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CHAPTER 117 Tendinopathy and Bursitis
Michael J. Schmidt and Stephen L. Adams
TENDINOPATHY
Perspective
Emergency physicians may see a wide variety of patients with
tendinopathies due to overuse and injury given the increased participation of people in athletics and fitness.1 Approximately half
of all sports participants will be injured at some time, and of these
injuries, up to half will involve a tendinopathy. Tendinopathies
have been implicated in approximately 40% of tennis injuries, and
between 37 and 79% of participants in running will suffer an
injury, with most of these injuries related to overuse.1,2 In the
workplace, the incidence of work-related musculoskeletal disorders is higher in occupations that involve repetitive motion, localized contact stress, awkward positions, vibrations, and forceful
exertion. Ergonomic and medical intervention programs may
reduce the incidence of work-related injuries.3
Complicating the acute pain and functional limitations, tendinopathies often become chronic and can be disabling. Patients
may have symptoms for extended periods despite appropriate
therapy. The management of tendinopathy focuses on identification of the cause of discomfort; elimination of sources of primary
tendinopathy; institution of treatment modalities, such as analgesic medication, protection, relative rest, application of ice, compression, and elevation as necessary; modification of behavior to
minimize or to eliminate sources of continuing irritation; and,
importantly, referral for appropriate follow-up care and early
rehabilitation.4,5
Principles of Disease
Tendons are collagenous structures that connect muscle to bone.
They transmit the forces originating in the muscle to the bone,
which enables joint motion. The diagnosis of tendinitis, a commonly used term implying an “inflammation of the tendon,” has
long been attached to many overuse injuries. Many practitioners
now advocate use of the term tendinosis as a more accurate reflection of the pathologic process, given that histologic findings consistent with inflammation are not clearly evident in pathoanatomic
studies. Although it has been noted that reliable, well-conducted
epidemiologic studies have not been performed for most tendinopathies, the histopathologic substratum, in many cases, is
degenerative.1 The term tendinopathy is used throughout this
chapter to refer to the impaired tendon, as it encompasses the
variety of pathologic processes.
Mechanical overload and repetitive microtrauma to the musculotendinous unit are thought to be the major precipitating causes
of most tendinopathies. This is a result of extrinsic and intrinsic
factors that modify the pathophysiologic state. Intrinsic factors,
1518
such as age, gender, malalignment, joint laxity, muscle weakness,
and imbalance, can result in excessively high or frequent mechanical loads during normal activity. Extrinsic factors, such as ergonomics, abnormal movements, excessive duration of activity, and
increased frequency or intensity of activity, can also contribute to
the development of a tendinopathy. Many injuries have a multifactorial origin.6 An increased incidence of tendinopathy and
tendon rupture, particularly of the Achilles tendon, is reported in
patients taking fluoroquinolone antibiotics, particularly in individuals receiving steroid treatment or those with renal disease.7
Under optimal conditions, such as appropriate athletic training,
the musculotendinous units are able to adapt to tension overload
because of the ability of bone to increase its load-bearing capacity
and because of an increase in size and strength by hypertrophy of
existing muscle fibers. An enhancement of tendon and ligament
strength occurs by an increase in collagen content, collagen crosslinking, and mucopolysaccharide content. Unfortunately, many
athletes may not allot sufficient time for this adaptive process to
occur. For instance, a runner may increase mileage, intensity, or
both with excessive alacrity, not allowing time for the cellular
changes that are required to adapt to the increased stresses. Poor
technique and improper equipment may also contribute to the
development of an overuse syndrome.
The pathophysiologic mechanism of tendon healing has mainly
been described in the literature in the context of acute injury (e.g.,
rupture), and correlation to the healing process in tendinopathies
remains unclear. Acutely injured tendons go through several stages
in the healing process, and it may take 6 to 12 weeks for structural
organization and collagen cross-linking to return the tendon to its
preinjured strength.8 As the healing process ensues, unrestricted
activity is generally avoided. However, atrophy associated with
immobilization should also be avoided because the strength in
healing tendons and ligaments increases faster when controlled
forces are applied. Consequently, flexibility forces, eccentric
strength training, and a measured return to resistive exercises have
been suggested as long as pain is not produced. Most patients with
overuse tendinopathies fully recover within 3 to 6 months.9 In
summary, a prescription for good follow-up with proper rehabilitation is important in caring for the patient with tendinopathy.
Some areas with common presentations of tendinopathies are
diagrammed in Figure 117-1.
Clinical Features
General Tendinopathy
The history of the patient presenting with a tendinopathy can be
variable, although certain clinical aspects are characteristic. A
Chapter 117 / Tendinopathy and Bursitis 1519
“Bursitis of the shoulder”
supraspinatus tendon and
subdeltoid bursa
“Student’s elbow”
olecranon bursa
“Tennis elbow”
extensor tendons
Posteriorly at
ischial tuberosity;
“ischial bursitis,”
located medial to
the sciatic nerve
“Trochanteric
bursitis”
gluteus medius
and minimus
tendons
“Housemaid’s knee”
prepatellar bursa
“Bicipital tendinopathy”
tendon of long head
of biceps
“Iliopectineal bursitis”
located lateral to
femoral vessels
“de Quervain’s
tenosynovitis”
tendons of extensor
pollicis brevis and
abductor pollicis longus
“Acute tendinopathy
of the wrist”
flexor carpi ulnaris
and other wrist
flexor tendons
“Infrapatellar bursitis”
infrapatellar bursa
“Anserine bursitis”
anserine bursa
“Bursitis of the heel”
Achilles tendon
Figure 117-1. Location of common sites for tendinopathy or bursitis. (Modified from Branch WT: Office Practice of Medicine, 2nd ed.
Philadelphia, WB Saunders, 1987.)
recent history of repetitive stress may be obtained by inquiring
about changes in sports or other recreational activities, work activities, or changes in the workplace. Many patients initially report
no such changes, but when they are prompted to consider activities during several weeks or months (including sports equipment
used, workplace ergonomic features, protective boots, or other
features), a potential inciting change or activity may be elicited.
