Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5181_Библиотеки_им_академика_М_И_Перельмана.pdf
9 The Shoulder
Fig. 9.6 Algorithmic approach to the diagnosis and treatment of atraumatic shoulder pain
213
and full-thickness tears of the rotator cuff become
more prevalent with increasing age. It is unusual
for patients under the age of 40years to present
with rotator cuff tears in the absence of signicant trauma. Conversely, older patients may present with massive rotator cuff tears after an
innocuous event. There are two main theories
which attempt to explain such degenerative cuff
tears. The external impingement model suggests
an extrinsic cause of rotator cuff tears such as
abrasion of the anterosuperior cuff under the
acromion and coracoacromial arch. The intrinsic
model suggests that a relatively poor blood supply to the critical zone of the rotator cuff in combination with high stresses across the cuff leads
to RC tears. The true pathophysiology likely
results from a combination of these models.
History
The chief complaint is usually anterosuperior
shoulder pain which often radiates to the lateral
deltoid region. The pain is typically worse with
overhead activities, arm movements away from
the body, and at night. The patient may recall a
minor traumatic event, or the pain may have
started insidiously.
Examination
Inspection of the shoulder girdle usually reveals
symmetry, but patients with degenerative cuff
tears may present with atrophy of the supra- or
infraspinatus fossae. The patient typically has discrete tenderness at the cuff insertion on the greater
tuberosity. The active range of motion is generally
normal; however, some patients with large RC
tears may exhibit loss of active motion with preservation of passive motion. In this setting, the clinician may be able to document lag signs. Strength
testing may reveal weakness of the supraspinatus
or infraspinatus tendons. Special tests include the
Neer and Hawkins’s impingement signs. If the
patient has concomitant biceps tendon pathology,
there may be tenderness at the bicipital groove
and Speed’s test may be positive. Tenderness over
the AC joint may indicate that the AC joint is contributing to the painful condition. A cross-body
adduction test recreating pain at the AC joint is
considered conrmatory.
Dierential Diagnosis
The differential diagnosis varies with the age of
the patient. In older patients, the differential diagnosis includes arthritis, cervical spine pathology,
214
E. Michaelson and B. Wiesel
metastatic disease, and visceral pathology such
as cardiac disease. In younger patients, instability
and labral pathology should be considered. In
any age group, the differential diagnosis includes
adhesive capsulitis, calcic tendinitis, and a variety of other less common shoulder problems
(avascular necrosis, scapulothoracic dysfunction,
and infection).
Imaging
The AP radiograph may reveal sclerosis, hypertrophy, and cyst formation of the greater tuberosity. The Y-outlet view shows the acromial
morphology with potential narrowing of the subacromial space. In patients with longstanding RC
tears, there may be superior migration of the
humeral head and the distance between the
humerus and acromion on the AP view may be
narrowed. The axillary view illustrates the joint
space and may reveal an os acromiale. An MRI
scan is useful for a number of reasons.
Conrmation of rotator cuff disease (and exclusion of other etiologies) is reassuring, but not
necessary. The MRI scan is extremely useful for
assessing the RC tendons and muscle bellies
(Fig.9.7). The presence, size, and chronicity of a
RC tear directly impacts patient care (surgical
options), recovery, and, ultimately, prognosis.
Patients with smaller tears and less muscle degen-
Fig. 9.7 A tear of the supraspinatus tendon with uid in
the gap is appreciated in this coronal oblique magnetic
resonance imaging (MRI) scan of the glenohumeral joint
eration, seen on MRI as fatty inltration of the
muscle belly, are more likely to experience better
outcomes after rotator cuff repair surgery compared to those patients with signicant muscular
degeneration or larger, retracted tears.
Treatment
The goal of treatment is to return the patient to
pain-free activity. Initially, treatment consists of
education, activity modications and physical
therapy. If the pain is signicant, an oral antiinammatory medication can be prescribed.
Once the painful period subsides, the patient
may benet from a course of physical therapy to
strengthen the rotator cuff and scapular stabilizers, stretch any stiff regions, and improve posture. A subacromial corticosteroid injection can
be considered in a patient who fails to respond
to the initial treatment over 1–2 months or
patients with so much initial pain that they cannot participate in physical therapy. Patients who
fail to respond to nonoperative management
over 3–6 months may benet from surgical
treatment. Most surgeons will obtain an MRI
scan to assess the degree of rotator cuff pathology or tear prior to surgical treatment. For
patients who present with rotator cuff symptoms
and weakness after an initial traumatic event,
MRI may be warranted to assess for rotator cuff
tearing and to determine if surgical intervention
is indicated.
