Anterior Glenohumeral Instability
Background
The shoulder is the most commonly dislocated joint in the
body. When shoulder dislocation occurs in adolescents and children, it has the worst
natural history of any injury; the rate of recurrence in later years is at
least 70%. As many as 95% of shoulder dislocations are anterior. Anterior
dislocations often lead to recurrent anterior glenohumeral instability.
Recurrent anterior glenohumeral instability accounts for the largest portion of
the shoulder laxity spectrum. Excessive deviation of the humeral head on the
glenoid occurs in all or 1 of 3 directions: anterior, posterior, or inferior.
Although certainly not life threatening, recurrent subluxation or dislocation
is clearly lifestyle threatening and can effectively disable an otherwise
active individual.
See the images below.
Upper
- Type I superior labrum anterior posterior lesion. Lower - Type II superior
labrum anterior posterior lesion.
Upper
- Type III superior labrum anterior posterior lesion. Lower - Type IV superior
labrum anterior posterior lesion.
Normal shoulders have a certain degree of laxity due to minimal
bony restraint of the joint, which in turn allows the widest range of motion of
any joint in the body. The result is a tremendous need for competent
soft-tissue balance and control. Traumatic damage leads to laxity in the
soft-tissue and bony restraints; thus, recurrent subluxation and dislocation
ensues. Atraumatic etiologies also exist, but this article focuses on recurrent
subluxation and dislocation due to trauma.
Nonoperative and operative therapies both play a role in treatment
of anterior shoulder instability. Both have been studied extensively. Surgical
management has gone through an evolutionary process involving multiple methods
of fixation. This evolution has led to operative fixation that achieves a
stable repair with little restriction of motion.
For patient education resources, see the Breaks, Fractures, and Dislocations Center, as
well as Shoulder Dislocation.
Reports of anterior glenohumeral instability and
its many repair methods date back to Hippocrates' treatise, "On
Joints." Hippocrates described the practice of using cautery to cause the
capsule to scar and thus tighten around the joint. He wrote, "grasp the
skin at the armpit between the fingers and draw it in the direction towards
which the head of the humerus gets dislocated, then pass the cautery right
through the skin thus drawn away."
Since Hippocrates' description of capsule repair,
a multitude of new techniques have been reported, all aimed at preventing
recurrent dislocation or subluxation. These repairs can be divided into
anatomic and nonanatomic. Anatomic repairs focus on repairing the structure
that has been disrupted. With nonanatomic repairs (eg, Putti-Platt,
Magnuson-Stack, and Bristow procedures), an attempt is made to shorten or
tighten certain anterior structures regardless of the specific shoulder
pathology.
Early in the evolution of capsular repair, loss
of motion was considered acceptable and even desired as a necessary part of
stabilizing a shoulder. As new techniques followed, shoulder stability was
achieved without significant loss of motion. Postoperative motion restriction
is now considered a complication.
In 1923, Bankart described the lesion of
traumatic shoulder dislocation in theBritish Medical Journal, as follows: "The essential lesion
is the detachment of the capsule from the fibro-cartilaginous glenoid
ligament." He goes on to say, "... the only rational treatment is to
reattach the fibrous capsule to the glenoid ligament whence it has been
torn."
In 1965, du Toit and Roux reported a similar
procedure in which staples were used to attach the capsule to the anterior
glenoid rim. This method had the potential to simplify the procedure, but it
also added complications, such as glenoid damage from the staples and
loosening.
The Magnuson-Stack procedure was described next,
in 1943. This procedure involves transferring the subscapularis from its
attachment on the lesser tuberosity to a point lateral to the bicipital groove.
The goal was to produce a sling effect on the humeral head. Like the
Putti-Platt procedure that would follow, it decreased external rotation by
design.
In 1948, the Putti-Platt procedure was described.
Here, the subscapularis tendon and capsule are divided longitudinally at the
mid portion. The lateral free end is attached to the anterior rim of the
glenoid, and the medial free end is attached over the lateral end. The
Putti-Platt operation led to low dislocation recurrence rates, but it also led
to decreased external rotation.
In 1954, Latarjet proposed the Bristow procedure.
This procedure was later popularized by Helfet, in 1958. This involved
transferring the tip of the coracoid process with its muscular attachments. A vertical
slit in the subscapularis allowed the osteotomized coracoid to be attached to
the anterior glenoid with sutures. This procedure thus provided a bony block to
anterior glenohumeral translation.
The term anterior glenohumeral instability describes
the shoulder in which soft-tissue or bony insult allows the humeral head to
sublux or dislocate from the glenoid fossa. Function of these shoulders is
compromised. Patients typically experience apprehension, recurrent
subluxations, and frank dislocations. This pathology limits many activities,
including overhead arm motions, external rotation, and, thus, physical or
athletic activities.
In studies of anterior glenohumeral instability,
a wide array of incidences have been proposed. Most report an average age of
initial shoulder dislocation early in the third decade of life. The vast
majority, 85-95%, of these are anterior dislocations. One fourth of all
patients with dislocations present with a family history of the same problem. Rowe's
1956 analysis of 500 shoulder dislocations found only 8 occurred in children
younger than 10 years; the largest cohort of dislocations occurred in the
subsequent decade of life, in patients aged 10-20 years.
The age at the time of dislocation is the biggest
determinant of future recurrence. Recurrences result from anterior glenohumeral
instability and occur most commonly in patients younger than 20 years. Reported
recurrence rates in patients younger than 20 years vary from 70-100%.
The cause of anterior glenohumeral instability
can be traumatic or atraumatic. Either mechanism leads to the loss of balance
in the surrounding muscular and capsular structures.
Traumatic injury to any one component of the
shoulder soft tissue leads to instability. This traumatic insult most commonly
comes in the form of an anterior shoulder dislocation.
Atraumatic causes leading to multidirectional instability are not the focus of this article.
These causes include repetitive atraumatic injury, Ehlers-Danlos syndrome, Marfan syndrome, congenital absence of the
glenoid, deformities of the proximal humerus, and emotional and psychiatric
instability.
In an unstable shoulder, many findings are
possible. Each finding can occur alone or in combination with other lesions.
These lesions include the Bankart lesion (in 85% of cases), Hill-Sachs lesion
(in 77% of cases), anterior glenoid rim damage (in 73% of cases), capsular
redundancy, subscapularis deficiency, and glenoid fossa deficiency. Absence of
pathological findings is also possible.
In 1923, Bankart described the "essential
lesion" in posttraumatic anterior glenohumeral instability as the
detachment of the capsule from the fibrocartilaginous glenoid ligament. In this
lesion, the humeral head translates forward, shearing the inferior glenohumeral
ligament (IGHL) with the anteroinferior labrum from the glenoid rim.
Rowe's review of 28 patients in which he examined
shoulder pathology after traumatic anterior dislocation disputed Bankart's
claim to the essential lesion. Rowe's results showed "there was no
evidence that there is a single essential lesion responsible for the recurrent
dislocations of the shoulder." The Bankart lesions occurred in 27-100% of
cases.
Other lesions were just as variable.
Subscapularis laxity ranged from being present in every case to not being
present in any cases. Hill-Sachs lesions were present in 26-100% of cases.
Anterior glenoid trauma of all variations occurred in 2-52% of cases.
The next logical question is which of these
lesions actually causes the recurrent instability observed after traumatic
dislocations. This remains a debated topic. The most accurate conclusion is the
one Rowe came to in 1978 when he declared that no single lesion is responsible
for the recurrent dislocations of the traumatized shoulder.
Several lesions have been suggested. Baker et al
devised a system of classification for the Perthes-Bankart lesion, as follows:
·
Type I - Pure
capsular lesion
·
Type II - Partial
labral detachment
·
Type III - Complete
detachment of the inferior glenohumeral-labral complex
Other lesions include attenuation of capsule and
capsular ligaments, Hill-Sachs lesions, attenuation of the subscapularis, and
humeral avulsion of the IGHL.
Children presenting with a dislocated shoulder may
relate a couple of possible mechanisms. These mechanisms occur in a number of
ways and are similar to those in adults. Most commonly, the child falls on the
outstretched hand, forcing the arm into abduction and external rotation,
levering the humeral head out of the glenoid cavity. Activities promoting this
injury include contact sports, falls from heights, fights, and motor vehicle
accidents. Other mechanisms have been described, including elevation with
external rotation and direct blows.
A history of prior dislocations suggests a high
likelihood of anterior glenohumeral instability. Studies have shown a 70-100%
recurrence rate in various population groups of patients younger than 20 years.
As with physical examinations of any joint,
beginning by observing the shoulder is important. Note any atrophy of the
biceps, supraspinatus, or infraspinatus. Gross deformities can also suggest the
direction of a dislocation.
Range of motion of the shoulder must be tested
for restriction or hypermobility. Atraumatic instability generally manifests
with hypermobility of the shoulder, whereas traumatic instability typically
results in bilaterally symmetric motion. Generalized joint laxity is
demonstrated by extending the elbow, wrist, metacarpal-phalangeal, and distal interphalangeal
joints. External rotation can be increased as much as 28° or decreased as much
as 14° after dislocation.
Next, the examiner manually assesses translation
of the humeral head in the glenoid fossa. The humeral head is grasped in one
hand, and the clavicle and scapula are stabilized in the other as the examiner
pushes anteriorly and posteriorly. This is known as a shoulder drawer sign.
Compared with the unaffected shoulder, the affected shoulder often demonstrates
increased laxity. Remember that as much as 50% of posterior translation may be
normal.
A sulcus sign is demonstrated by pulling
inferiorly on the relaxed shoulder. A sulcus observed between the acromion and
proximal humeral head is considered a positive finding. This finding indicates
that the shoulder has multidirectional instability.
The key finding in anterior glenohumeral
instability is a positive apprehension test. The arm is placed in abduction,
extension, and external rotation while stressing it in anterior translation. If
the patient becomes apprehensive and reports pain, this is considered a
positive finding.
The relocation test involves placing the shoulder
in the position of apprehension and applying a posteriorly directed force on
the humeral head. The result is considered positive if this relieves the
patient's apprehension.
Impingement signs must also be evaluated because
as many as 10% of patients experience impingement after dislocation. Evaluate
for the Hawkins sign and perform the Neer impingement test.
The indications for open surgical repair depend
on the individual surgeon. Shoulders in which conservative therapy has failed
or any shoulder rendered unstable may undergo open repair.
Frequently, classifying patients into one of two
categories helps to determine treatment. Young patients with heavy physical
demands may forego conservative therapy and proceed to immediate surgical
repair. This recommendation is based on the high recurrence rate and the
patient's desire to return to activity.