On occasion, no cause is identified for an inciting mechanical
overload. A history of fluoroquinolone therapy, infectious disease,
or other systemic illness should also be obtained as initial presentations of rheumatologic disorders or infections, such as those
from Mycobacterium, have been described.7,10-12
Pain is the most common symptom of the patient who presents
with tendinopathy. Increasing discomfort, nonradiating, at the site
of the affected tendon is a general symptom.4 The discomfort is
frequently described as more severe subsequent to periods of rest.
Unlike the discomfort of morning stiffness associated with arthritis, the pain of tendinopathy may resolve after initial movement,
only to be manifested as a throbbing pain after completion of
exercise. The patient may have had prior similar episodes. Continued episodes may be accompanied by an increased severity in pain.
Consequently, it may be helpful to know whether a diagnosis was
made (and how) and which treatment rendered (if any) was
successful.
In the evaluation of the patient with a tendinopathy, a thorough, directed musculoskeletal examination yields important
information. Inspection searching for signs of edema, effusion,
erythema, atrophy, deformity, symmetry, or trauma can be
helpful. Palpation of the tendon, noting warmth or evidence of
crepitation on movement, is important. Evidence of tenderness
over the tendon, especially localized, reproducing the patient’s
pain should be elicited.4 Underlying bone tenderness (and consideration of other differential diagnoses, including avulsion
fracture and osteomyelitis) should be assessed as well. Motor
function, particularly passive and active range of motion (and
symptoms elicited during the examination), strength (and evidence of weakness or pain), and joint involvement and stability
should be noted.
In narrowing the diagnosis, it is important to determine whether
the source of pain is articular (within the joint capsule) or periarticular (around the joint capsule). In general, arthritis produces
generalized joint pain, warmth, swelling, and tenderness. The discomfort of arthritis increases with both passive and active motion
of the joint. In contrast, the pain of a tendinopathy tends to be
more localized.4 Tenderness and swelling do not occur uniformly
across the joint, and pain may be produced only with certain
movements, most commonly with resisted active contraction or
passive stretching of the affected muscles or tendons.
1520 PART III ◆ Medicine and Surgery / Section Nine • Immunologic and Inflammatory
Specific Tendinopathies
Shoulder. Tendinopathies of the shoulder joint include impingement syndrome, which includes subacromial bursitis or rotator
cuff tendinopathy, bicipital tendinopathy, calcific tendinopathy,
and adhesive capsulitis.
Impingement Syndrome and Rotator Cuff Tendinopathies. The shoulder joint is predisposed to soft tissue injury
because of its extensive range of motion and unique anatomic
structure. Although it is inherently unstable, the muscles of the
rotator cuff (supraspinatus, infraspinatus, teres minor, and subscapularis) and the glenohumeral ligaments serve to stabilize the
joint. The muscles of the rotator cuff originate from the scapula
(hence their nomenclature), and their tendinous insertion is
found on the fibrous capsule of the glenohumeral joint after
traversing through the subacromial space. The presence of the
subacromial bursa, as for all bursae, serves to ensure fluidity of
movement, but it may become inflamed as a part of an impingement syndrome.13 Impingement of the tendons occurs because of
their unique position interposed between the humeral head and
the acromion, which may predispose to a chronic tendinopathy.
The functional arc of the elevated shoulder is forward and in the
anterior plane. As a result of this position, the greater tuberosity
of the humerus may compress (impinge) the tendons of the
rotator cuff (usually the supraspinatus) against the undersurface
of the anterior third of the acromion. Because of the insertion of
the tendon of the long head of the biceps, it too may be involved
as part of the impingement syndrome.13 Development of this tendinopathy may be a result of overuse of the extremity that leads
to microtrauma of the tendinous fibers, or it may be due to individual anatomic differences (congenital or from the process of
aging, such as osteophytic changes) that predispose to tendinopathy, or both. Other entities that may coexist and complicate an
impingement syndrome include subacromial bursitis, bicipital
tendinopathy, and calcific tendinopathy.14
More than 30 years ago, Neer noted that 95% of rotator cuff
tears are associated with impingement (excluding tears due to a
one-time traumatic event). He described three progressive stages
of the impingement syndrome as a result of overuse.15 The first
stage is frequently seen in athletes younger than 25 years who
participate in sports that require repetitive overhead motions of
the shoulder (e.g., swimming and baseball).15,16 It is characterized
by edema and hemorrhage within and around the tendon. The
pain is usually described as a dull ache over the anterolateral
shoulder, extending from the shoulder to the middle upper arm,
often occurring after an activity involving flexion and abduction
of the arm. Point tenderness may be elicited over the greater tuberosity. No weakness or loss of motion is generally present. This
condition is generally believed to be reversible with appropriate
treatment. In the second stage, as mechanical trauma continues,
fibrosis and thickening of the tendon and subacromial bursa can
occur. This generally affects patients between 25 and 40 years of
age. The pain becomes constant and may worsen at night. Active
motion may be limited by pain, and any activity involving overhead movement exacerbates the symptoms. Passive range of
motion should be preserved, and on physical examination, pain is
more diffuse and intense. The third stage has symptoms similar to
those of the second stage but may involve a prolonged history of
shoulder problems. The range of motion of the shoulder is usually
decreased because of either disuse or a partial rotator cuff tear. On
pathologic examination, tendon degeneration and attrition may
be present. Partial-thickness tears may occur or extend with minor
trauma or stress. Complete tears of the rotator cuff, biceps tendon
rupture, and osteophytic bone changes are sometimes seen.
