CHAPTER 44 Tennis Elbow Tendinosis
Tennis elbow is a common term used to describe what was originally introduced as lawn tennis arm in 1883.39 Over the years, it has been used to describe a variety of maladies that occur in and about the elbow.6,10,12,13,19,66 The accurate diagnosis of this entity requires a thorough understanding of the epidemiology and clinical presentation as well as the pathophysiology of this condition. The traditional terms tendinitis and epicondylitis do not accurately reflect the true pathology of this condition. On the basis of clinical and surgical experience,16,25,37,50,51 it can be stated with confidence that the pathology of classic tennis elbow resides primarily in tendon tissue. Associated intra-articular issues such as synovial plica or capsular defects or degeneration, may be noted in a small percentage of patients. Therefore, rather than being inflammatory the demonstrated changes are degenerative (E. R. Stay, personal communication).34,37,63 The absence of inflammatory cells and findings of dysfunctional vascular and fibrous elements with total distortion of collagen has prompted us to describe this pathology as angiofibroblastic tendinosis.34,35,37
Lateral tendinosis typically affects approximately 2% of the general population. The dominant arm is affected in more than half of the patients. The peak incidence of this condition is during the fourth and fifth decades of life. A random study of 200 tennis players in three tennis clubs revealed that half of the players older than 30 years of age had experienced symptoms of characteristic tennis elbow at one time or another.47,50 Of this group, half noted minor symptoms with a duration of less than 6 months, and the rest had had major symptoms with an average duration of 2½ years. A larger statistical analysis of 2500 patients performed by Priest at the Vic Braden Tennis Camps revealed similar data.61,62 A study performed by Gruchow and Pelletier29 correlated playing time with the incidence of tennis elbow in club players. Not restricted to tennis and racquet sports, the incidence of the malady varies among other sports and oc-cupations that require repetitive forearm and wrist movements, including baseball, fencing, and swimming. Stressful repetitive uses of the forearm, such as computer keyboard use, carpentry, plumbing, meat cutting, textile production, and constant handshaking (e.g., politicians) are occupations related to the occurrence of tennis elbow.
The primary structure involved in all cases is the extensor carpi radialis brevis tendon origin. The anterior edge of the extensor digitorum communis may be involved in approximately 50% of the cases as well. Occasionally, the underside of the extensor carpi radialis longus and, rarely, the origin of the extensor carpi ulnaris are also involved.
The flexor-pronator mass origin, which is located about the medial epicondyle, includes the structures most commonly related to medial elbow tendinosis. The primary structures involved in the majority of cases are the flexor carpi radialis and the pronator teres origin. The flexor carpi ulnaris origin is involved in 5% of cases.
An additional complicating factor associated with medial elbow tendinosis is ulnar nerve compression neuropraxia (cubital tunnel syndrome). This phenomenon is evident in approximately 30% of all cases51–53 (see Chapter 45).
It is common to have combined signs and symptoms of both lateral and medial tennis elbow tendinosis occurring simultaneously. Beause this combination commonly occurs in recreational golfers and tennis players, we have coined the term “country club elbow.”
A thorough history and physical examination of the neck, shoulder and entire upper extremity is essential. Several associated abnormalities are often found in combination or as separate entities. These abnormalities include:
The association of carpal tunnel syndrome and trigger finger, as well as the association of rotator cuff tendinosis, bilateral elbow tendinosis and cubital tunnel syndrome, has led me (R. N.) to the conclusion that a constitutional factor may play a significant role in certain patients with elbow tendinosis.46,51,53 This combination of pathology has been coined mesenchymal syndrome (R. P. Nirschl, unpublished data).