In contrast, older patients who are less
physically demanding may try conservative therapy prior to assuming the risks
of surgical repair. These patients have a lower likelihood of recurrence and
may only require conservative therapy.
Surgery is also indicated if the patient is
symptomatic with activities of daily living or if overhead stability is
specifically needed. The patient must understand that overhead stability cannot
be guaranteed.
The shoulder joint is a simple structure that
provides complex function. It is the most mobile joint of the body, and it is
also the joint that is most frequently dislocated. The gross anatomy consists
of 3 main components: musculature, capsule/ligaments, and bone.
Capsuloligamentous structures provide the primary
stabilization for the joint. The capsule of the shoulder joint extends from the
periphery of the glenoid around the articular surface of the proximal humerus.
Within this capsule are 3 distinct thickenings that constitute the superior
glenohumeral ligament (SGHL), middle glenohumeral ligament (MGHL), and IGHL.
The SGHL and MGHL attach proximally at the
anterosuperior portion of the glenoid labrum. The proximal attachment of the
SGHL has 2 origins, including the one at the apex of the labrum that is joined
with the long head of the biceps brachii and a second origin at the base of the
coracoid process. Distally, the SGHL attaches just superior to the lesser
tuberosity at the edge of the articular surface. The MGHL inserts just medial
to the lesser tuberosity.
The IGHL is the key stabilizer of the shoulder,
preventing anterior glenohumeral instability. The IGHL attaches proximally to
the anterior, inferior, and posterior margins of the glenoid labrum. Distally,
it attaches to the inferior margin of the anatomic neck of the humerus.
Together, the glenohumeral ligaments function to
limit lateral rotation of the shoulder. Each of the 3 ligaments is relied upon
for stability, depending on the position of the arm. In 1910, Delorme found
that the MGHL tightens as the arm is externally rotated or dorsally flexed. If the arm is then
abducted, the IGHL becomes the primary stabilizer, with the upper fibers tight
at slight abduction and the whole ligament tightening at about 45° of
abduction.
The secondary stabilizers of the shoulder joint
are the surrounding musculature. This consists of the rotator cuff muscles. The
supraspinatus, infraspinatus, teres minor, and subscapularis are intimately
associated with the capsule. These muscles provide dynamic secondary
stabilization. Conservative therapy focuses on strengthening the rotator cuff
muscles to prevent recurrent dislocation.
The subscapularis is the most important
contributor of the rotator cuff muscles to anterior shoulder stability. With
the arm adducted, it tightens with external rotation. Cutting it results in
15-20° of increased external rotation. At 45° of abduction, the subscapularis
becomes taught over the anterior joint surface and ascends so its inferior
margin lies at the inferior margin of the glenoid. External rotation raises it
even further and makes it more taught. Finally, at 90° of abduction, the
inferior portion of the subscapularis no longer covers the inferior humeral
head. It continues to provide anterior stabilization by remaining taught.
The glenoid fossa provides a shallow socket in
which the humeral head articulates. It is composed of the bony glenoid and the
glenoid labrum.
The labrum is comparable to the menisci of the
knee. It is a fibrocartilaginous structure surrounding the periphery of the
glenoid. Like the menisci of the knee, it is flexible but constant; when torn,
it generally does not heal. The stability of the glenohumeral joint is greatly
increased by the labrum, which provides a 50% increase in the depth of the
concavity. The bony concavity measures approximately 2.5 mm and has been
measured at 5.0 mm with an intact labrum.
In 1923, Bankart claimed that anterior inferior
detachment of the labrum from the glenoid was the essential lesion in anterior
glenohumeral instability. It has since been proven that this is true in most
cases of instability but is not required for instability.
The labrum is closely related to the joint
capsule and the glenohumeral ligaments. It is anchored to the bony rim of the
glenoid and can be attached to the capsular structures as well.
Finally, understand the supporting musculature of
the scapula that allows such a wide range of motion at the shoulder. A total of
16 muscles move and stabilize the scapula.
Surgical repair is relatively contraindicated in
older patients with low physical demand, who have little chance of recurrence.
Conservative therapy, including physical therapy to strengthen the rotator
cuff, is indicated rather than exposing these patients to the risks of
operation.
Patients who have been asymptomatic in their
activities of daily living also need not be exposed to the risks of surgery.
These patients are best monitored for any recurrent dislocations.
A certain contraindication exists in the case of
multidirectional instability of the shoulder. In these atraumatic dislocations,
patients are able to voluntarily dislocate and relocate their shoulder.
Predisposing factors include psychiatric dislocations, laxity due to repetitive
injury as occurs in competitive swimmers, and congenital collagen abnormalities
such as Ehlers-Danlos syndrome and Marfan disease. The history and physical
examination must be used to identify these patients.
If these patients are treated as patients with
unidirectional dislocations, operative therapy will fail. The amount of
inferior capsular redundancy in multidirectional instability requires an
operative procedure addressing the possibility of future inferior instability.
Rotator Cuff Pathology
The first description of rupture of the rotator
cuff tendon was by Smith in 1834. With history, degenerative changes of the rotator
cuff have been better characterized by Duplay, Von Meyer, Codman, and Neer. The
exact mechanisms leading to the degeneration of the rotator cuff, however, are
still being debated.
Shoulder pain is the third most common cause of
musculoskeletal disorders (MSDs) after low back pain and cervical pain. Estimates of the
cumulative annual incidence of shoulder disorders vary from 7-25% in the
Western general population. The annual incidence is estimated at 10 cases per
1000 population, peaking at 25 cases per 1000 population in persons aged 42-46
years. In persons aged 70 years or older, 21% of persons have shoulder
symptoms, most of which were attributed to the rotator cuff. In cadaver
studies, the rate of full thickness tears varies from 18-26%. The rate of
partial thickness tears varies from 32-37% after age 40 years. Before age 40
years, tears are rare. In magnetic resonance imaging (MRI) studies, tears have
been observed in 34% of asymptomatic individuals of any age. After age 60
years, 26% of patients have partial thickness tears, and 28% demonstrate
full-thickness tears.
As mentioned, shoulder pain is the third most
common cause of MSDs after low back and neck pain. Although considered a benign
condition, according to a study on the long-term outcome of rotator cuff
tendinitis, 61% of the patients were still symptomatic at 18 months, despite
receiving what was considered sufficient conservative treatment. Moreover, 26%
of patients rated their symptoms as severe. MSDs are the primary disabling
conditions of working adults. The prevalence of rotator cuff tendinitis has
been found to be as high as 18% in certain workers who performed heavy manual
labor.
Webster and Snook estimated that the mean
compensation cost per case of upper extremity work-related MSDs was $8070 in
1993; the total US compensable cost for upper extremity, work-related MSDs was
$563 million in the 1993 workforce. The compensable cost is limited to the
medical expenses and indemnity costs (lost wages). When other expenses (eg,
full lost wages, lost production, cost of recruiting and training replacement
workers, cost of rehabilitating the affected workers) are considered, the total
cost to the national economy becomes much greater.[7]
The impact of rotator cuff
disease on quality of
life is even more difficult to assess than its cost. Further studies using
valid methods such as the Medical Outcomes Study (MOS) 36-item short-form
health survey (SF-36), which measure the impact of the disorder on general
health, should help assess this issue.
No known racial variation associated with rotator
cuff disease is cited in the literature. In one study, a predominance of male
patients (66%) seeking consultation for rotator disease is reported, but in
other studies, the male-to-female ratio is 1:1. Rotator cuff disease is more
common after age 40 years. The average age of onset is estimated at 55 years.
The rotator cuff, as shown in the image below, is
composed of 4 muscles—the subscapularis, supraspinatus, infraspinatus, and
teres minor—and their musculotendinous attachments. The subscapularis muscle is
innervated by the subscapular nerve and originates on the scapula. It inserts
on the lesser tuberosity of the humerus. The supraspinatus and infraspinatus
are both innervated by the suprascapular nerve, originate in the scapula, and
insert on the greater tuberosity. The teres minor is innervated by the axillary
nerve, originates on the scapula, and inserts on the greater tuberosity. The
subacromial space lies underneath the acromion, the coracoid process, the
acromioclavicular joint, and the coracoacromial ligament. A bursa in the
subacromial space provides lubrication for the rotator cuff.
Rotator cuff anatomy.
Understanding the functional anatomy of the
rotator cuff assists in understanding its disorders. The rotator cuff is the
dynamic stabilizer of the glenohumeral joint. The static stabilizers are the
capsule and the labrum complex, including the glenohumeral ligaments. Although
the rotator cuff muscles generate torque, they also depress the humeral head.
The deltoid abducts the shoulder. Without an intact rotator cuff, particularly
during the first 60° of humeral elevation, the unopposed deltoid would cause
cephalad migration of the humeral head, with resulting subacromial impingement.
Piasecki et al found that arthroscopic-revision
rotator cuff repair may be a reasonable treatment option even after previous
open repairs, providing improved pain relief and shoulder function. In the 54
patients, studied, the American Shoulder and Elbow Surgeons scores improved
from 43.8 ± 5.7 to 68.1 ± 7.2, and the Simple Shoulder Test improved from 3.56
± 0.8 to 7.5 ± 1.1. Visual analog pain scale scores improved from 5.17 ± 0.8 to
2.75 ± 0.8 (P = .03), and forward elevation increased from 121.0º ±
12.3º to 136º ± 11.8º. The authors noted that female patients
and those who had undergone more than 1 ipsilateral shoulder surgery had poorer
results.[10]
De Jesus et al performed a meta-analysis study to
compare the diagnostic accuracy of MRI, MR arthrography, and ultrasound in
diagnosing rotator cuff tears. The literature showed that MR arthrography is
the most sensitive and specific technique for diagnosing both full- and
partial-thickness rotator cuff tears and that ultrasound and MRI are comparable
in both sensitivity and specificity. Summary ROC (receiving operating
characteristic) curves for MR arthrography, MRI, and ultrasound for all tears
showed the area under the ROC curve is greatest for MR arthrography (0.935),
followed by ultrasound (0.889) and then MRI (0.878); however, pairwise
comparisons of these curves showed no significant differences between MRI and
ultrasound (P >.05).
In a systematic review of the published
literature, Nho et al compared single-row (SR) with double-row (DR) suture
anchor fixation in arthroscopic rotator cuff repair. The authors found no
clinical differences between the SR and DR suture anchor repair techniques.
They concluded that the data in the published literature do not support the use
of DR suture anchor fixation to improve clinical outcome, although they noted
that there are some studies reporting that DR suture anchor fixation may
improve tendon healing.