Physical examination in the evaluation of a rotator cuff tendinopathy includes maneuvers that can exacerbate the symptoms of
impingement.17 Because the supraspinatus tendon is most often
involved, a physical examination sign (sometimes referred to as
Jobe’s sign, after Frank Jobe, team physician of the Los Angeles
Dodgers, or the empty can test, describing the position of emptying aluminum cans) is helpful in assessing the supraspinatus
tendon with resistance testing. With the arms abducted at 90
degrees in the scapular plane (30 degrees anterior to the coronal
plane), the arms are internally rotated with the thumbs pointed
downward. The examiner places a downward force on the arms,
and the patient is instructed to resist the examiner and to keep the
arms parallel to the floor. Weakness or pain is considered a positive
finding. If the patient is unable to resist the force of the examiner,
supraspinatus weakness should be suspected.
Another sign of rotator cuff tendinopathy is elicited by the Neer
test, which suggests mechanical impingement with decrease of the
subacromial space. The examiner forward flexes the arm, which
causes impingement of the greater tuberosity of the humerus with
the anterior and inferior edge of the acromion. The patient’s
shoulder should then be fully flexed to 180 degrees. A positive
result occurs if there is pain produced at the end range of the arc.
The Hawkins test, also indicative of mechanical impingement,
is performed by forcibly internally rotating the proximal humerus
while the shoulder is forward flexed to 90 degrees and the
elbow flexed to 90 degrees. Pain with this maneuver indicates a
positive finding.
A complete rotator cuff tear is evaluated by the drop arm test,
in which the arm is passively abducted at 90 degrees and the
patient is asked to maintain the abduction. If the arm drops to the
side, a large rotator cuff tear should be considered.17
The shrug sign is exhibited when a patient with acute macrotrauma to the rotator cuff is asked to abduct the arm at 90 degrees
and appears to be giving a shrug with that side. This movement
results from the scapula’s attempting to abduct the arm without
the assistance of the rotator cuff. Although this has historically
been associated with rotator cuff disease, it is somewhat nonspecific and can be associated with other shoulder disease.18 Patients
with adhesive capsulitis (frozen shoulder) have limitation of active
and passive range of motion.19
Bicipital Tendinopathy. The tendon of the long head of the
biceps, given its insertion into the humerus in proximity to
the rotator cuff, can be associated with the impingement syndrome. The patient with bicipital tendinopathy may report
pain in the anterior shoulder that radiates down to the radius.
Discomfort occurs when the individual rolls on the shoulder at
night or attempts to reach a hip pocket or a back zipper. Focal
tenderness can be obtained by palpation in the groove between
the greater and lesser tuberosities of the humerus while testing for
Yergason’s sign, which is elicited by having the patient flex the
elbow to 90 degrees with the arm against the body and resisting
supination of the forearm. Pain in the area of the proximal tendon
is considered to be a positive finding and indicative of bicipital
tendinopathy.17
Another physical examination tool in the diagnosis of bicipital
tendinopathy is the Speed sign. With the elbow extended and the
forearm supinated, the patient is instructed to resist forward
flexion of the adducted shoulder at 60 degrees. Pain in the area
of the proximal biceps tendon (bicipital groove) is indicative
of a positive finding. This may also be suggestive, however, of
labral disease.20
Calcific Tendinopathy. Calcific tendinopathy is an acute or
chronically painful condition associated with deposition of
calcium crystals that occurs in or around the tendons of the
rotator cuff. The cause is unknown but has been postulated to be
related to tissue hypoxia and degeneration due to overuse.21
Although it can affect any of the rotator cuff tendons, it seems to
have a predilection for the supraspinatus. The symptoms are
similar to those of an impingement syndrome, and the condition
generally affects people older than 40 years. Calcium deposition
Chapter 117 / Tendinopathy and Bursitis 1521
Figure 117-2. Plain radiograph of the shoulder showing calcium
deposits of the rotator cuff in a patient with acute shoulder pain,
consistent with calcific tendinopathy.
occurs over time and then undergoes spontaneous resorption.
This resorptive phase is thought to be the painful aspect, but the
severity of the symptoms is not related to the size of the deposit.
Pain is believed to be in response to the local chemical pathologic
disorder and direct mechanical irritation.22
On physical examination, there may be specific tenderness
over the greater tuberosity as well as symptoms consistent with
impingement. Radiographic evaluation may show evidence of calcification in or around the rotator cuff tendons (Fig. 117-2). The
presence of calcium in the tendon does not necessarily affirm
the origin of the pain because asymptomatic patients may have
evidence of calcification on a routine radiograph.22
Elbow. Increasingly, athletes of all ages and skill levels are
participating in sports involving overhead arm motions; consequently, elbow injuries are increasingly seen.23 From an anatomic
and functional perspective, the extensors and supinators of the
wrist attach to the lateral elbow, and the flexors and pronators
attach medially.