In the absence of a rotator cuff tear, surgeons may recommend arthroscopic subacromial decompression. This involves removing
the inamed subacromial bursa, releasing the
coracoacromial ligament, and shaving the
undersurface of the acromion (acromioplasty)
to create more room in the subacromial space
for the rotator cuff. Subacromial decompression is rarely needed as an isolated procedure
since the vast majority of patients without a
full-thickness rotator cuff tear will improve
with the nonoperative management strategies
described above.
Patients who have reparable RC tears are
treated with primary repair, and most surgeons
will perform an acromioplasty, especially if there
is a downsloping acromion or large bone spur,
9 The Shoulder
215
although several studies suggest this may be
unnecessary. RC repairs can be done with open,
mini-open, and arthroscopic techniques (Fig.9.8).
Arthroscopic rotator cuff repair has become the
standard of care as it allows for better visualization of the tear pattern and a more anatomic repair.
Results of arthroscopic repair are now equivalent
or superior to open repair in recent studies.
Care should be taken to preserve the CA
ligament in patients with large tears and multiple tendon tears to prevent superior migration
of the humeral head if the repair fails. There are
a variety of options for patients with irreparable
tears, including arthroscopic debridement, partial tendon repair, superior capsular reconstruction, and tendon transfers. Rotator cuff
arthropathy is the end-stage of irreparable rotator cuff disease, and will be discussed, along
with treatment options, in the next section. If
biceps tendon pathology is found at the time of
surgery, either tenodesis or tenotomy can be
performed. Patients who are noted to have AC
joint arthropathy and pain prior to surgery may
benet from a distal clavicle resection, which
can also be done arthroscopically. Recovery
a
b
from RC surgery can take anywhere from 4 to
6months. The goal of early (4–10weeks) postoperative physical therapy is recovery of passive shoulder motion. Restoration of strength
and function is the goal of subsequent postoperative therapy. Failure of the patient to adhere
to postoperative physical therapy can result in a
poor outcome. New work is underway to
explore biological augmentation to rotator cuff
repair in order to improve healing rates, especially in degenerative and irreparable tears.
Rotator Cu Arthropathy
Rotator cuff arthropathy (RCA) is the end-stage
outcome of rotator cuff disease often resulting in
signicant shoulder pain and dysfunction. The
primary roles of the rotator cuff are to stabilize
the humeral head in the glenoid fossa throughout
shoulder motion and to create a force couple with
the deltoid to enable effective overhead shoulder
motion. When chronic rotator cuff injury with
degeneration is present, a variety of clinical and
radiographic ndings can be seen. The spectrum
of dysfunction ranges with the severity of the
condition and the physical demands on the individual patient. Although less active patients are
sometimes able to compensate for their dysfunction with scapulothoracic mobility or the contralateral arm, many patients present with complaints
of pain with motion, signicant weakness, or
pseudoparalysis. There is characteristic anteriorsuperior escape of the humerus, as the shoulder
loses the inferior and medial directed stabilizing
force of the rotator cuff.
Fig. 9.8 (a) Arthroscopic photography of a right shoul-
der with a full-thickness tear of the supraspinatus tendon.
(b) Arthroscopic photography following arthroscopic
repair of the tear with suture anchors
History
Patients will often complain of chronic pain and
weakness with shoulder elevation and movements away from the body. In patients without
associated arthritis, pain will often be limited at
rest. Night pain is common and patients often
report being unable to sleep on the affected side.
Examination
Inspection may demonstrate disuse atrophy of
the shoulder girdle. Passive range of motion will
216
E. Michaelson and B. Wiesel
be intact prior to the development of arthritis,
with signicantly limited active range of motion,
especially in forward elevation. As arthritis progresses, passive range of motion will become
progressively restricted. There will be signicant
weakness in rotator cuff testing, and lag signs can
be seen most commonly in forward exion,
external rotation at the side, and Hornblower’s
sign in abduction and external rotation. A thorough motor and neurovascular exam should be
performed including strength testing of all three
heads of the deltoid.
Dierential Diagnosis
The spectrum of rotator cuff disease including
tendonitis and rotator cuff tear will have a similar
presentation. Adhesive capsulitis may cause a
similar degree of dysfunction, but with limited
passive motion and lacking radiographic pathology. It is important to differentiate RCA from
osteoarthritis (where the rotator cuff is typically
intact), as this distinction may inuence surgical
decision-making.