A meta-analysis, including 3 randomized
controlled studies and 2 controlled clinical cohort studies, compared outcomes between
single-row and double-row rotator cuff repair. The results found that while the
double-row technique significantly increased operative time, it provided
greater external rotation, improved tendon healing, and decreased recurrence
rate. However, no significant differences were found between the 2 techniques
with regard to shoulder function, muscle strength, forward flexion, internal
rotation, patient satisfaction, or return to work.
One study analyzed the structural and functional
outcomes after arthroscopic rotator cuff repair between single-, double-, and
combined double-row/suture-bridge techniques. After an average follow-up of
38.5 months, the data noted that repair with combined double-row and
suture-bridge technique resulted in an overall decreased retear rate,
especially for large and massive tears. This combined technique proved to be an
effective option for arthroscopic rotator cuff repair.
Schofer et al, in a prospective, randomized,
controlled study, compared high-energy extracorporeal shock-wave therapy (ESWT)
with low-energy ESWT in the treatment of rotator cuff tendinopathy. Patients in
the high-energy group received 6000 impulses of ED+ 0.78 mJ/mm2 in 3 sessions, and patients in the
low-energy group received 6000 impulses of ED+ 0.33 mJ/mm2. An
increase in function and a reduction of pain were found in both groups (P < .001). Although the improvement
in Constant score was greater in the high-energy group, statistical analysis
showed no significant difference between the 2 groups regarding Constant score,
pain reduction, and subjective improvement after 12 weeks and after 1-year
follow-up.
Drake et al reviewed the use of reverse total
shoulder arthroplasty (RTSA) in patients with rotator cuff disease. The authors
found that modern RTSA designs restore deltoid tension and a functional fulcrum
to the rotator cuff-deficient shoulder, allowing recovery of active shoulder
elevation and restoring function. The authors noted that contraindications to
RTSA include severely impaired deltoid function, an isolated supraspinatus
tear, and the presence of full active shoulder elevation with a massive rotator
cuff tear and arthritis. They concluded that for properly selected patients who
have symptomatic and disabling rotator cuff deficiency, RTSA can result in
life-changing improvements in pain, motion, function, and patient satisfaction.
Wellmann et al concluded that for patients with
symptomatic and disabling rotator cuff deficiency, RTSA can result in a
significant reduction in pain and improvements in motion and function.
Using propensity-matching methods, one study
compared the outcomes of patients with pseudoparalytic large-to-massive tears
with those of nonpseudoparalytic tears after rotator cuff repair and whether
the presence of pseudoparalysis negatively affected the outcome. The study
observed evidence of recovery from pseudoparalysis in a large portion of the
study group; similar outcomes were noted in postoperative function and cuff
healing, whether pseudoparalysis was present or not. Considering the possible
complications from treatment with RTSA, the study authors suggest that rotator
cuff repair should be the first-line treatment option for large-to-massive
tears.
Data from one study noted that the failure rate
after arthroscopic rotator cuff repair was significantly higher in patients
with lower bone mineral density, a higher grade of fatty infiltration of the
infraspinatus, and greater amount of retraction.
Rotator cuff pathology can be caused by extrinsic
(outside) or intrinsic (from within) causes. Extrinsic examples include a
traumatic tear in tendons from a fall or accident. Overuse injuries from
repetitive lifting, pushing, pulling, or throwing are also extrinsic in nature.
Intrinsic factors include poor blood supply, normal attrition or degeneration
with aging, and calcific invasion of tendons.
Rotator cuff tendinitis is the term used to describe
irritation of tendons either from excessive pressure on the acromion or, less
commonly, from intrinsic tendon pathology. Irritation of the adjacent bursa is
known as subdeltoid or subacromial bursitis. Repetitive overhead activities
resulting in irritation of tendons and bursae from repeated contact with the
undersurface of the acromion is termed impingement syndrome.
Rotator cuff dysfunction is typically a continuum
of pathology ranging from tendinitis and bursitis, to partial tearing, to a
complete tearing in one or more of the tendons. Although the earlier stages may
resolve with conservative care, actual tearing of the tendon can be more
problematic. These tears most commonly occur at the tenoperiosteal
(tendon-to-bone) junction. Because this area has a relatively poor blood
supply, injury to the tendon at this location is very unlikely to actually
heal. Additionally, the constant resting tension in the muscle-tendon unit, or
muscle tone, pulls any detached fibers away from the bone, preventing their
reattachment. Finally, joint fluid from within the shoulder may seep into the
tear gap and prevent the normal healing processes from occurring.
Possible causes of rotator cuff pathology are as follows:
·
Outlet impingement
·
Subacromial spurs
·
Type 2 and type 3
acromions
·
Osteoarthritic
spurs of the acromioclavicular joint (includes subacromial spurs)
·
Thickened or
calcified coracoacromial ligament
·
Nonoutlet
impingement
·
Loss of rotator
cuff causing superior migration of the humerus (ie, tear, loss of strength)
·
Secondary
impingement from an unstable shoulder
·
Acromial defects
(os acromiale)
·
Anterior or
posterior capsular contractures (ie, adhesive capsulitis)
·
Thick subacromial
bursa
Patients with rotator cuff pathology commonly
present with an activity related dull ache in their upper lateral (outer) arm
and shoulder. Activity is usually most difficult above shoulder level. Many
people have little or no discomfort with below-shoulder-level activities such
as golf, bowling, gardening, writing, or typing. Conversely, tennis,
baseball/softball, basketball, swimming, and painting are more problematic.
A complete medical history should be obtained to direct the
physical examination and make the correct diagnosis. Most of the time, the
diagnosis can be made following a systematic history. Relevant history
findings, treatments, and test results should complement the history of the
present injury. Sometimes, relevant social and family histories are necessary.
Patients with degenerative rotator cuff disease are almost always
older than 40 years. Fifty percent of patients have a progressive onset of
shoulder pain, whereas the other 50% can identify a specific event responsible
for the onset of pain. The evolution of rotator cuff disease is characterized
by variable episodes of recurrence following more intensive shoulder
activities, followed by remission with rest or treatment.
As the disease progresses, shoulder pain becomes more constant.
Overhead and arm-length activities typically increase the pain. Discomfort and
night pain can also be present. With time, the individual can notice some
weakness during shoulder elevation. Crepitus can also be noted. With evolution
of the disease, shoulder pain can be accompanied by cervical and mid-back pain.
The following questions should help the physician assess the
patient:
·
What is the
patient's age? Shoulder pain in young overhead athletes suggests underlying
shoulder instability. In older patients, degenerative rotator cuff disease or
frozen shoulder is suggested by shoulder pain.
·
What is the
patient's occupation or sport? Repetitive overhead activities and sports
predispose to rotator cuff tendinitis.
·
What was the
mechanism of injury? A fall on an outstretched arm could indicate a dislocation
of the glenohumeral joint or a fracture of the humeral neck. Repetitive
overhead motions can cause tendinitis and, in the long run, chronic
degenerative changes. A fall or a trauma on the tip of the shoulder can result
in an acromioclavicular sprain.
·
What was the onset?
Insidious, slow onset may suggest tendinitis or osteoarthritis. Sudden onset is
usually due to a trauma causing a fracture, dislocation, or a rotator cuff
tear.
·
Where is the pain
located? Pain located on the superior or lateral aspect of the shoulder
suggests rotator cuff tendinitis. Pain on the anterior aspect of the shoulder
may result from bicipital tendinitis, an acromioclavicular sprain, or anterior
instability. Neck pain and radicular pain or paresthesias suggest a cervical
spine disorder.
·
What is the
severity of the pain? An acute burning pain could indicate an acute bursitis.
An intermittent dull pain may be due to a degenerative rotator cuff disease.
·
What is the type of
pain? Sharp, burning pain suggests a neurologic origin. Bone and tendon pain is
deep, boring, and localized. Muscle pain is dull and aching, is not localized,
and may be referred to other areas. Vascular pain is aching, cramplike, and
poorly localized, and it may be referred to other areas.
·
What is the
duration of the symptoms? Frozen shoulder has 3 stages that can last up to 3-4
years. Acute bursitis has a short-term evolution and responds well to
nonsteroidal anti-inflammatory drugs (NSAIDs).
·
What is the timing
of the pain? Predominantly night pain suggests frozen shoulder. Morning pain
and stiffness improved by activity may be caused by a synovitis. Pain that
increases with activity is usually the result of a rotator cuff tendinitis.
·
Which
activities/positions increase the pain? Pain increased by overhead activities
or arm-length activities suggests rotator cuff tendinitis. Pain increased when
throwing is likely to be due to anterior instability. Pain increased by lying
on the affected shoulder may be caused by an acromioclavicular sprain.
·
Which
activities/positions relieve the pain?
·
Is there any
weakness or paresthesia in the upper extremities? Neurologic symptoms are
caused by a cervical radiculopathy or peripheral nerve entrapment/lesion.
·
Are the symptoms
constant or intermittent? Intermittent symptoms usually result from soft-tissue
or joint disorders. Constant symptoms suggest a neurologic lesion.
·
Is joint-motion
restriction present? Passive and active joint restriction in all directions of
range of motion (ROM) is caused by a frozen shoulder or glenohumeral synovitis.
Restriction in internal rotation suggests an impingement syndrome due to
rotator cuff tendinitis. The inability to perform active abduction suggests a
rotator cuff tear or a frozen shoulder.
·
Is some crepitus
noted? Crepitus is the result of degenerative rotator cuff changes. Crepitus is
not a normal finding in the shoulder.
·
Have any changes in
the color of the arm occurred? Color changes may be due to ischemia secondary
to vascular insufficiency. Reflex sympathetic dystrophy (also termed complex
regional pain syndrome, type 1) can cause skin-color changes.
·
Has the patient had
any treatments such as oral medication, injections, or physical therapy to
date?
·
Has the patient had
any diagnostic tests performed to date?
·
What is the
evolution of the symptoms?
·
Has the pain
changed?
·
Has the pain spread
or moved?
·
Has the pain
subsided or increased? The last 3 questions help in deciding the appropriate
treatment and management.
The importance of obtaining a systematic and detailed history
cannot be overemphasized. Any attempt to shortcut the process leads to a
nonfocused physical examination and an inaccurate diagnosis. Remember that a
recent study assessing the interobserver agreement of a diagnostic
classification of shoulder disorders based on history and physical examination
showed only moderate agreement between experienced observers.
A systematic examination of the shoulder region
includes careful observation; palpation of the bones and soft tissues;
assessment of passive and active ROM; and impingement and topographic tests
complemented, as needed, by instability tests, labrum tests, and special tests.
The examination is completed by a cervical spine examination, along with
neurologic and vascular examination.
The observation begins from the moment the
patient enters the room. The smoothness and symmetry of the shoulders and the
movements of the upper extremities are evaluated, as is the patient's gait. The
examiner must be aware of any signs of painful posturing and irregularity of
motion of the affected shoulder. Bilateral examination allows for comparison of
the affected shoulder with the unaffected one.