Lateral Epicondylitis. Lateral epicondylitis (“tennis elbow”) is
a painful elbow condition that occurs at the insertion of the
common extensor tendon (extensor carpi radialis brevis) onto the
lateral epicondyle of the humerus. Although it occurs in many
tennis players, epidemiologic studies suggest that less than 5% of
patients with such a syndrome actually play tennis. Activities such
as driving in screws, use of a wrench, and repetitive work on an
assembly line have also been implicated. Symptoms often begin as
a dull ache on the outer (lateral) aspect of the elbow.24,25 The discomfort can be exacerbated by activities that involve extension or
supination of the wrist, such as grasping and twisting. Cozen’s test
is performed by having the patient keep the fist clenched while
extending the wrist. The examiner grasps the forearm with the left
hand while the right hand pulls the patient’s hand toward flexion
against the patient’s resistance. A positive finding is pain at the
lateral epicondyle, reproducing the patient’s symptoms.26
Active extension of the long finger against resistance with the
elbow in extension can also reproduce the pain over the lateral
epicondyle at the insertion of the extensor carpi radialis brevis. In
addition, patients will typically have tenderness to palpation just
distal to the lateral epicondyle, over the origin of the extensor carpi
radialis brevis.26
Radiographs can be helpful in cases with atypical or prolonged
symptoms and to rule out other pathologic conditions. Approximately 20% of patients demonstrate tendon calcification or a
reactive exostosis at the tip of the epicondyle.24
The differential diagnosis of lateral epicondylitis includes
posterior interosseus nerve entrapment (motor aspect of radial
nerve in forearm). Other associated lesions include plica, synovitis,
chondromalacia, and adolescent osteochondral defect.24
Medial Epicondylitis. The pain of the less common medial
epicondylitis (“pitcher’s elbow” or “golfer’s elbow”) can result
from microtrauma at the site of the insertion of the flexor carpi
radialis on the medial epicondyle. It is important to differentiate
medial epicondylitis from other causes of medial elbow pain,
including medial ulnar collateral ligament injury. As a result of
repetitive valgus stress placed on the joint, microtraumatic injury
and valgus instability at the ligament can occur. With disruption
of the medial ulnar collateral ligament, abnormal stress is placed
on the articular surfaces, which may lead to degenerative changes
and the formation of osteophytes.27 In the case of medial epicondylitis, patients will generally have tenderness over the flexorpronator origin slightly distal and anterior to the medial
epicondyle. Pain can be reproduced by having the patient attempt
wrist flexion and forearm pronation against resistance.28
Wrist
de Quervain’s Tenosynovitis. The wrist and hand comprise
several tendons that pass through thick, fibrous retinacular
tunnels. These help prevent subluxation of the tendons and act as
a pulley system. Overuse syndromes are thought to result from
changes of the synovial lining between these tendons and retinaculum. de Quervain’s tenosynovitis involves the synovial lining
of the abductor pollicis longus and extensor pollicis brevis.
Although the term tenosynovitis indicates an inflammation of the
tendon sheath, it has been noted that there are many potential
forms of tenosynovitis. Classic acute inflammatory changes
that are characteristic of tenosynovitis may be related to systemic
manifestations of disease (e.g., rheumatoid arthritis and gout);
tenosynovitis related to de Quervain’s syndrome is referred to by
some practitioners as stenosing tenosynovitis. The pathologic
process of de Quervain’s tenosynovitis does not generally involve
inflammation because the primary change is thickening of the
extensor retinaculum covering the first dorsal compartment of the
wrist. It has been suggested that de Quervain’s disease is a result
of intrinsic degenerative mechanisms rather than extrinsic inflammatory ones.29
The history may consist of chronic, repetitive trauma or unaccustomed repetitive efforts, such as firm grasping and movement
of the hand in a radial direction. Direct trauma, such as a direct
blow or fall, has occasionally been implicated.30 The discomfort of
de Quervain’s tenosynovitis can be localized over the radial styloid
process. Radiation of pain proximally to the forearm or distally
down the thumb has been noted. The pain is generally constant
but may be exacerbated by maneuvers that include grasping,
abduction of the thumb, and ulnar deviation of the wrist. In most
cases of de Quervain’s tenosynovitis, the onset is gradual and not
associated with a history of acute trauma.
On physical examination, slight swelling may be seen over the
radial styloid. Crepitation may be palpable over the tendons with
flexion and extension of the thumb. An increase in the tensile load
(passive stretching or active contraction) in the abductor pollicis
longus or extensor pollicis brevis increases pain. The Finkelstein
test, which exacerbates the discomfort of de Quervain’s tenosynovitis, is the most pathognomonic physical sign. The patient is
instructed to hold the affected thumb in the palm by the fingers
and then to ulnar deviate the wrist. Pain will occur near the radial
styloid, which is also the point of tenderness. Pain with this
maneuver is considered to be a positive finding. Radiographs are
characteristically normal.
1522 PART III ◆ Medicine and Surgery / Section Nine • Immunologic and Inflammatory
The differential diagnosis includes scaphoid fracture and osteoarthritis of the carpometacarpal joint, which has pain caused by
longitudinal traction and compression. Rarely, infections such
as tuberculosis or disseminated gonococcal infections can be
manifested as tenosynovitis.
Knee
Patellar Tendinopathy. Patellar tendinopathy or “jumper’s
knee” occurs in sports that have jumping as a part of the activity,
although it can also occur as a result of other sporting activities.31
Patients complain of pain at the inferior pole of the patella. The
discomfort may abate with activity early in the tendinopathy but
later progresses to the point of discomfort during exercise and at
rest. With the knee flexed at 30 degrees, which relaxes the quadriceps, tenderness may be localized to the deep surface of the pro­
ximal attachment of the patellar tendon at the inferior pole of
the patella. However, healthy active athletes sometimes have
tenderness on examination as well.31,32
The differential diagnosis includes patellofemoral syndrome,
which arises from imbalances in the forces controlling tracking
during knee flexion and extension. The patient usually complains
of anterior knee pain, described as “behind” or “around” the
patella, which is classically worse on ascending or descending stairs
or on rising from a seated position. On occasion, there is tenderness of the medial or lateral retinacula or facets.33
Imaging with ultrasonography and magnetic resonance imaging
(MRI) may reflect collagen degeneration but is generally adjunctive to the distinctive history and physical examination findings.