Imaging
A standard shoulder X-ray series combined with
physical examination is usually sufcient for
diagnosis. The AP radiograph may show superior
translation of the humerus, calcication of the
CA ligament, and acetabularization of the CA
arch with femoralization of the humeral head.
The Scapular-Y view will show loss of the subacromial space, and the axillary view may show
anterior escape of the humeral head. As RCA
progresses, all views may demonstrate arthritic
progression (Fig. 9.9). Glenoid wear should be
evaluated on the AP and axillary radiographs, as
superior glenoid wear frequently occurs. If there
is severe glenoid deformity, a CT scan can be
obtained for surgical planning purposes. Once
superior migration of the humeral head is seen on
the AP radiograph, MRI of the shoulder is not
needed to make the diagnosis of RCA.If an MRI
is obtained, it will demonstrate signicant rotator
cuff pathology often involving massive tears of 2
or more tendons with retraction of the tendon
edges past the joint line and atrophy of the rotator
cuff muscle bellies.
Treatment
Initial treatment is nonoperative combined with
activity modication. Physical therapy includes
strengthening the deltoid and remaining rotator
cuff muscles to improve function. Oral antiinammatories and intra-articular steroid injections may provide pain relief. Nonoperative
treatment measures generally provide mild and
temporary symptomatic improvement. When
nonoperative intervention and activity modication fail to provide adequate relief, operative
intervention is indicated.
The primary surgical option for patients with
RCA is reverse total shoulder arthroplasty
(RTSA). In RTSA, the ball-and-socket anatomy
of the shoulder is reversed (Fig. 9.10). The
rounded implant, known as the glenosphere, is
placed on the glenoid, and the socket is implanted
on the humeral side of the shoulder. Reversing
the anatomy of the shoulder creates a few signicant advantages in the setting of RCA. The
shoulder joint becomes more constrained, recreating stability lost with rotator cuff dysfunction
and enabling elevation of the shoulder by the
deltoid without superior translation of the
humeral head. The center of shoulder rotation is
moved inferiorly and medially, thereby partially
substituting for the inferior, medial, and compressive force of the rotator cuff that enables
effective force coupling with the deltoid in the
native shoulder. An increased deltoid moment
arm and higher deltoid muscle tension increases
the stability of the shoulder and efcacy of the
deltoid to elevate the arm without the assistance
of the rotator cuff musculature. Overall, RTSA is
a highly effective procedure that provides durable relief for patients with signicant pain and
functional limitations.
Osteoarthritis
Degenerative arthritis, or osteoarthritis (OA),
occurs in the glenohumeral joint but is less common than in the hip or knee joints. Osteoarthritis
of the glenohumeral joint has the same pathophysiology as in other joints with progressive
articular cartilage destruction.
9 The Shoulder
Fig. 9.9 AP, scapular-Y,
and axillary radiographic
views of a shoulder with
rotator cuff arthropathy.
Characteristic superior
and anterior escape can
be seen as well as
greater tuberosity
hypertrophy and
coracoacromial
calcication
217
History
Patients with early osteoarthritis may have a clinical syndrome that is virtually indistinguishable
from impingement syndrome. In patients with
advanced osteoarthritis, pain is more likely to be
chronic, occur at rest, and be resistant to standard
analgesics and anti-inammatory medications. In
addition, loss of shoulder motion is a common
complaint. Patients may have trouble sleeping,
often not able to sleep on the affected shoulder.
Examination
Patients with early osteoarthritis may examine
similarly to those with impingement syndrome.
In more advanced OA, generalized disuse atro-
phy of the shoulder girdle may be noticeable and
there is often signicant crepitus of the glenohumeral joint. In general, there is a progressive loss
of active motion in all planes, but loss of external
rotation with the arm at the side is often the most
dramatic. Passive motion is similarly decreased
and there is often a signicant amount of pain
associated with passive stretching of the joint
capsule near the end ranges of motion. It is
important to look for scars indicative of prior
surgeries to the shoulder. A thorough strength
and neurovascular exam should also be performed, paying specic attention to axillary
nerve function, along with deltoid and rotator
cuff strength.
218
Fig. 9.10 AP,
scapular-Y, and axillary
views of a patient with
rotator cuff arthropathy
after reverse total
shoulder arthroplasty
E. Michaelson and B. Wiesel
Dierential Diagnosis
Adhesive capsulitis can have a similar presentation
to and is distinguished from glenohumeral arthritis
via radiography. Inammatory arthropathy and
septic arthritis can have similar presentations, with
medical history, onset, and signs of infection differentiating these conditions. The examiner must
have a high index of suspicion for locked posterior
shoulder dislocations in older patients who are
poor historians as a result of dementia or stroke.
