582-587.

     

     

32. Rhyou IH, Kim KW. Is posterior synovial plica excision necessary for refractory lateral epicondylitis of the elbow? Clin Orthop Relat Res 2013;471:284-290.

     

     

33. Sasaki K, Onda K, Ohki G, et al. Radiocapitellar cartilage injuries associated with tennis elbow syndrome. J Hand Surg Am 2012;37:748-754.

     

     

34. Snyder KR, Evans TA. Effectiveness of corticosteroids in the treatment of lateral epicondylitis. J Sport Rehab 2012;21:83-88.

     

     

35. Thurston AJ. The early history of tennis elbow: 1873 to 1950s. Aust N Z J Surg 1998;68:219-224.

     

     

36. Tosti R, Jennings J, Sewards JM. Lateral epicondylitis of the elbow. AJM 2013;126:357.e1-357.e6.

     

     

37. Tsuji H, Wada T, Oda T, et al. Arthroscopic, macroscopic, and microscopic anatomy of the synovial fold of the elbow joint in correlation with the common extensor origin. Arthroscopy 2008;24:34-38.

     

     

38. Walz DM, Newman JS, Konin GP, et al. Epicondylitis: pathogenesis, imaging, and treatment. Radiographics 2010;30:167-184.

     

     

39. Wang CJ. Extracorporeal shockwave therapy in musculoskeletal disorders. J Orthop Surg and Res 2012;7:11.

     

     

40. Yeoh KM, King GJ, Faber KJ, et al. Evidence-based indications for elbow arthroscopy. Arthroscopy 2012;28:272-282.