The patient then must be asked to remove the
appropriate amount of clothing to facilitate proper assessment of the bone and
soft tissues. The shoulder, cervical region, and entire upper extremity must be
assessed. The examiner should assess bones and joints for possible asymmetry or
deformities and should assess for soft-tissue changes (eg, swelling, erythema,
white shiny skin, loss of hair, atrophy) suggestive of vasomotor abnormalities.
Scars and abrasions also must be noted. The observer should assess bony
contours first and then soft tissues. Observation of the patient must be
completed from the front, side, and back.
Looking at bony contours, the examiner makes a
general assessment. The dominant side may be lower than the nondominant one;
the head and neck should be in the midline; the clavicle should be symmetric
without any deformity of the acromioclavicular joint and sternoclavicular
joint.
Each of these parts is then examined in more
detail. Because of its superficial location, a fracture of the clavicle or a
subluxation or dislocation of both ends is easy to identify. A step deformity
of the acromioclavicular or sternoclavicular joint, with the clavicle side of
the joint migrating superiorly, is due to a dislocation of these joints.
Observation of the soft tissues is directed first
at the contours of the deltoid. The mass of the deltoid should be round, with
the anterior and posterior aspects symmetric. Flattening of the muscle suggests
atrophy of the deltoid and is usually due to a neurologic lesion such as an
axillary nerve neuropathy, an upper trunk brachial plexopathy (Erb palsy), or a
C5-6 radiculopathy. An anterior dislocation of the glenohumeral joint produces
flattening of the deltoid with bulging of the anterior aspect of the muscle due
to the dislocated head of the humerus, with the patient holding the shoulder in
slight adduction and across the trunk. A bulge observed in the middle third of
the belly of the biceps when the elbow is flexed suggests rupture of the long
head of the biceps tendon.
The side view allows the examiner to assess
thoracic spine kyphosis, which is indicated by a protraction of the head or the
shoulders. Deltoid atrophy also can be observed.
Looking at bony contours, the examiner seeks
evidence of a scoliosis of the thoracolumbar spine and then observes the
scapulae. Each scapula extends from the spinous process of T2 (superomedial
angle) to the spinous process of T7 (inferomedial angle). The scapulae should
be at the same height and at the same distance from the spine. The examiner
should check for a winging of the scapula (ie, a displacement of the medial
side of the scapula away from the thorax). When the winging is present with
medial displacement of the scapula toward the spine, a serratus anterior muscle
palsy is suggested. This palsy usually is due to a long thoracic nerve injury.
When the winging is noted with lateral displacement of the scapula, a trapezius
muscle palsy or, more rarely, a rhomboid muscle palsy must be suspected.
A trapezius muscle palsy can be due to a spinal
accessory nerve (cranial nerve XI) injury, and a rhomboid muscle palsy can be
due to a dorsal scapular nerve injury. A prominent spine of the scapula may be
due to a supraspinatus and infraspinatus muscle atrophy caused by a
suprascapular nerve injury in the suprascapular notch or a rotator cuff tear.
Observation of the soft tissues is directed at
the posterior aspect of the deltoid muscle. The trapezius muscle is then
observed. Atrophy resulting from palsy of the muscle has been discussed
previously. Because the rhomboid is overlapped by the trapezius, atrophy of the
rhomboids is more difficult to assess.
Like observation, palpation must be performed in
an orderly manner, beginning with the anterior structures and finishing with
the posterior structures. Palpation must include bony structures and soft
tissues. Irregular joint surfaces, swelling, heat, crepitus, pain, tenderness,
and muscle tension and spasms must be sought. Palpation can be performed more
conveniently with the patient standing. In this position, the examiner can more
easily move around the patient. The examiner should stand behind the patient
for the palpation.
Beginning with the anterior structures, the
examiner palpates the sternoclavicular joint. Superior migration of the medial
end of the clavicle is palpated if the joint is dislocated. The examiner must
remember that the clavicle is superior to the manubrium. Always compare the
affected side with the contralateral side. The sternocleidomastoid muscle also
must be palpated, looking for tension and spasms. The muscle contracts to turn
the head on the contralateral side. The muscle is easier to identify and
palpate in this position. The sternal and clavicular heads of the muscle must
be palpated. Hands can be moved medially to palpate the suprasternal notch. The
first rib, the costochondral joints, and the sternum also should be assessed.
The clavicle should be palpated along its whole
length, looking for bumps (suggesting callus formation resulting from
fracture), loss of continuity, and crepitus. The acromioclavicular joint is a
common site of pain and must be palpated with care. Because the
acromioclavicular joint is a superficial joint, swelling, synovial thickening,
and/or crepitus can be palpated. Step deformities with superior migration of
the lateral end of the clavicle, seen in dislocation or subluxation, are easily
palpable.
The coracoid process can be palpated
approximately 2.5 cm (1 in) inferior and just medial to the acromioclavicular
joint. The coracoid process is the site of origin of the short head of the
biceps tendon, the coracobrachialis muscle, and the insertion of the pectoralis
minor. The pectoralis major and minor also must be palpated. Muscle tension and
spasms are commonly associated with shoulder disorders.
The acromion and subacromial space are palpated.
The subacromiodeltoid bursa can be palpated indirectly in the subacromial
space. Because it is overlapped by the deltoid muscle, the bursa cannot be felt
under the fingers; however, the examiner, through pressure on the deltoid
muscle, applies indirect pressure on the inflamed bursa, causing pain.
The examiner follows by palpating the greater
tuberosity, the long head of the biceps tendon, and the lesser tuberosity.
These structures can be identified easily in a lean patient by an experienced
examiner. This identification may be more difficult in an overweight patient or
one with abundant muscle mass. By rotating the shoulder medially (eg, by putting
the dorsal aspect of the hand on the buttock), the examiner can feel the
greater tuberosity on the anterior aspect of the shoulder, just inferior to the
acromion. The supraspinatus, infraspinatus, and teres minor tendons all insert
into this structure and, when inflamed, can produce pain upon palpation of the
greater tuberosity.
Keeping the fingers on the greater tuberosity,
the examiner rotates the shoulder laterally. The fingers feel the bicipital
groove where the long head of the biceps tendon can be palpated. Pain or
thickening of the tendon sheet indicates an inflamed tendon, whereas its
absence suggests a rupture or dislocation. By rotating the shoulder more
laterally, the examiner can palpate the lesser tuberosity. The tendon of the
subscapularis inserts on that structure, and when it is inflamed, the tendon is
painful to palpation. With the shoulder back to a neutral position, extension
of the shoulder allows palpation of the subacromiodeltoid bursae under the
anterior edge of the acromion.
All of these structures must be palpated gently
because they may be tender. Any painful palpation must be compared with the
contralateral shoulder. A positive finding is when pain is more significant on
the affected side than on the contralateral shoulder. Any excessive pain caused
by a vigorous palpation makes the examination less sensitive.
The biceps muscle should be palpated, looking for
any bulging that indicates a long head of the biceps tendon rupture. The
deltoid muscle also must be palpated to look for painful spasm or tension. Tone
and atrophy also are assessed.
The examination is continued by palpation of the
posterior structures. Bony structures can be rapidly assessed because they are
rarely a source of pain. The spine of the scapula is palpated, followed by
palpation of the superior medial angle of the scapula. The levator scapulae
muscle that inserts on this angle is a common site of pain. The medial border
of the scapula is then palpated from the superior to the inferior medial angle.
The bony palpation is completed by palpation of the spinous processes of the
dorsal and cervical spine.
Because muscle spasm and tension are frequently
associated with a rotator cuff disease, the posterior muscles must be palpated
with care to identify and treat those muscles. The superior trapezius is
commonly tense and painful and must be palpated from its cervical and occipital
origin to its insertion on the spine of the scapula and the acromion. Under
this muscle, lying in the supraspinatus fossa, the supraspinatus muscle also
should be palpated.
The rhomboid muscles, from C7 to T5, run downward
to attach on the medial border of the scapula. These muscles, often a source of
pain, are difficult to distinguish from the overlying middle trapezius muscle.
The rhomboid muscles can be identified by asking the patient to put his or her
hand behind the back, with the shoulder internally rotated and the elbow
flexed, and to push posteriorly against a resistance. The muscle belly of the
rhomboid muscles then becomes palpable. Muscle palpation is completed by
assessing the infraspinatus, teres major and minor, and latissimus dorsi
muscles.
Both active and passive ROM must be evaluated.
Although some authors suggest that an assessment of passive ROM is not necessary
if the patient is able to perform complete active ROM without pain, passive ROM
must be assessed systematically. Some patients with glenohumeral ROM
restrictions have learned to compensate with increased scapulothoracic mobility
and seem to have near-normal active ROM.
Movements (with the normal ranges provided) that
should be assessed are abduction (70-180°), adduction (30-45°), flexion
(160-180°), extension (45-50°), external rotation (80-90°), and internal
rotation (90-110°).
Active movements are evaluated first. With the
observer behind the patient (who is standing), active abduction is performed.
The scapulohumeral rhythm is observed. If a
painful arc (ie, pain or inability to abduct because of pain) is observed at
45-120°, a subacromial impingement syndrome is suggested. If the pain is
greater after 120°, when full elevation is reached, an acromioclavicular joint
disorder is suggested.
If a reverse scapulohumeral rhythm (ie, an
abduction initiated by the scapulothoracic joint rather than by the glenohumeral
joint) is observed, a frozen shoulder is suggested. Look for a winging of the
scapula caused by trapezius or rhomboid muscle weakness. Active flexion is also
evaluated. In the presence of a subacromial impingement syndrome, this movement
can also be painful. Active flexion may elicit a winging of the scapula caused
by a serratus anterior weakness.
Other motions can be evaluated through a
combination of active movements. The Apley scratch test is probably the most
well known. This test combines internal rotation and adduction of one shoulder
with external rotation and abduction of the other.
The evaluation for passive ROM can be performed
with the patient standing, sitting, or lying down. For practical purposes, the
examination is performed with the patient standing. Passive abduction is
assessed with the observer behind the patient. Full abduction is performed
first to evaluate the combination of scapulothoracic and glenohumeral motion.
Then, the scapulothoracic joint is locked by putting one hand over the scapula
and the clavicle to resist any motion of this joint. This maneuver allows for a
more selective evaluation of the glenohumeral joint (90-120°).