Entrapment of the motor branch of the radial nerve in the radial tunnel at the canal of Froshe (posterior interosseus nerve) may coexist with and can cause symptoms similar to those seen with lateral elbow tendinosis. Diagnosis is confirmed by findings of electromyographic abnormality. Roles and Maudsley64 reported a surgical experience with 33 cases in 1972. In the Roles report, specific care was taken to decompress the radial tunnel by releasing the origin of the extensor carpi radialis brevis. Thus, the success of the reported operation may be due to an alteration of the origin of the extensor brevis rather than decompression of the nerve. Entrapment of the posterior interosseous nerve has also been implicated as the cause of lateral elbow pain by Werner,77 Dobyns (personal communication), and others (see Chapter 46). Entrapment of the radial nerve proximal to the sensory-motor bifurcation of the radial tunnel syndrome has also been described. A random sample of 20 electromyographic studies in patients with the classic signs of clinical lateral tennis elbow and suggested radial tunnel symptoms, however, failed to reveal any radial nerve abnormality (R. P. Nirschl, unpublished data). In most instances, if posterior interosseus nerve entrapment does occur, it is not associated in a major statistical way with classic lateral tennis elbow. In his classic study, Werner77 did report that the two coexist in about 5% of patients. When, on occasion, entrapment of the posterior interosseous nerve does occur, it may present as an entirely separate entity with vague aching symptoms that are more diffuse and felt more distally over the extensor muscle mass, tenderness in the same more distal forearm area, and a provocative handshake stress test that elicits symptoms in resisted supination. Most commonly, electromyographic studies tend to be normal in both radial tunnel syndrome and posterior interosseus nerve entrapment, thereby clouding the opportunity for objective laboratory diagnostic clarity.
As noted earlier, multiple areas of tendinosis often occur in association with tennis elbow.46,51,53 As noted earlier, the term mesenchymal syndrome has been employed to identify this subset of patients.46 It is the author’s clinical hypothesis, that this entity is hereditarily based and probably represents a slight collagen distortion—perhaps cross-linkage—as it relates to tendons. The practical ramifications of this entity include the necessity of rehabilitative exercise dedicated to the shoulder as well as the elbow when one formulates a treatment plan.
Gunn and Milbrandt30 have reported pain relief in 53 cases of tennis elbow by directing treatment to osteoarthritis of the cervical spine. Because the greatest incidence of tennis elbow occurs in individuals in the fourth and fifth decades of life, coincidental cervical osteoarthritis is common. Because the findings of lateral tennis elbow are usually specific, including response to local elbow tendon injections, it is unlikely that osteoarthritis in the cervical spine is anything but a coincidental finding. The report, however, reinforces the concept that shoulder and neck problems often occur in combination and must be addressed by rehabilitation.
Individuals who use the arm with high torque and shearing forces, as in the aggressive activities of baseball or javelin throwing, are vulnerable to associated intra-articular problems. These generally take the form of synovitis, traumatic osteoarthritis,45 and osteocartilaginous loose bodies present in the lateral or, more rarely, medial elbow compartments, as well as in the posterior olecranon fossa when associated with ligamentous laxity of the medial ulnar collateral ligamentous structures. Ulnar nerve neuropathy (cubital tunnel syndrome) commonly complicates the medial tendinosis clinical picture. Appropriate history, physical, and imaging examinations identify this subset of patients, and treatment should be adjusted accordingly. In a review, Baker and Cummings1 demonstrated that in some, there is arthroscopic evidence of capsular degeneration and synovial plica coexists with degeneration of the extensor carpi radialis brevis.1 In a review of his arthroscopic findings, Cummins16 reported a low incidence of intra-articular pathology, and this report is consistent with my observation (e.g., less than 5%).16 Nonetheless, the intra-articular component does exist.
The characteristic age at onset of classic uncomplicated tennis elbow is between 35 and 50 years, with a median of 41 years.47,61 Although the condition is most common in the third, fourth, and fifth decades, tennis elbow occurs in patients as young as 12 and as old as 80 years. Depending on a given patient population, the overall male-to-female ratio is usually equal.
The overall intensity and duration of arm use associated in some instances with a constitutional predisposition is the major cause of tendinosis. In this regard, younger patients such as competitive tennis players and professional baseball athletes characteristically place high demands on the upper extremities and are at increased risk. Inadequate, marginal, or compromised musculoskeletal fitness also appears to play a role in the etiology of medial and lateral elbow tendinosis.