It is noted that some asymptomatic jumping athletes have imaging
appearances similar to those of affected individuals and that prognosis and outcome are not predicted by such imaging.31
Ankle
Achilles Tendinopathy. Achilles tendinopathy is a common
overuse syndrome that typically affects male athletes. The Achilles
tendon, named for the mythological Achilles, whose heel was not
immersed in the river Styx as his mother dipped him in the river
for its protective powers, arises from the medial and lateral heads
of the gastrocnemius muscle and the deep layers of the soleus
muscle and inserts on the calcaneal tuberosity. A major function
is plantar flexion of the foot. It is the strongest and largest tendon
in the body and can withstand tensile loads more than 12 times
the body’s weight during running.34
The Achilles tendon is vulnerable to injury from either trauma
or overuse. A tendinopathy can also develop as a result of systemic
disease (e.g., ankylosing spondylitis, Reiter’s syndrome, gout, and
pseudogout). The use of fluoroquinolones has also been related to
Achilles tendinopathy.7
The occurrence of Achilles tendinopathy is highest among individuals who participate in middle- and long-distance running,
orienteering, track and field, tennis, badminton, volleyball, and
soccer. Some studies have noted an almost 10% annual incidence
of Achilles disorders in elite runners.34 The most common Achilles
disorders are tendinopathy (55-66%) and insertional problems,
such as retrocalcaneal bursitis and insertional tendinopathy (2025%).34 Many cases of Achilles tendinopathy are thought to be
multifactorial in origin. Body mechanics and environmental
factors (e.g., uneven terrain) may apply valgus or varus stress to
the tendon. Technique, equipment, and body mechanics can also
contribute to the development of this tendinopathy. Anatomically,
the vascular supply to the tendon creates a watershed area approximately 2 to 6 cm above the calcaneal insertion. This is thought to
be responsible for clinical symptoms and the pathologic disruption commonly seen at this site.
The patient’s history provides most of the information necessary to make the diagnosis of Achilles tendinopathy. Pain, a cardinal symptom of Achilles tendinopathy, may lead the patient to
seek medical help. Some practitioners have noted that the patient’s
symptoms reflect the degree of the tendon abnormality. As with
many tendinopathies, pain after strenuous activities is reported in
the early phase, whereas pain in the later phase occurs during
activity and even at rest. At this point, the patient is often unable
to perform sporting activities.34
On physical examination, inspect the contour of the muscletendon unit and note areas of swelling and erythema. In acute
Achilles tendinopathy, the tendon may be diffusely swollen and
exhibit tenderness on palpation, usually greatest in the middle
third. Typically, in the patient who has acute symptoms of tendinopathy, the area of swelling and tenderness does not move with
dorsiflexion of the ankle joint. On palpation, local heat, crepitation, and palpable tendon nodules or defects may be noted. Examination for ankle instability and biomechanical faults should be
considered.34
Achilles Tendon Rupture. Although rupture of the Achilles
tendon most often occurs when it is preceded by tendon damage,35
it is possible for untrained athletes to apply excessive force and to
rupture the tendon in the absence of prior changes of tendinopathy. Partial and complete rupture may occur, most commonly in
30- to 40-year-old men. Complete rupture is more common in the
middle-aged recreational athlete. Historically, the patient may
note a “popping” sensation followed by acute weakness and inability to continue the exercise or sport. The patient may report that
it felt as though someone kicked him or her in the back of the
ankle or, if playing a racket sport, as if he or she were struck on
the calf by a ball.
On physical examination, a defect in the tendon can sometimes
be palpated. If enough time has elapsed to allow hematoma formation, bogginess may be noted over the injured area of the tendon.
The ability to plantar flex the foot is not incompatible with a
complete rupture of the Achilles tendon. There are multiple
plantar flexors of the foot and toes. Muscles such as the tibialis
posterior, flexor digitorum longus, flexor hallucis longus, peroneus
brevis, and peroneus longus can remain functional and therefore
disguise a complete rupture with the ability to plantar flex the foot.
The Simmonds (Thompson) test can be performed to evaluate for
complete rupture. With the patient prone and feet hanging over
the edge of the bed, the examiner squeezes the calf muscles at their
widest point and looks for passive plantar flexion. The absence of
plantar flexion is considered a positive finding, indicative of a
complete tear of the Achilles tendon. The presence of plantar
flexion does not, however, negate the possibility of a partial tear
of the Achilles tendon.
Diagnostic Strategies
The diagnosis of tendinopathy is generally made on clinical
grounds. Although plain radiographs may be helpful in excluding
bone abnormalities, ultrasonography has been recommended by
some practitioners as the modality of choice for evaluation of
pathologic tendon conditions.36 Ultrasonography can be especially
useful when other conditions (e.g., gouty arthritis) obscure the
findings of concomitant tendinopathy. Although ultrasound
imaging is employed in the emergency department (ED), the use
of this imaging technique for soft tissue evaluation in this setting
is relatively unstudied, and thus it is not frequently used.37,38
In cases of acute or chronic tendinopathy, one or more of the
following features can be seen: loss of the fibrillar echotexture,
focal tendon thickening, diffuse thickening, focal hypoechoic
areas, extended hypoechogenicity, irregular and ill-defined
borders, microruptures, and peritendinous inflammatory edema.39
Hypoechoic areas surrounding tendons provide evidence for surrounding soft tissue inflammation. In addition to tendinopathy,
tendon tears, both partial and complete, can be delineated by
ultrasonography.39
MRI has been used to visualize pathologic conditions of the
tendon. It is able to provide high intrinsic tissue contrast, which
Chapter 117 / Tendinopathy and Bursitis 1523
permits the distinction between normal tendons and abnormal
tendons, and the high spatial resolution that permits detailed anatomic structures to be identified. MRI has superb resolution of the
soft tissue structures and can aid in a variety of tendon disorders.
Cost, availability, the need to have the patient be still during examination, and the loss of the interactive and dynamic component
compared with ultrasound examination are disadvantages to use
of this modality.40
Differential Diagnosis
The differential diagnosis for tendinopathy includes tendon ruptures, bursitis, ligamentous injuries, septic and inflammatory
arthritis, nerve entrapment syndromes, and bone abnormalities
(such as fracture, foreign body, tumor, and osteomyelitis).
Management
General Tendinopathy
The management of tendinopathy focuses on identification of the
cause of discomfort; elimination of sources of primary tendinopathy; institution of treatment modalities, such as analgesic medication, protection, relative rest, application of ice, compression, and
elevation as necessary; modification of behavior to minimize or
to eliminate sources of continuing irritation; and, importantly,
referral for appropriate follow-up care.5
Cryotherapy (cold treatments, 20 minutes at a time every
several hours, for the first 24 to 48 hours) may be beneficial. Nonsteroidal anti-inflammatory drugs (NSAIDs) are also sometimes
indicated to provide pain relief, although there is little evidence to
support a beneficial effect with their use because tendinopathies
tend to represent a degenerative rather than an inflammatory
process.41 Graduated range-of-motion exercises may be useful
after the period of immobilization. Although corticosteroid injection is often used, its role for most tendinopathies is unclear.42,43
The use of corticosteroid injection is controversial. Steroids should
not be injected into a major tendon such as the Achilles tendon
or the patellar tendon, which may be at risk for spontaneous
rupture if it is already weakened.