The same procedure can be used to evaluate full
flexion that combines scapulothoracic and glenohumeral motion and flexion
performed selectively by the glenohumeral joint. This maneuver is followed by
an evaluation of adduction. The external rotation is tested with the elbow held
close to the waist and flexed at 90°. Then, the arm is rotated externally. The
examination is followed by an evaluation of the extension and an assessment of
the internal rotation. The full range of internal rotation is achieved with the
forearm passing behind the trunk with the shoulder slightly extended.
Positive impingement tests result from the
reproduction of impingement of the rotator cuff tendon by different provocative
maneuvers.[25] With
anterosuperior impingement syndrome, the impingement occurs underneath the
coracoacromial arch. With posterosuperior impingement syndrome, the impingement
is on the posterosuperior border of the glenoid cavity. Finally, with
anterointernal impingement syndrome, the impingement occurs in the subcoracoid
space or in the coracohumeral interval.
Impingement tests confirm an impingement
syndrome; however, they do not determine the location of the rotator cuff
lesion.
A of cadaveric shoulders has shown that some
provocative impingement tests—namely, the Neer and Hawkins-Kennedy tests—appear
to elicit contact consistent with impingement.
The Neer impingement test is described as
follows:
·
With the examiner
standing behind the patient, the shoulder is passively flexed. Although not
originally described by Neer, this author positions the shoulder in internal
rotation.
·
When the result is
positive, this test produces pain caused by contact of the bursal side of the
rotator cuff on the anterior third of the undersurface of the acromion and the
coracoacromial ligament, as well as by contact of the articular side of the
tendon with the anterosuperior glenoid rim.
·
A positive test
result suggests an anterosuperior impingement syndrome. The sensitivity of this
test, assessed based on operatively observed anatomic lesions, is 89%.
The Hawkins-Kennedy test is described as follows:
·
With the examiner
standing behind the patient, the shoulder is flexed passively to 90°, followed
by repeated internal rotation.
·
When the result is
positive, this test produces pain caused by contact of the bursal side of the
rotator cuff on the coracoacromial ligament and by contact between the
articular surface of the tendon and the anterosuperior glenoid rim. Contact
between the subscapularis tendon and the coracoid process is also observed.
·
A positive test result
suggests an anterosuperior or an anterointernal impingement test.
·
This author uses a
modified version of this test with the shoulder positioned initially at 90° of
abduction and 30° of flexion in the plane of the scapula. Along with repeated
internal rotation motion, the shoulder is brought progressively to 90° of
flexion. If pain is present when the shoulder is flexed at 30°, it is caused by
an anterosuperior impingement syndrome. If the pain is present only when the
shoulder is brought to 90° of flexion, reducing the coracohumeral interval, an
anterointernal impingement syndrome is suggested.
·
The sensitivity of
this test is 87%.
The Yocum test is described as follows:
·
With the examiner
standing behind the patient, the hand on the ipsilateral side of the examined
shoulder is placed on the contralateral shoulder. The elevation of the elbow is
resisted by the examiner.
·
When the result is
positive, this test produces pain caused by contact of the bursal side of the
cuff tendon with the coracoacromial ligament and possibly the undersurface of
the acromioclavicular joint.
·
A positive test
suggests an anterosuperior or an anterointernal impingement syndrome. The
sensitivity of this test is only 78%; however, the sensitivity of the 3 tests
together is 100%, which justifies that the 3 tests should be systematically
performed together.
The posterior impingement test is described as
follows:
·
With the patient
lying down, the shoulder is positioned at 90-100° of abduction and maximally
externally rotated.
·
When the result is
positive, this test produces pain in the posterior aspect of the shoulder
caused by impingement of the articular side of the cuff tendon between the
greater tuberosity and the posterosuperior glenoid rim and labrum. Relocation
of the humeral head, performed by applying a posteriorly directed force to the
humeral head, causes a reduction in pain.
·
The sensitivity of
this test is 90%.
Using resisted isometric contraction of specific
muscles of the rotator cuff, the location of the tendon lesion causing the
impingement can be identified.
To identify the supraspinatus tendon, use the
Jobe test or the full-can test.
In the Jobe test, the shoulder is placed at 90°
of abduction and 30° of flexion in the plane of the scapula. Shoulder elevation
is resisted. The test result is considered positive if pain is noted. When
compared with surgical observations, the sensitivity of this test is 86% and
the specificity is 50%. The positive predictive value (the ratio of true
positive tests on all the positive tests) of the Jobe test is 96%, and its
negative predictive value (the ratio of all the true negative tests on all the
negative tests) is 22%.
Full-can test: The shoulder is placed at 90° of
flexion and 45° of external humeral rotation (thumb pointing upward, as if
someone is holding a full can right-side-up). Shoulder elevation is resisted.
The test result is considered positive if it produces pain. Electromyography
(EMG) studies show that this test results in the greatest supraspinatus
activation with the least activation from the infraspinatus.
To identify the infraspinatus tendon, use the
infraspinatus isolation test or, less optimally, the Patte test.
In the infraspinatus isolation test, the shoulder
is positioned at 0° of elevation (elbows against the waist flexed at 90°) and
45° of internal rotation. Shoulder external rotation is resisted. The test
result is considered positive if it produces pain. EMG shows this to be the
optimal infraspinatus isolation test.
In the Patte test, the shoulder is placed at 90°
of abduction, in neutral rotation, and in the plane of the scapula. The
examiner holds the elbow of the patient, and the external rotation is resisted.
The test result is considered positive if it produces pain. The sensitivity of
the test is 92%, but its specificity is only 30%. The positive predictive value
is 29%, and its negative predictive value is 93%. A palsy of the external
rotator also can be tested. With the elbow held against the waist, the shoulder
is positioned passively in external rotation. The test result is positive if
the patient is unable to maintain the shoulder in external rotation, suggesting
a full tear of the external rotators.
To identify the teres minor tendon, use the same
tests used for the infraspinatus tendon. No specific teres minor isolation
tests have been developed.
To identify the subscapular tendon, use the
Gerber lift-off test or the Gerber push-with-force test.
In the Gerber lift-off test, the shoulder is
placed passively in internal rotation and slight extension by placing the hand
5-10 cm from the back with the palm facing outward and the elbow flexed at 90°.
The test result is positive when the patient cannot hold this position, with
the back of the hand hitting the patient's back. The sensitivity and specificity
of this test are 100% when the subscapularis is fully torn.
In the Gerber push-with-force test, the shoulder
is placed in the same position as the lift-off test; however, the patient must
keep the hand away from the back and must resist a push in the palm of the
hand. EMG shows that this is the optimal subscapularis isolation test, with
minimal activation of the pectoralis and latissimus dorsi muscles.
To identify the long head of the biceps tendon,
use the Speed palm-up test.
In the speed palm-up test, the shoulder is placed
at 90° of flexion with the elbow in extension and the forearm in supination,
bringing the palm of the hand up. The flexion of the shoulder is resisted. The
test result is positive if the maneuver produces pain. The sensitivity of this
test is 63%, but its specificity is only 35%. The positive predictive value is
43%, and its negative predictive value is 55%.
The Yergason test, in this author's opinion, is
technically difficult and ineffective; therefore, it is not described. Generally,
the topographic tests are sensitive but not specific, except for the Gerber
lift-off test. The combination of impingement tests and topographic tests helps
determine whether a patient's symptoms are caused by rotator cuff disease. As
mentioned, the examination must be completed by instability and labrum tests,
special tests (eg, thoracic outlet syndrome tests), a cervicothoracic spine
examination, and a neurologic and vascular examination, but it is not the
purpose of this section to describe them all.
A wide variety of radiologic examinations are
offered to image the rotator cuff. Each of them has advantages and limitations.
To prescribe the most useful examination, one must start with a good clinical
history and physical examination. Imaging should be used to confirm the anomaly
and to describe its extension and the associated findings. The following
paragraphs briefly explain the indications, the technique, and the findings for
each modality available to image the rotator cuff in radiology.
Plain films are not very specific or
sensitive for rotator cuff disease, but they remain the first examination to
perform. Radiographs are used for gross evaluation of the mineralization of the
bone, the alignment, posttraumatic changes, the normal variant of the acromion
shape, the presence of degenerative changes, and the presence of fine soft
tissue calcifications that could be missed with by other modalities. This is
the most useful test in trauma situations or to assess chronic complete tears.
In the last stage of complete chronic rotator cuff tear, it could be the only
imaging modality needed to confirm the diagnosis (see the image below).
In this patient's shoulder radiography, the humeral head no longer matches up with the glenoid because the rotator cuff is torn and the strong deltoid muscle is pulling the head superiorly toward the acromion. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.
Plain films are acquired routinely in 3 planes (ie, neutral,
internal, external rotation).
The main indication of arthrography is to
identify complete rotator cuff tears and intra-articular infiltration of the
corticoid. As a diagnostic tool, it is combined generally with CT arthrography
scanning.
Arthrography is performed by injecting iodine
contrast medium, air, or both into the glenohumeral joint. From 8-12 mL of
contrast (or 3-4 mL of contrast and 10-12 mL of air) is injected to distend the
joint capsule. If air and contrast are injected, the term double-contrast study
is used. Then, plain films are taken in different positions, such as external
rotation, internal rotation, and subacromial views, before and after motions.
The image below shows an intact capsule.
This image depicts the channel between the articular
capsule and the subacromial-subdeltoid bursa in a complete rotator cuff tear.
Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.
In the presence of a complete tear, the contrast floods from the
glenohumeral joint into the subacromial-subdeltoid bursa (see the images
below).
Even
if the channel cannot be always identified, the presence of contrast medium in
the subdeltoid-subacromial bursa signals the presence of a complete rotator
cuff tear. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.
CT-arthrography of the shoulder in the axial plane. Note the presence of air and contrast in the subacromial-subdeltoid bursa. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.
With a partial tear, the contrast is seen as a
line or small, filled cavity within the tendon but without contrast in the
subacromial-subdeltoid bursa. This finding is more difficult to demonstrate in
a complete tear. Intratendon tears and tears on the superior aspect of the tendon
(bursal side) are not visualized with this technique. Arthrography can also
provide some information about the long portion of the biceps tendon, loose
bodies, and synovial disorders, such as inflammatory synovitis,
osteochondromatosis, or villonodular pigmented synovitis.
This study, although very accurate (100%
sensitivity, 100% specificity) in depicting complete rotator cuff tears, is
limited in the evaluation of tendinitis and partial tears, for which its
sensitivity drops to 17-43%. On the other hand, this test yields more
information than arthrography regarding the joint itself and the soft tissues
around it. The ability to evaluate the labrum, the glenohumeral ligaments, the
long head of the biceps tendon, and the bony structures, as well as the
presence of loose bodies, makes this a useful study.