Imaging
A standard shoulder series is recommended.
Joint space narrowing, subchondral sclerosis,
osteophytes, and subchondral cyst formation are
classic ndings in osteoarthritis and are best
seen on the AP and axillary view (Fig.9.11). In
the glenohumeral joint, inferior humeral osteophytes predominate. Often, eccentric posterior
glenoid wear is present. MRI scans are generally
not used in the evaluation of OA.A CT scan to
assess the glenoid for eccentric wear or bone
loss is common during preoperative evaluation
for shoulder arthroplasty. In patients with greater
deformity, many surgeons will utilize 3-D surgical planning software prior to shoulder replacement surgery to create preoperative shoulder
templates from CT scans.
9 The Shoulder
219
Fig. 9.11 All of the classic ndings of osteoarthritis are
present in this true AP X-ray of the glenohumeral joint,
including joint space narrowing, subchondral sclerosis,
osteophyte formation, and subchondral cyst formation
Treatment
Initial treatment for OA includes education, rest,
activity modication, and anti-inammatory
medications. Physical therapy for stretching and
maintenance of motion is an important component of nonoperative treatment. Intra-articular
corticosteroid injections often delay the need for
surgical intervention but provide inconsistent and
incomplete pain relief in this setting. When nonoperative management is no longer able to control the patient’s pain, surgical management is a
reasonable option. In select younger patients with
concentric wear, some joint space preservation,
and reasonable motion, improved symptoms may
be obtained from arthroscopic debridement. The
goal of debridement is pain relief and postponement of prosthetic joint arthroplasty. This intervention may include a combination of loose body
removal, osteophyte debridement, chondroplasty,
capsular releases, subacromial decompression,
biceps tenodesis, and axillary neurolysis.
In the setting of painful, end-stage OA, prosthetic joint replacement with either an anatomic
total shoulder arthroplasty (aTSA) (Fig.9.12) or
RTSA is recommended, depending on the amount
Fig. 9.12 A total shoulder arthroplasty is demonstrated in
this true AP X-ray of the glenohumeral joint. This metallic
humeral component is placed via press-t into the proximal humerus but may also be cemented. The pegged polyethylene glenoid component is cemented into the glenoid
and is represented by the reproduction of the joint space.
The central peg of the polyethylene glenoid component is
identied by the horizontal radiopaque marker
of bony deformity and status of the rotator cuff.
For aTSA, a plastic glenoid component is
cemented onto the patient’s glenoid in addition to
replacement of the humeral head. aTSA introduces the risk of glenoid-sided prosthetic loosening and wear which may require revision surgery
and, similar to a native shoulder, requires a wellfunctioning rotator cuff for good shoulder function. Similar to the reverse shoulder arthroplasty,
surgery is performed via the deltopectoral interval. The subscapularis muscle must be detached
in order to access the joint. The muscle is repaired
following placement of the implant, but the repair
must be protected during the early phase (rst
6 weeks) of postoperative rehabilitation, as the
survival of the anatomic arthroplasty is dependent on the healing of the subscapularis. In many
situations, especially in older patients who may
have degeneration of the rotator cuff or patients
with signicant boney deformity, RTSA is now
being used to treat patients with glenohumeral
arthritis.
220
E. Michaelson and B. Wiesel
Miscellaneous Arthropathy
A variety of other disease processes can lead to
glenohumeral joint destruction. Inammatory
arthropathy, such as rheumatoid arthritis, can
lead to joint destruction as a result of synovial
disease. While the clinical presentation may be
similar to osteoarthritis with pain and loss of
motion, there are some important differences. In
particular, rheumatoid arthritis can result in rotator cuff deciency and incompetence. In these
patients, anatomic total shoulder arthroplasty is
contraindicated since glenoid loosening in the
setting of rotator cuff deciency is a common
problem. If arthroplasty is required in the setting
of signicant destruction of the rotator cuff, then
reverse total shoulder arthroplasty is the procedure of choice. Progressive bony destruction of
the humeral head and glenoid can result from
rheumatoid arthritis, making prosthetic arthroplasty difcult. Avascular necrosis can occur as a
result of trauma, corticosteroid use, alcoholism,
and other less common etiologies. Avascular
necrosis of the humeral head can lead to pain and
loss of motion in the glenohumeral joint.
Hemiarthroplasty is an option for young patients
with humeral head collapse and chronic pain.