Specific Tendinopathies
Impingement Syndrome and Rotator Cuff Tendinopathies. The treatment of rotator cuff tendinopathies and the impingement syndrome follows the treatment of tendinopathy in general. Emphasis
is placed on physical rehabilitation and strengthening exercises. A
significant proportion of patients will improve with conservative
management. In those who do not, surgical intervention, such as
acromioplasty or repair, may be indicated.44,45
Calcific Tendinopathy. The initial treatment of calcific tendinopathy is mainly conservative and consists of analgesia and brief
sling immobilization because prolonged immobilization may
result in adhesive capsulitis. The use of corticosteroids is controversial. Ultrasonography and extracorporeal shock wave therapy
have been used with some success.22 A small percentage of
patients who do not respond to these interventions may need
surgery. As well as arthroscopic treatment, localized disruption
in the resorptive phase by needle lavage under fluoroscopic guidance or in the operating room has been noted to be an efficacious
therapy.21,22 Follow-up care is important because calcific tendinopathy has been described as the best known cause of reactive
cuff failure.
Lateral and Medial Epicondylitis. In up to 95% of patients, epicondylitis will improve with conservative therapy.24 Initial efforts
include making the patient more comfortable with the standard
principles of protection, relative rest, cryotherapy, compression,
elevation, medication (NSAIDs), and modalities of physical
therapy. The term relative rest implies the avoidance of abuse and
not the absence of activity. Activities that aggravate the pain
should be eliminated, and an attempt to protect the tendon
through such strategies as a reduction in playing time or intensity
should be considered. Control of force loads by bracing, improved
performance technique, and use of appropriate equipment should
also be considered.24 Follow-up evaluation should be ensured.
de Quervain’s Tenosynovitis. The initial treatment of de Quervain’s tenosynovitis consists of immobilization with a thumb spica
splint, anti-inflammatory medications, and prompt referral. Corticosteroid injection has been shown to be an effective treatment
of de Quervain’s disease, and failure to respond may be due to
anatomic variation or poor technique.29,46 Surgical decompression
of the first dorsal compartment may be indicated if these treatments fail.29
Achilles Tendinopathy and Rupture. In addition to routine conservative treatment, patients with Achilles tendinopathy should
be referred for orthopedic evaluation and correction of limb
malalignment with the use of orthotics or heel lifts. Eccentric
loading exercise and low-energy shock wave therapy are effective
therapies for Achilles tendinopathy.47-49
The management of Achilles tendon rupture may be either
operative or nonoperative, depending on the patient involved.
Appropriate consultation with an orthopedist is essential. A conservative approach, including immobilization in a short or long
leg cast in the equinus position, may be indicated.50 Some authors
note that complete ruptures in active athletes should be treated
surgically in most cases.51 Although other risks and benefits must
be taken into consideration, some studies indicate that early
surgery may be indicated because the risk for Achilles tendon
re-rupture is less.50,51
Disposition
Most patients with tendinopathy are safely discharged home
with proper discharge instructions, relative rest of the tendon,
analgesia, and appropriate follow-up. The exception is elderly or
disabled patients who are rendered unable to perform the activities of daily living by the tendinopathy. Although appropriate rest
and analgesia provide symptomatic relief, underlying causes
should be sought and modified.
BURSITIS
Perspective
Bursae are closed, round, flat sacs lined by synovium.52 They occur
at areas of friction between skin and underlying ligaments and
bone. The bursa permits lubricated movement of soft tissues over
areas of potential impingement (e.g., subacromial bursa) and friction (e.g., olecranon bursa and prepatellar bursa). Many bursae
are nameless, and new bursae can form as a result of frequent
irritation. The two most common identifiably inflamed bursae are
the olecranon and the prepatellar. When these bursae are inflamed,
they are generally recognizable over the extensor surface of the
elbow or the knee, respectively.
Principles of Disease
Many cases of bursitis are idiopathic in nature, but common identifiable causes of inflammation include infection (most often due
to Staphylococcus aureus), trauma (which may predispose to infection), rheumatologic disorders (e.g., gout, pseudogout, ankylosing
spondylitis, and rheumatoid and psoriatic arthritis), and other
systemic diseases.
1524 PART III ◆ Medicine and Surgery / Section Nine • Immunologic and Inflammatory
Clinical Features
Olecranon and Prepatellar Bursitis
Less than half of patients who present with olecranon or prepatellar bursitis show signs of an infectious origin.53,54 Distinguishing
septic from nonseptic bursitis is not always straightforward, either
on clinical grounds or as a result of diagnostic testing. Patients
with septic bursitis generally present earlier in the clinical course
and have more pain, tenderness, erythema, and warmth compared
with those who have an inflammatory process. The most important predisposing factor in septic bursitis is trauma, which precedes septic bursitis in up to 70% of cases.52 Other predisposing
factors for septic bursitis include chronic illness such as diabetes
mellitus or alcohol abuse, chronic skin conditions such as atopic
dermatitis, and previous noninfectious inflammation of the
bursae such as rheumatoid arthritis or gout.52 It may also be seen
more commonly in people in occupations in which repetitive knee
or elbow trauma is common.