CT arthrography is performed exactly like a
double-contrast (air and iodine contrast) arthrography but is followed by
tomodensitometry imaging (CT scanning). For this examination, the shoulder is
imaged in the axial plan in internal and external rotation. Thin slices as
small as 2-3 mm are acquired throughout the entire joint. With new CT scanning
technology, it has become easy to reformat images in multiple planes.
The semiologic signs of rotator cuff tears are
essentially the same as seen with conventional arthrography. The presence of
contrast in the subacromial-subdeltoid space confirms the diagnosis of complete
rotator cuff tears (see images below). The contrast can also facilitate determination
of the size and location of the tear to help the surgeon plan the surgery.
Degenerative findings such as osteophytes, geodes, sclerosis, and articular
space narrowing are also well depicted.
CT-arthrography
of the shoulder in the axial plane. Note the presence of air and contrast in
the subacromial-subdeltoid bursa. Courtesy of Dr Thomas Murray, Orthopaedic
Associates of Portland.
CT-arthrography of the shoulder in the axial plane. Note the presence of air and contrast in the subacromial-subdeltoid bursa. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.
In addition to conventional arthrography, this
technique can identify labral and glenohumeral ligament tears. The presence of
contrast between the labrum and the articular space indicates the presence of a
tear. The axial views also permit a good visualization of the long head of the
biceps tendon in its groove. Therefore, subluxation of this tendon, or rupture,
can also be diagnosed. Finally, the shape of the acromion can be evaluated on
the oblique sagittal reformatted study, which requires a special acquisition.
MRI is the state-of-the-art diagnostic tool for a
full evaluation of the shoulder. MRI allows a fine evaluation of the bone marrow,
tendons, muscles, ligaments, capsules, bursae, and labrum. MRI combines the
advantage of visualization of the bony structures and of all the soft tissues
about the shoulder and in any plane desirable. With this imaging modality, the
full continuum of rotator cuff disease, from simple tendinosis to complete
tears, can be diagnosed. MRI is much more powerful than the previous modalities
when used to identify partial tears, and it also can identify intratendon tears
or tears on the bursal aspect of the tendon. As with CT scanning and plain
radiography, the bone structures resulting or contributing to the impingement
syndrome can be evaluated.
MRI can also yield information about retraction
of the muscle, atrophy, bursitis, and bone marrow abnormalities (eg, edema,
contusion), which all are associated findings of rotator cuff disease.
MRI is somewhat limited in the evaluation of the
labrum and glenohumeral ligaments. MRI arthrography is the study of choice for
the evaluation of labrum and glenohumeral ligaments.
This technique takes advantage of the properties
of hydrogen protons submitted to a magnetic field and radiofrequency waves.
Therefore, the patient is not subjected to radiation exposure. Multiple
sequences are available to highlight different substances, such as water, fat,
blood, or solid structures. Mainly spin-echo T1, spin-echo T2, and
gradient-echo sequences, in axial, sagittal, and coronal oblique plans, are
acquired in different combinations. Inversion recovery, fat saturation, and
injection of gadolinium (intravenous or intra-articular) can be added if
necessary.
MRI shows great detail of the anatomy in multiple
plans. MRI also allows better visualization of the nature of a structure or an
anomaly (ie, according to its intrinsic property). Therefore, the examiner
should know some characteristics of the MRI signals for the most common
structures.
Fat, methemoglobin, melamine, gadolinium, and
some forms of calcium all are hyperintense in T1-weighted images. On the
contrary, water appears at low signal intensity. In T2-weighted images or in
gradient echo, the liquids are hyperintense, as are most lesions, meaning that
edema, inflammatory processes, tumors, tendinitis, and tendon tears are
hyperintense in T2-weighted images and hypointense in T1-weighted images.
Therefore, the presence of fluid in a bursa or articular joint is hyperintense
in T2 or gradient echo and indicates inflammatory or posttraumatic fluid. A
full-thickness tear of the tendon is demonstrated by a hypersignal intensity in
T2 that extends throughout the tendon (see image below).
Full-thickness tear of the supraspinatus as seen as a
hyperintensity line through the full thickness of the tendon in a flash
2-dimensional MRI sequence in coronal oblique plane. Courtesy of Dr Thomas Murray,
Orthopaedic Associates of Portland.
Tendinitis is recognized as a gray signal in the tendon. Finally,
calcification and cortical bone appear hypointense in all sequences (see image
below).
Calcifications are seen as hypointense foci in flash
2-dimensional images. Courtesy of Dr Thomas Murray, Orthopaedic Associates of
Portland.
MRI arthrography is the gold standard as an imaging modality for diagnosis
of a rotator cuff tear. It follows the same principle as CT arthrography. This
modality can help identify labral tears (see image below) and glenohumeral
tears.
MRI arthrography can help to identify labral tears, as seen in this image. The contrast medium penetrates between the labrum and the articular surface. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.
The size and morphologic features of rotator cuff
tears may influence treatment selection and affect final outcomes. Magnetic
resonance arthrography allows observation of these features and other
intra-articular structures. In one series, Toyoda and colleagues compared MRI with MRI arthrography. To assess the utility of
magnetic resonance imaging in assessing size and morphologic features, the
authors did a retrospective analysis of 41 shoulders in 37 consecutive
surgically treated patients (mean age, 63.2 years) who had MRI followed by
magnetic resonance arthrography. The maximum rotator cuff defect size in the
anteroposterior direction defined transverse size, and the maximum rotator cuff
defect size in the mediolateral direction defined longitudinal size.
Sensitivity for detecting full-thickness rotator cuff tears by MRI was 90.2%,
compared with 100% for magnetic resonance arthrography.
Magnetic resonance arthrography also allowed
morphologic classification of the torn tendon as blunt end, tapering end,
indistinct end, horizontal tear, and global tear. There was good agreement in
classifying torn edges: the imaging findings agreed with findings at surgery.
Magnetic resonance arthrography was more accurate in evaluating both rotator
cuff tear size and morphologic features than MRI.
With the aid of fat-suppressed imaging, full
thickness and partial cuff tears can be identified with 100% sensitivity and
specificity. Fat-suppressed images also showed intratendinous contrast material
imbibition in 3 torn cuffs with frayed, friable tendon margins. Fat suppression
in MR arthrography is valuable in the differentiation between partial and
full-thickness cuff tears and in the detection of small partial tears of the
inferior tendon surface.
Ultrasound uses the same principles as radar. The
images are created using a high-resolution transducer that first sends a sound
signal and then receives the echo produced when the sound hits the different
structures at different depths.
The advantages of this technique reside in its
low cost, high availability, and high resolution. Ultrasound is a dynamic study
for demonstrating impingement syndrome. The disadvantages are that it is time
consuming for the radiologist and is operator-dependent. Ultrasonography cannot
study bone structures because sound does not penetrate bone very well.
With ultrasound, the normal tendon is an echoic
structure, whereas the cartilage and fluids are hypoechoic. All of the tendons,
bony landmarks (eg, humerus, greater tuberosity), and intra-articular or
intrabursal effusions are easily recognized. Tendinitis is diagnosed when the
tendon loses its echogenicity and becomes diffusely hypoechoic. Calcifications
appear as bright foci within the tendon, accompanied by a posterior shadowing,
because the sound cannot pass through the calcium.
The main, and most sensitive, sign of a complete
rotator cuff tear is an interruption in the tendon that fills with fluid,
producing a hypoechogenic foci extending from the cartilage surface to the
subdeltoid-subacromial bursa (see image below). The secondary signs include the
uncovered cartilage (cartilage appears hyperechoic at the site of the tear),
bursa herniation, loss of convexity of the tendon and bursa, and effusion
within the glenohumeral articulation and the subacromial-subdeltoid bursa.
Ultrasound
is another modality to demonstrate a complete rotator cuff tear, as seen here
with a gap of more than 2 cm between both extremities of the torn tendon.
Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland.
The diagnosis of a partial rotator cuff tear is
made when the hypoechoic or bursal herniation does not cross the full width of
the tendon. The use of ultrasound also allows the operator to demonstrate, in
real time, the impingement of the supraspinatus tendon on the acromion when the
arm is positioned in internal rotation and moved in abduction or flexion.
Bone scintigraphy is not used routinely in rotator cuff disease
imaging.
Physical therapy can be a useful adjunct in the
conservative treatment of patients with degenerative rotator cuffs. Although
numerous studies have been performed on conservative treatment and surgical
approaches of the painful shoulder and, more specifically, the rotator cuff,
the conclusion of a review of randomized, controlled trials of interventions
for painful shoulder was that little evidence supports or refutes the efficacy
of common interventions for shoulder pain.
Drawing firm conclusions about the efficacy of
any of these interventions remains difficult because of, among other reasons,
the lack of definition and strict diagnostic criteria for the different painful
shoulder conditions, valid randomization procedures, blinding, valid scales for
outcome measurement, and heterogeneous populations. In their approach to
conservative patient treatment, clinicians must be critical and try to use an
evidence-based medicine approach as much as possible. The clinician must also
use a combination of experience and intuition to compensate for the lack of
scientific evidence supporting the different therapeutic modalities.
Conservative treatment of the degenerative
rotator cuff involves pain relief; avoidance of painful motions and activities;
simple analgesics and NSAIDs; manual physical therapy for the glenohumeral,
scapulothoracic, acromioclavicular, and sternoclavicular joints and the
parascapular and scapula-stabilizer muscles; subacromial corticosteroid
injection; bupivacaine suprascapular nerve block; restoration of motion and
normal scapulohumeral rhythm; stretching of the glenohumeral capsule and
muscles; and manual therapy of the cervicodorsal spine (often necessary because
of its close relationship with the shoulder).
Ebenbichler showed in a randomized,
doubled-blind, placebo-controlled study that the use of a pulsed ultrasound
performed 5 times a week for 15 minutes (0.89 MHz frequency, 2.5 W/cm2,
pulsed mode 1:4) significantly resolves calcification of the shoulder,
decreases pain, and improves the short-term quality of life.[37,
38]Long-term follow-up did not show significant differences;
however, in the long term, the symptoms of calcifying tendinitis may be
self-limiting and may improve independently from the resolution of the calcium
deposit. This theory may explain why the use of ultrasound is only
significantly effective in the short term. The short-term efficacy of
ultrasound therapy has been demonstrated only in calcifying tendinitis. Its
efficacy in other shoulder disorders has not been shown.
Another modality that looks promising is
extracorporeal shockwave therapy. Passing a strong electric current through a
flat coil induces a magnetic field and generates shock waves. Shock waves were
used first for the treatment of delayed union and nonunion of fractures by
stimulating osteogenesis.