Lateral tennis elbow is directly related to activities that increase tension loads, and hence the stress, of the wrist and finger extensors and, possibly, the supinator muscles. Funk and associates22 revealed that the extensor carpi radialis brevis is active with flexion, extension, varus, and valgus stress, hence, supporting the notion of overuse or overexertion of this anatomic structure.
Medial tennis elbow characteristically occurs with wrist flexor activity and active pronation, as in baseball pitching, the tennis serve and overhead strokes, and the pull-through strokes of swimming.
Posterior tennis elbow consists of extension overload of the triceps attachment that occurs in sports such as javelin throwing, baseball pitching, and football that incorporate techniques that initiate a sudden forceful elbow extension.
The primary overload abuse in tendinosis is caused by intrinsic muscular contraction. These muscular contractile overloads may occur concentrically or ec-centrically. Micro tears that occur within the tendon intercellular substance as a consequence of these overloads may be the inciting factor to tendon degeneration. Other forces such as valgus tensile extrinsic overload common in baseball (e.g., valgus instability or macro trauma) are more likely to cause excessive joint torque forces, leading to ligamentous rupture and traumatic osteoarthritis. In these sports activities, therefore, a distinction from classic tendinosis occurs because combination pathologies are present. Therefore, the etiologies in these circumstances also include both intrinsic and extrinsic factors.
Repetitive overuse is clearly associated with the development of tennis elbow.50,61,62 A typical sports patient is an active recreational tennis player who plays at least three or four times per week.6,61,62 Less commonly, acute onset may be associated with a direct blow to one of the epicondylar areas or a sudden extreme effort or activity.
Before 1964, defined pathoanatomy was not known precisely. In 1922 Osgood,57 and in 1932 Carp,13 related the condition to radiohumeral bursitis. Goldie,25 in his classic 1964 report, was the first to describe pathology adjacent to the lateral elbow. Goldie used longitudinal incisions and binocular magnification for more thorough assessment of the tissues.25 Before Goldie’s report, previous release techniques described by Bosworth8 and Hohmann31 failed to observe specific pathologic tendon abnormalities.
Careful gross surgical inspection of the abnormal tendinosis specimen reveals a characteristically grayish color and homogeneous and generally edematous tissue (Fig. 44-1). This typical gross pathologic appearance is present in lateral, medial, and posterior tendinosis. Indeed, similar visual characteristics are present in tendinosis involving the rotator cuff, and patellar and Achilles tendons, and even in plantar fasciosis (fasciitis). In my original surgical series of lateral tennis elbow, 97% of cases demonstrated varying degrees of this pathologic tissue at the origin of the extensor brevis tendon (which was ruptured in some degree in 35%).53 Observations in these and subsequent surgical cases also revealed that approximately 50% of cases also had associated tendinosis changes in the anteromedial edge of the extensor digitorum communis or extensor aponeurosis (usually 10% to 20% of the volume of the extensor digitorum communis tendon).51–53 Radiographic examination revealed that 22% of patients had some form of bony exostosis at the tip of the lateral epicondyle.51–53 Soft calcification in the substance of the tendon can also occur, but this finding is rare. Today, in some cases, the use of magnetic resonance imaging (MRI) may be helpful in demonstrating pathology at the lateral epicondyle. In the editor’s (B. F. M.) experience, this image is very rarely indicated to diagnose epicondylitis (Fig. 44-2).
FIGURE 44-1 Gross pathologic appearance. The brevis origin is exposed by retracting the extensor longus anteriorly (closed arrows). The characteristic visual appearance of angiofibroblastic hyperplasia (open arrow) is a grayish, homogeneous, edematous, and friable tissue. This appearance has led us to coin the phrase thick unhappy gray tendon, weeping with edema.