The olecranon bursa, on the extensor surface of the elbow, is
the only bursa of the elbow joint and is easily traumatized, resulting in inflammation, pain, and swelling. Infection can occur from
local trauma (e.g., puncture wound and laceration) but may also
be present in the absence of visible trauma. Hematogenous bacterial seeding is rare and is probably due to the limited vascular
supply of the bursal tissue.55
On physical examination, localized swelling and fluctuance
are usually present. Evidence of trauma may or may not be
present. Tenderness and warmth are seen in most patients
with septic bursitis. Erythema with overlying cellulitis is also
common in septic bursitis, and approximately 40% of patients will
also have a fever. Whereas tenderness, erythema, and warmth can
also be seen in patients with purely inflammatory causes of bursitis, both the frequency and degree of these findings are less,
and patients with septic bursitis will usually present earlier in the
clinical course.52,54
Passive range of motion should not produce much pain, with
the exception of full flexion, at which point there may be discomfort as the inflamed bursa is compressed. Evidence of significantly
diminished range of motion, generalized joint swelling, or other
signs and symptoms of joint involvement (e.g., joint pain, warmth,
and joint effusion) should raise a concern for septic arthritis.
Although the olecranon and prepatellar bursae generally do not
communicate with the joint space, one must consider this possibility in the differential diagnosis, especially if trauma is involved
and the integrity of the underlying joint is disrupted. Arthrocentesis to rule out septic arthritis should then be considered.
Diagnostic Strategies
When signs of acute inflammation are present, aspiration of the
bursa is indicated to exclude the presence of infection or crystalinduced disease.52,53 Although a discussion of the technique of
bursal aspiration is beyond the scope of this chapter, it should be
performed with sterile technique. An 18- to 20-gauge needle can
be used to perform this procedure. A lateral approach has been
recommended to lower the risk of iatrogenic sinus track formation, although the relation between the two is still somewhat
unclear. A distal approach can also be used when the olecranon
bursa is aspirated. In cases of septic bursitis, the aspirate usually
appears purulent but can occasionally appear serosanguineous
or straw colored. In the case of nonseptic bursitis, the aspirate
may vary from bloody aspirate to straw colored. The aspirate
of an inflamed bursa should be sent for evaluation of white
blood cell (WBC) count with differential, microscopy for crystals
(if crystalline disease is suspected), Gram’s stain, appropriate
cultures and sensitivities, and glucose level. A bursal fluid
glucose–to–serum glucose ratio of less than 50% is almost exclusively seen in septic bursitis.
Organisms found on either Gram’s stain or culture are diagnostic for septic bursitis. There are no definitive guidelines about use
of the WBC count to distinguish between septic and nonseptic
bursitis. A bursal fluid WBC count higher than 1000/µL3 is almost
always seen, and one higher than 5000/µL3 suggests bursal fluid
infection, even in the presence of a negative Gram’s stain, but
counts can be much lower in septic bursitis and above this level
in nonseptic cases. Culture is the definitive test but will not be
available during the initial evaluation. S. aureus is by far the most
common organism in bursal infection, followed by other staphylococcal and streptococcal species, and this bacteriology has not
changed in the last several decades.56-58
Because most cases of septic bursitis occur in the olecranon and
prepatellar bursae, the diagnosis is made clinically in conjunction
with aspiration. MRI can be used to aid in the diagnosis of inflammation or infection of deep bursae.59,60 Ultrasonography has also
been used as a modality for aspiration of deep bursae.61
Differential Diagnosis
Conditions that mimic bursitis include underlying fracture
and osteomyelitis. Radiography and bone scan or MRI may be
necessary to exclude these conditions. Other causes of the
nontraumatic, nonseptic bursitis include rheumatoid arthritis,
gout, pseudogout, scleroderma, ankylosing spondylitis, systemic
lupus erythematosus, hypertrophic pulmonary osteoarthropathy,
Whipple’s disease, oxalosis, and idiopathic hypereosinophilic
syndrome.
Management
Septic Bursitis
The optimal treatment of septic bursitis is uncertain because
large-scale clinical prospective trials in this area are lacking. Debate
remains about the use of outpatient (oral) versus inpatient (intravenous) administration of antibiotics, duration of therapy, use of
needle aspiration and incision and drainage, and use of operative
intervention.54
Patients who have bursal inflammation with suspicion (clinical
or laboratory) of infection should be treated with appropriate
antibiotics. Empirical therapy (including coverage for S. aureus
and Streptococcus species) may be indicated until definitive
culture results are available. The frequency of methicillin-resistant
S. aureus (MRSA) in septic bursitis is unclear, although recent
literature suggests that rates are low.56-58 MRSA was found to be
the most common cause of community-onset adult septic arthritis in one case series from an ED population, so empirical coverage for this organism in septic bursitis should be considered.62 A
trial of oral antibiotic therapy (up to 14 days) and treatment on
an outpatient basis in the patient with uncomplicated bursitis
and no underlying disease is reasonable. However, failure rates up
to 67% have been reported for outpatient treatment of septic
bursitis.54 One of the largest observational studies on the successful outpatient treatment of septic bursitis showed an admission
rate of only 1 of 118 patients, but all patients in this study received
sequential intravenous antibiotics for approximately 4 days at an
outpatient clinic followed by oral antibiotic therapy.63 Treatment
in an observation unit or inpatient setting with intravenous antibiotics therefore is a consideration for patients with significant
symptoms, with overlying cellulitis, or unlikely to receive close
follow-up.
Needle aspiration is a commonly used technique for the management of septic bursae. Successful treatment of septic bursitis
can be achieved in patients receiving outpatient oral antibiotics
Chapter 117 / Tendinopathy and Bursitis 1525
63
after initial needle aspiration. Laupland and Davies showed no
difference between patients who received aspiration (51% of total
patients) and those who did not, but the authors conceded that
patients who had more severe disease were likely to be selected for
drainage. Also, the diagnosis of septic bursitis was confirmed by
culture in only 26% of these patients, potentially underestimating
the importance of bursal drainage in patients with true septic
bursitis.52 Because needle aspiration is used for the diagnosis of
septic bursitis, initial drainage at the same time seems warranted.