In an uncontrolled study, shockwave therapy (1500
impulses of 0.28 mJ/mm2) reportedly disintegrated calcium deposits
partially or completely in 62% of patients, and 75% had significant improvement
in pain, power, ROM, and shoulder function. The authors of the study concluded
that a larger-scale, placebo-controlled trial should be conducted to analyze
the benefits of this modality. A prospective, randomized, controlled study
using a valid functional shoulder scale showed the efficacy of extracorporeal
shockwave therapy. At 3-6 months, significant improvement occurred in pain and
function. At 6 months, calcium deposits disappeared or disintegrated in up to
77% of patients' radiographs. Comparing different regimens of shockwaves, the
authors concluded that the improvement in pain and function and the radiologic
disintegration of calcification were dose-dependent.
Extracorporeal shockwave therapy appears to be a
promising treatment for calcifying tendinitis. Similar to ultrasound, its
efficacy in other shoulder conditions has not been established.
Randomized, controlled studies have shown the
efficacy of topical steroids, NSAIDs, and acetic acid iontophoresis, as
compared with placebo, in different MSDs; however, the studies were not
specifically on rotator cuff disease. Moreover, a recent trial did not show any
difference in outcomes between no treatment and treatment with acetic acid
iontophoresis followed immediately by 9 sessions of ultrasound therapy in a
constant mode (0.8 W/cm2 at
a frequency of 1 MHz for 5 min) over a period of 3 weeks. Some authors could
not show any effect of iontophoresis on steroid migration through in vivo and
in vitro studies, whereas others did. Thus, no conclusions can be made
regarding the efficacy of iontophoresis in the treatment of rotator cuff disease.
As with NSAID therapy, many of the studies on the
efficacy of corticosteroid injection for various shoulder conditions are of
poor methodological quality. Green, van Der Heijden, and Sibilia performed a
systematic review of all the randomized clinical trials on corticosteroid
injection. Although the trials selected were essentially the same in the 3
studies, their conclusions differ because of the different assessment methods.
Two of these articles suggested that corticosteroid injection may be superior
to placebo in the short-term treatment of rotator cuff tendinitis, whereas one
suggested that no conclusive evidence was found regarding the efficacy of
corticosteroid injection.
Subacromial corticosteroid and local anesthetic
agent injection also appear to be more effective than an injection of a local
anesthetic alone, although some authors disagree. Corticosteroid injection also
appears to be significantly more effective than NSAIDs. Therefore, subacromial
corticosteroid injection appears indicated when pain persists after simple
analgesics and NSAIDs have been used.
Because some authors have reported poorer
surgical outcome in patients who have had 3 or more corticosteroid injections,
the recommendation is that no more than 2 injections be given. No trials have
compared the different routes of corticosteroid injection; thus, the physician
should select his or her preferred route. Additionally, no trial has compared
the efficacy of different corticosteroids. Triamcinolone acetonide is the agent
most frequently studied.
The action mechanism is inhibition of
prostaglandin formation by selective cyclooxygenase (COX)–2 activity. The
optimal dose has not been evaluated. Recommended doses vary from 20-80 mg in
the different trials. This author recommends 20-40 mg of triamcinolone
acetonide. Adverse effects can be local or systemic. Although systemic adverse
effects can occur following a subacromial injection, only local adverse effects
are discussed here. Possible adverse effects include dermal atrophy, necrosis
and loss of pigmentation, synovitis, septic arthritis, hemarthroses, cartilage
damage and degeneration, tendon rupture, and Charcot arthropathy.
The bupivacaine suprascapular nerve block is a
relatively unknown, although effective, method to treat different painful
shoulder disorders. A few randomized controlled trials have demonstrated its
efficacy for painful shoulder associated with rheumatoid arthritis, for chronic
rotator cuff disease, and for frozen shoulder. Preliminary data of a study on
chronic impingement syndrome conducted at the Montreal Rehabilitation Institute
show its efficacy compared with placebo. At 3 months, a significant improvement
in pain and function, measured by a valid functional shoulder scale, was
observed. The efficacy of this procedure is supported by randomized controlled
studies, and it appears to be a very promising new approach in the treatment of
rotator cuff disease.
The technique for nerve block is very
inexpensive, simple, and safe. It consists of injecting 10 mL of bupivacaine
0.5% in the supraspinatus fossa of the scapula to produce an indirect
suprascapular nerve block. In rotator cuff disease, 2 injections are
administered 4 weeks apart
Patients with more advanced rotator cuff disease
or a more significant injury may not respond to conservative therapies. If the
patient believes that his or her quality of life is being significantly
impacted by the shoulder dysfunction, then surgical intervention is a
reasonable consideration. In some cases, simple debridement of a frayed or
partially torn cuff tendon, along with smoothing of the undersurface of the
acromion (acromioplasty) above the tendon, may be all that is needed. More significant
partial tearing (>50% of tendon thickness) and complete tears require
reattachment of the tendon ends back to the humeral head.
Rotator cuff repair is most commonly performed
using an open surgical procedure, which typically requires a 2- to 4-in
incision at the top of the shoulder. The deltoid muscle is split, and the
undersurface of the acromion is smoothed. Strong stitches are placed in the
torn ends of the rotator cuff tendons, and they are attached back to the bone
of the humerus through specially created tunnels or commercially available
suture anchors.
Because the entire shoulder cannot be visualized
through the open approach, many surgeons perform an initial diagnostic
arthroscopy of the shoulder at the time of the repair to be sure no other
coexisting problems are present within the shoulder that could also be
addressed at the open procedure. This technique may be performed in an
inpatient setting or in an outpatient surgery facility, providing that the
patient is comfortable enough to return home the same day.
Standard tendon repair techniques combined with
anterior acromioplasty, postoperative limb protection, and monitored
physiotherapy can produce consistent and lasting pain relief and improvement in
range of motion. Open rotator cuff repair has been known to have excellent
outcomes and patient satisfaction since the early 80s. Romeo and colleagues
have reported 94% patient satisfaction 4 years after open rotator cuff repair,
with lasting relief of pain and improved function.[52] In another series, Baysal
has reported that 96% of patients were satisfied or very satisfied with the
results of their repair; 78% of patients who were working before surgery
returned to work without modification by 1 year postoperatively. For the most
part, patient age and size of tear did not influence postoperative range of
motion or health-related quality of life.
Arthroscopic surgery involves the use of a
special camera attached to a long, narrow surgical telescope to visualize the
inside of a joint. Working through small incisions about the size of
dress-shirt buttonholes, the surgeon can use specially created instruments to
repair damaged cartilage, capsule, tendon, and other tissues. The camera
transmits the signal to a video monitor for improved visualization and to allow
photographic and videographic documentation of the surgical findings and the
procedure. In orthopedic surgery, arthroscopy was first used to treat conditions
of the knee. With new technology and refined techniques, arthroscopic surgery
has become quite common for treating many knee, shoulder, elbow, wrist, hip,
ankle, and foot problems.
Arthroscopic treatment of rotator cuff disease
initially consisted of rotator cuff inspection and debridement and arthroscopic
acromioplasty. If a repairable rotator cuff tear was discovered, an open or
mini–open repair of the tendon was then performed. As surgeons' skills improved
and more specialized instrumentation was developed, it became possible to fix
relatively small tears using arthroscopic techniques to insert anchors, pass
sutures, and tie knots. In current practice, surgeons can now perform shoulder
arthroscopy to repair even large rotator cuff tears using these techniques.
Arthroscopic rotator cuff repair is a technically
challenging procedure (see images below) that requires advanced arthroscopic
surgical skills, careful preoperative planning, and a step-wise, systematic
approach. The procedure may be performed with the patient in a "beach
chair" (sitting) or a lateral decubitus (side-lying) position. Usually,
the patient is under general anesthesia.
View
of large tear from posterior (behind). Socket is to the right. Courtesy of Dr
Thomas Murray, Orthopaedic Associates of Portland.
Visualizing
torn rotator cuff from within the joint. The biceps tendon is running
vertically on the left. Courtesy of Dr Thomas Murray, Orthopaedic Associates of
Portland.
Motorized
burr removing under-surface of acromion. Courtesy of Dr Thomas Murray,
Orthopaedic Associates of Portland.
View
of large tear from the "50 yard line." Courtesy of Dr Thomas Murray,
Orthopaedic Associates of Portland.
The
side-to-side stitches begin to close the large tear defect. Courtesy of Dr
Thomas Murray, Orthopaedic Associates of Portland.
An
arthroscopic knot-tying instrument is used to pass tie knots in the suture to
secure the repair. Courtesy of Dr Thomas Murray, Orthopaedic Associates of
Portland.
Small
metallic anchors (5 mm) with sutures attached are then inserted into the
humerus at the site desired for tendon reattachment. The anchors are recessed
below the surface, so only the suture is visible. Courtesy of Dr Thomas Murray,
Orthopaedic Associates of Portland.
Sutures
are anchored with the metallic anchors. Courtesy of Dr Thomas Murray,
Orthopaedic Associates of Portland.
Small (5-mm) incisions are created in the back,
side, and front of the shoulder, and the arthroscope and instruments may be
switched between each of these positions as necessary. A complete diagnostic
arthroscopy and bursoscopy (inspection of bursa) is initially performed. Care
is taken to inspect the biceps tendon within the shoulder, the fibrous ring or
labrum that surrounds the glenoid, the capsule and ligaments, the cartilage
surfaces of the head and glenoid, and the rotator cuff tendons. Any pathology
is addressed only after a complete inspection, so as not to miss any
significant findings.
Careful preoperative radiographic evaluation of
the shape and size of the acromion, along with a notation of any spurs, serves
as a guide for the extent of any acromioplasty (undersurface smoothing)
necessary. Because the arthroscope magnifies the structures seen,
irregularities in the surface of less than 1 mm can be seen and are removed.
The goal is to smooth and flatten the undersurface of the acromion to provide
more room for the repair and to relieve pressure from the healing tendon. An
overly aggressive acromioplasty must be avoided because excessive removal of
the anterior acromion can result in the humeral head sliding forward, up, and
out of the socket (anterosuperior subluxation).
The rotator cuff tear is then visualized through
the lateral (side) portal from the "50-yard-line view." The size and
pattern of the tear are assessed. Any thin or fragmented portions are removed,
and the area where the tendon will be reattached to the bone is lightly
debrided to encourage new blood vessel ingrowth for healing.
The sutures are once again passed through the
tendon and systematically tied. The sutures pull the tendon down to the
prepared bone surface, closing the defect. This completes the repair.
At the completion of the procedure, the shoulder
is injected with a long-acting local anesthetic to assist with postoperative
pain management. Each portal incision is closed with a single nylon stitch and
covered with a sterile bandage tape, followed by a dry, sterile dressing. A
cryotherapeutic shoulder pad (Cryocuff) is applied to provide postoperative
cold therapy. This assists in management of pain and swelling. Finally, a sling
(Don Joy UltraSling II) is applied for immobilization and protection. The
patient is then taken to the recovery room.