An understanding of the dense connective tissue that makes up the fibrous portion of the tendon is necessary for a better appreciation and definition of the pathologic process that is present in tennis elbow (E. R. Stay, personal communication). In tendons, collagen fibers and primary tendon bundles run parallel courses. In normal tendons, nerves and blood vessels extend through the major connective tissue septa but do not invade the fascicles (E. R. Stay, personal communication).67 On gross examination, the tendon appears firm, taut, and yellowish white or beige.51,53,54
In tendinosis, the abnormal tissue ordinarily can be identified easily by its appearance and is distinct from the normal tendon. Visual examination usually reveals gray, dull, sometimes edematous and friable, immature-appearing tissue that grossly resembles firm granulation tissue.51,53,54 Microscopically, the normal orderly tendon fibers are disrupted by a characteristic invasion of fibroblasts and vascular granulation-like tissue, which may be described as an angiofibroblastic hyperplasia-tendinosis34,37,50,51,54,67 (Fig. 44-3). Adjacent to this early proliferating vascular reparative tissue, the tendon appears hypercellular, degenerative, and microfragmented. The degree of angiofibroblastic infiltration appears to correlate generally with the duration of symptoms.47,50,53 In advanced lesions, adipose, connective, and even musculoskeletal tissue can reveal infiltration by this pathologic proliferative tissue.37
Others have noted the neovascular channels but emphasized that the mesenchymal cell proliferation indicated that the appearance was one of a healing process.67 On the other hand, Regan and colleagues63 compared 12 patients having surgery for lateral epicondylitis with 12 control patients. The unequivocal changes of hyaline degeneration were interpreted as demonstrating that the basic pathologic lesion was one of degeneration, although the increased vascularity noted by others also was reported. These investigators emphasized the fact that there is no microscopic evidence of inflammation associated with tennis elbow (Fig. 44-4).63 Evidence of acute or chronic inflammation is virtually absent in all cases.
In cases treated with corticosteroid injection, non-polarizable amorphous eosinophilic material can be identified, often without any foreign body response and usually without evidence of calcification (Fig. 44-5). Indeed, the proliferating vascular reparative tissue often insinuates itself between normal and abnormal tissues in regions close to the injection site.67
In 1999, Kraushaar and Nirschl37 reported a study of the histology, immunohistochemistry, and electron microscopy of tennis elbow tendinosis in nine surgical resection specimens. The origin of the extensor carpi radialis brevis was compared with 10 cadaveric specimens of the same anatomic region. These studies revealed that myofibroblasts are present in tendinosis material, a cell type with contractive properties not usually found in healthy tendons. Tendinosis material, therefore, contains hyperplasia of nonfunctional vascular elements, active distorted fibroblasts, and a lack of lymphocyte or neutrophilic populations that is clearly distinct from inflammatory tendinitis and/or normal tendon.37 This study reinforces the prior original hematoxylin and eosin (H&E) stain microscopic observations that “tendinosis” or degeneration is the histopathologic lesion in tendon overuse.51,54,67
We have pondered this question for a matter of years. The initial presumption of causation was that of regional anoxia with a production of noxious chemicals (e.g., soft tissue avascular necrosis). Khan and Cook34,35 have agreed that the histopathology is devoid of inflammatory cells and have suggested that noxious agents including chemical mediators, matrix substances and disrupted collagen may stimulate nociceptors. Voloshin and associates73 have advanced a similar suggestion concerning rotator cuff and bursal pain. Tasto and colleagues,71 in preliminary basic science investigations, report the possibility of free nerve endings, as noted by the identification of immunohistologic markers for nerve. However, the identification of free nerve endings themselves has not been supported by our electron microscopy evaluations.37 The work of Lian and associates38 on patellar tendinopathy identifies the ingrowth of substance P fibers with the presumption that this may play a nociceptive role.
A complete evaluation of the patient includes range of motion and strength testing of the neck, shoulder and wrist. Grip strength and pain rated on a continuous scale as well as forearm circumference should be documented.
The area of maximal tenderness in lateral elbow tendinosis typically lies 5 mm distal and anterior to the midpoint of the lateral epicondyle (e.g., the pathoanatomy typically is not at the epicondyle). Provocative stress testing consists of resisted wrist and finger extension with the elbow in flexion with marked accentuation as the elbow is brought into extension (Fig. 44-6). Increased pain with extension is common even with mild tendinosis. When provocative tests are positive in flexion, the need for surgical intervention is more likely in our experience.