Those with a purulent aspirate may require repeated aspiration at
1- to 3-day intervals if the effusion persists. In all cases, appropriate follow-up to assess response to therapy should be arranged.
Warm soaks and wound care are also indicated. Surgical incision
and drainage or bursectomy may also be necessary in severe,
recurrent, or refractory cases.54
Nonseptic Bursitis
The optimal treatment of nonseptic bursitis has not been clarified.
Most cases improve with conservative therapy, although complete
recovery can take many months. Aspiration can be considered in
the initial treatment of acute nonseptic bursitis. Further conservative therapy includes the administration of NSAIDs and application of a compression dressing with an elastic bandage to prevent
recurrent swelling. Systemic causes of bursitis (e.g., crystalline
disease) should be treated appropriately. Avoidance of local trauma
is important for treatment and successful prevention of bursitis.
Recurrent olecranon bursitis may be caused by underlying anatomic disorders such as bone spurs. Steroid injection into a nonseptic bursa has been used as a treatment modality, but multiple
complications have been described, including skin atrophy over
the bursa, chronic pain, development of septic bursitis, bleeding,
postinjection flare as a result of release of microcrystals, and
tendon rupture.
as the lateral thigh. Lying on the hip and walking may exacerbate
the pain. Trochanteric bursitis can occur as a complication of
rheumatoid arthritis. On examination, the pain of superficial bursitis may be reproduced by hip adduction, and the pain of deep
trochanteric bursitis may be reproduced with hip abduction. The
hip joint has normal examination findings. Septic trochanteric
bursitis has been described in the literature.64
Ischiogluteal Bursitis
The ischiogluteal bursa is located adjacent to the ischial tuberosity
and overlies the sciatic and posterior femoral cutaneous nerves.
Inflammation, known as weaver’s bottom, is described as pain over
the center of the buttocks with radiation down the back of the leg.
Sitting on a hard surface exacerbates the pain, and palpation over
the ischial tuberosity causes discomfort.
Iliopsoas Bursitis
The iliopsoas bursa is the largest bursa around the hip. It lies
between the iliopsoas tendon and the lesser trochanter. The pain
of iliopsoas bursitis usually is manifested as anterior hip pain that
can radiate down the medial thigh to the knee and is increased on
hip extension.65
Anserine Bursitis
The anserine bursa lies deep to the three tendons (sartorius, gracilis, and semitendinosus) that form the pes anserinus (“foot of the
goose”) and superficial to the medial collateral ligament. The
patient with anserine bursitis usually complains of medial knee
pain approximately 2 or 3 cm distal to the joint line. There is
usually tenderness to palpation in this area and occasionally swelling. Diabetes mellitus and possibly obesity and osteoarthritis of
the knee are risk factors for development of this condition.66
Disposition
Patients without underlying medical problems who present with
uncomplicated septic bursitis can usually be discharged with
appropriate oral antibiotics. Those with underlying diseases
(e.g., immunocompromise, leukopenia, and diabetes) and those
with systemic toxicity or severe bursal infection (e.g., purulent
drainage) are candidates for intravenous antibiotics and inpatient
therapy. Patients with a purulent aspirate may need repeated
aspiration. Close follow-up is necessary to ensure response to
therapy. Patients with presumed nonseptic bursitis require close
follow-up as well.
Other Types of Bursitis
Subacromial Bursitis
The subacromial bursa lies between the supraspinatus tendon and
the acromion. Subacromial bursitis is thought to be nearly synonymous with supraspinatus tendinopathy and may be involved
in the stages of rotator cuff impingement. Pain and tenderness,
localized to the lateral aspect of the shoulder, and signs of impingement may be noted on physical examination.13 Although it is
uncommon, septic subacromial bursitis can occur.61
Trochanteric Bursitis
The trochanteric bursa has both deep and superficial components.
The deep bursa is located between the greater trochanter and the
tensor fascia lata; the superficial bursa is located between the
greater trochanter and the skin. In general, middle-aged or older
women report acute or chronic pain over the bursal area as well
KEY CONCEPTS
Tendinopathy
■ Mechanical overload and repetitive microtrauma are key
underlying mechanisms in the development of tendinopathy.
Patients most often present with a history of progressively
worsening localized pain after work- or sport-related activities
that are repetitive in nature.
■ Tendinopathy may also be associated with nonmechanical
causes, including systemic manifestations of diseases and the
use of fluoroquinolones.
■ Most patients with tendinopathy can initially be treated with
conservative measures, such as protection, relative rest,
application of ice, medication, and elevation. Overuse
syndromes can take at least 6 to 12 weeks to heal. Inform
patients of this and provide appropriate referral for
follow-up.
■ Operative treatment may be indicated for selected cases
of tendon injury that require primary repair (e.g., rupture of the Achilles tendon) or that have failed to respond to
conservative treatment (e.g., impingement syndrome) and are amenable to surgical amelioration.
Bursitis
■ Consider the possibility of an infectious cause in all cases of
acute bursitis.
■ The definitive diagnosis of bursitis is made by aspiration of
the bursa and evaluation of the fluid.
■ Septic bursitis is most commonly caused by Staphylococcus
aureus.
1526 PART III ◆ Medicine and Surgery / Section Nine • Immunologic and Inflammatory
■ Nonseptic bursitis may be traumatic, rheumatologic (e.g.,
gout and pseudogout), or idiopathic in nature. Other
conditions, such as septic arthritis, osteomyelitis, and
underlying fracture, are in the differential diagnosis of
bursitis.
■ The management of bursitis includes treatment with
appropriate medication (antibiotics for septic bursitis, NSAIDs
for nonseptic bursitis), rest, application of ice, compression,
and elevation as well as prompt referral for appropriate
follow-up. Hospitalization is considered for severe local
infections, for patients who are immunosuppressed, and in
the presence of high fever or systemic toxicity.
The references for this chapter can be found online by
accessing the accompanying Expert Consult website.
Chapter 117 / Tendinopathy and Bursitis 1526.e1
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