Arthroscopic rotator cuff repair has achieved
good-to-excellent results in a large percentage of patients (95% reported in
one series), with the results being independent of tear size. U-shaped tears
repaired by margin convergence have been shown to have results comparable to
those of crescent-shaped tears repaired directly by a tendon-to-bone technique.
There is a rapid return to full overhead function after arthroscopic rotator
cuff repair (average, 4 months for all tear sizes). A delay between the time of
injury and the time of diagnosis, even of several years, is not a
contraindication for arthroscopic rotator cuff repair.
The results from one study suggest that patients
who underwent arthroscopic rotator cuff repair with or without acromioplasty
experienced no difference in function or quality of life.[59]
In a prospective study of 88 patients, Castricini
et al showed that augmentation of a double row surgical repair of a small to
medium size tear of the rotator cuff with autologous platelet-rich fibrin
matrix (PRFM) did not improve the healing.[60]
Tissue-engineering techniques are being used to
develop therapies for tendon reconstruction. Biologic and synthetic scaffolds
can both repair tendon defects and improve healing by allowing for the
regeneration of the tendon's natural biologic composition to restore its
mechanical capacity. This process can be further enhanced through augmentation
methods such as cell seeding, growth factor implantation, and gene therapy.
There are many engineered prosthetic materials
being used, but there is no widely accepted treatment for massive irreparable
rotator cuff tears. Allografts have been used for repair of large defects but
with very little success.
Acetaminophen is recommended as initial treatment
because of the toxicity associated with NSAIDs, the need for an analgesic
rather than anti-inflammatory effect, the lower cost of a simple analgesic, and
the chronicity of degenerative rotator cuff disease.
While NSAIDs are known to be effective in
reducing pain and improving function and ROM, they may exert their effect
through their analgesic rather than their anti-inflammatory properties. One
study with poor methodologic quality showed no short-term superiority of NSAIDs
over acetaminophen in the treatment of painful shoulder syndrome. Long- and
short-term studies comparing the efficacy of NSAIDs with that of acetaminophen
for osteoarthritis of the knee have shown similar efficacy for the 2 agents.
Moreover, even the presence of inflammatory signs did not predict a better
response to treatment with NSAIDs, suggesting that improvements are not necessarily
dependent on an anti-inflammatory effect.
If the patient has no contraindications to the
use of ibuprofen, it is usually the drug of choice for the treatment of mild to
moderate pain. It inhibits inflammatory reactions and pain by decreasing
prostaglandin synthesis.
·
Adult dose - 400 mg
PO q4-6h, 600 mg PO q6h, or 800 mg PO q8h while symptoms persist; not to exceed
3.2 g/d
·
Pediatric dose -
For age 6 months to 12 years, 10-70 mg/kg/d PO divided tid/qid; begin at lower
end of the dosing range and titrate upward; not to exceed 2.4 g/d; for older
than 12 years, administer as in adults
·
Contraindications -
Documented hypersensitivity; peptic ulcer disease, recent gastrointestinal
bleeding or perforation, renal insufficiency, or high risk of bleeding
·
Interactions -
Coadministration with aspirin increases risk of inducing serious NSAID-related
adverse effects; probenecid may increase concentrations and, possibly, toxicity
of NSAIDs; may decrease effect of hydralazine, captopril, and beta blockers;
may decrease diuretic effects of furosemide and thiazides; may increase risk of
methotrexate toxicity; phenytoin levels may be increased when administered
concurrently; monitor prothrombin time closely (instruct patients to watch for
signs of bleeding)
·
Pregnancy category
B - Usually safe but benefits must outweigh the risks.
·
Precautions -
Category D in third trimester of pregnancy; caution in congestive heart
failure, hypertension, and decreased renal and hepatic function; caution in
anticoagulation abnormalities or during anticoagulant therapy
The analgesic effect of acetaminophen is mediated
by prostaglandin inhibition.
·
Adult dose -
325-650 mg PO q4-6h or 1000 mg tid/qid; not to exceed 4 g/d
·
Pediatric dose -
For those younger than 12 years, 10-15 mg/kg/dose PO q4-6h prn, not to exceed
2.6 g/d; for those older than 12 years, 325-650 mg PO q4h, not to exceed 5
doses in 24 h
·
Contraindications -
Documented hypersensitivity; known glucose-6-phosphate dehydrogenase deficiency
·
Interactions -
Rifampin can reduce analgesic effects of acetaminophen; coadministration with
barbiturates, carbamazepine, hydantoins, and isoniazid may increase
hepatotoxicity
·
Pregnancy category
B - Usually safe, but benefits must outweigh the risks.
·
Precautions -
Hepatotoxicity possible in chronic alcoholism following various dose levels;
severe or recurrent pain or high or continued fever may indicate a serious
illness; acetaminophen is contained in many over-the-counter products, and
combined use with these products may result in cumulative doses exceeding
recommended daily dose
Numerous studies on the efficacy of NSAIDs for
different shoulder conditions have been published, but because most of them
have poor methodologic quality, no conclusions can be drawn about the efficacy
of NSAIDs.
Recent review articles, using strict inclusion
criteria based on the quality of the methodology, concluded that the trials
with the best methodology show a superior short-term efficacy (2 wk) of NSAIDs
compared with placebo; however, at 4 weeks, results did not show any
statistical differences. Therefore, a short course (10-14 d) of NSAIDs is
indicated as a second-line treatment. No evidence supports longer use.
In case of persistent pain, other therapeutic
modalities should be sought. A comparison between different types of NSAIDs did
not show evidence of the superiority of 1 NSAID with respect to efficacy.
Therefore, an NSAID with the fewest adverse effects, such as the newer COX-2
selective molecules or an NSAID with a combination of prostaglandin E1 analogue
(diclofenac/misoprostol), should be the drug of choice.
In an aging population taking additional
medication that may interact with NSAIDs, drug interactions must be avoided.
From 40-60% of drugs consumed are over-the-counter medications, most often
analgesics and NSAIDs, increasing the risk of potential adverse
gastrointestinal side effects. The patient should be asked whether he or she is
taking any medications concomitantly, such as anticoagulants (hemorrhage),
corticosteroids (peptic ulcer), diuretics and antihypertensives (decreased
blood pressure control), ACE inhibitors (acute renal failure), high-dose
methotrexate (increased methotrexate toxicity), lithium, digoxin,
aminoglycosides (decreased renal clearance), phenytoin (decreased albumin
binding), and antacids (decreased NSAID levels). NSAIDs should be avoided, if
possible, in elderly patients with congestive heart failure or renal or hepatic
dysfunction and who are taking other medications.
Celecoxib primarily inhibits COX-2, which is
considered an inducible isoenzyme—that is, it is induced during pain and
inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID
gastrointestinal toxicity, but at therapeutic concentrations, celecoxib does
not inhibit the COX-isoenzyme; therefore, gastrointestinal toxicity may be
decreased. The lowest dose of celecoxib should be sought for each patient.
·
Adult dose - 200 mg/d
PO qd; alternatively, 100 mg PO bid
·
Pediatric dose -
Not established
·
Contraindications -
Documented hypersensitivity
·
Interactions -
Coadministration with fluconazole may cause an increase in celecoxib plasma
concentrations because of inhibition of celecoxib metabolism; coadministration
of celecoxib with rifampin may decrease plasma concentrations
·
Pregnancy category
C - Safety for use during pregnancy has not been established.
·
Precautions - Use
with caution in patients with compromised cardiac function, hypertension, and
conditions predisposing to fluid retention, because NSAIDs may cause fluid
retention and peripheral edema; use with caution in patients with severe heart
failure and hyponatremia, because NSAIDs may deteriorate circulatory
hemodynamics; use with caution in the presence of existing controlled
infections, because NSAIDs may mask the usual signs of infection; evaluate
symptoms and signs suggesting liver dysfunction, cardiac dysfunction or renal
dysfunction
Ketoprofen is used for relief of mild to moderate
pain and inflammation. Small initial dosages are indicated in small and elderly
patients and in persons with renal or liver disease. Doses of more than 75 mg
do not increase therapeutic effects. Administer high doses with caution and
closely observe patients for response.
·
Adult dose - 25-50
mg PO q6-8h prn; not to exceed 300 mg/d
·
Pediatric dose -
For those aged 3 months to 14 years, 0.1–1 PO mg/kg q6-8h; for those older than
14 years, administer as in adults
·
Contraindications -
Documented hypersensitivity; gastrointestinal disease
·
Interactions -
Coadministration with aspirin increases risk of inducing serious NSAID-related
adverse effects; probenecid may increase concentrations and, possibly, toxicity
of NSAIDs; may decrease effect of hydralazine, captopril, and beta blockers;
may decrease diuretic effects of furosemide and thiazides; may increase risk of
methotrexate toxicity; phenytoin levels may be increased when administered
concurrently; monitor prothrombin time closely (instruct patients to watch for
signs of bleeding)
·
Pregnancy category
B - Usually safe, but benefits must outweigh the risks.
·
Precautions -
Category D in third trimester of pregnancy; use with caution in patients with
congestive heart failure, hypertension, and decreased renal and hepatic
function; use with caution in patients with anticoagulation abnormalities or
during anticoagulant therapy
Differential diagnoses include the following:
·
Adhesive capsulitis
·
Biceps rupture
·
Bicipital
tendinitis
·
Cervical disk
disease
·
Cervical myofascial
pain
·
Cervical
spondylosis
·
Cervical sprain and
strain
·
Complex regional
pain syndromes
·
Fibromyalgia
·
Myofascial pain
·
Osteoarthritis
·
Rheumatoid
arthritis
·
Rotator cuff
disease
·
Shoulder and hemiplegia
·
Thoracic outlet
syndrome
Admit the patient to an orthopedic service in
preparation for the operating room (only required if surgery is the treatment
of choice).
Arrange outpatient follow-up care to an orthopedic
surgeon and rehabilitation services to continue conservative therapy. A
follow-up reassessment examination 6 weeks after beginning conservative therapy
is essential to determine if treatment is successful or if further surgical
treatment is needed.
All NSAIDs are equally effective.
Instruct patients to limit activities to ensure
rest of the affected shoulder.
Failure of conservative treatment requires
surgical intervention. Decreased ROM may occur.
An estimated 4% of cuff ruptures develop a cuff
arthropathy. Various authors report the success rate of conservative treatment
to be 33-90%, with longer recovery time required in older patients. Surgery
results in better function regardless of the patient's age.
Refer patients to a physical therapist for
conservative treatment and postoperative therapy.