Total shoulder arthroplasty is indicated when
secondary destruction of the glenoid is present.
Charcot or neuropathic arthropathy is typically a
painless condition that results in severe joint
destruction. Charcot arthropathy in the glenohumeral joint is commonly related to a cervical
spine syrinx and an MRI of the cervical spine
should be obtained in any patient presenting with
possible Charcot arthropathy. There are no reliable surgical options for Charcot arthropathy.
Adhesive Capsulitis
Adhesive capsulitis, or frozen shoulder, is a painful condition in which the synovial lining of the
glenohumeral joint is inamed. Adhesive capsulitis is a clinical diagnosis in which examination
reveals an equal loss of active and passive motion.
Primary adhesive capsulitis is idiopathic meaning that no trigger can be identied. It occurs in
middle-aged persons and is associated with dia-
betes and thyroid dysfunction. Secondary adhesive capsulitis implies that a trigger or cause of
the disease process can be identied. Trauma,
surgery, and concomitant shoulder girdle pathology may result in secondary adhesive capsulitis.
History
The patient reports an insidious onset of shoulder
pain and progressive decreased range of motion.
Pain often occurs during rotational movements
such as reaching behind the back, putting on a coat,
or fastening a bra. Often the patient may recall a
minor event that precipitated the condition. Pain at
night is common. It is important to obtain a past
medical and surgical history to identify possible
risk factors. Insulin-dependent diabetes is a strong
risk factor for adhesive capsulitis. Symptoms may
depend on the stage of the disease: the initial
inammatory phase will manifest as pain throughout the range of motion, whereas during the frozen
phase patients will report signicant motion restrictions and pain at the end range of motion.
Examination
In the absence of prior trauma or surgery to the
shoulder girdle, the inspection and palpation portions of the exam are usually unremarkable.
Active motion can be extremely limited in all
planes of motion, and the passive motion is similarly restricted. The patient often experiences
pain at the end range of motion (active or passive).
Rotator cuff strength is intact within the connes
of the limited motion.
Dierential Diagnosis
Early adhesive capsulitis can mimic rotator cuff
pathology. Subtle losses of internal and external
rotation in abduction may be the only clues to differentiate between the two diagnoses. Unrecognized trauma (locked posterior shoulder
dislocations) and glenohumeral joint arthropathy
can mimic adhesive capsulitis, but these entities
can be easily excluded with standard radiographs.
Imaging
A standard shoulder series is useful in excluding
other diagnoses; however, there are no radiographic ndings for adhesive capsulitis. MRI
may demonstrate general inammation and cap-
9 The Shoulder
221
sular thickening but is not routinely ordered
unless there is concern for concomitant pathology such as rotator cuff tear, and further studies
are generally not indicated unless additional
pathology is suspected.
Treatment
Once the diagnosis is made, education of the
patient is paramount. In general, the treatment
of adhesive capsulitis is twofold: treatment of
the synovial inammation and restoration of
motion. Anti-inammatory medications can be
used, but a corticosteroid injection into the glenohumeral joint space is more efcient and
effective for treating the synovial inammation.
Patients should be educated that the goal of
inammation control is to relieve pain, so they
are able to participate fully in stretching and
physical therapy. The patient must start a
stretching program to regain motion in all
planes. Initially, supervised physical therapy is
helpful, but the patient must independently perform a battery of home stretching exercises
daily. A gradual restoration of motion is the
anticipated course although this can often take
12–18months. In patients who fail to show any
response to nonoperative treatment after
3–6months, surgery may be a reasonable option.
Historically, patients with diabetes have a higher
failure rate of nonoperative treatment compared
to patients without risk factors. Additionally,
patients with secondary adhesive capsulitis
from trauma or prior shoulder surgery often fail
to respond fully to nonoperative treatment.
Manipulation of the shoulder under anesthesia
was once the preferred treatment and continues
to be a reasonable option. However, proximal
humerus fractures can occur with manipulations
under anesthesia, and osteoporosis is a risk factor for this complication. Arthroscopic capsular
release is a more invasive, yet more anatomic,
procedure. The surgery involves releasing the
shoulder capsule under direct vision with a
combination of biters and electrofrequency
devices. The axillary nerve is at particular risk
during release of the inferior capsule. Aggressive
physical therapy with active-assisted and active
range of motion is mandatory to maintain the
postoperative range of motion and should be
started on the day of surgery. Shoulder strengthening and resistance therapy is instituted only
after restoration of full, active shoulder motion.
Calcic Tendinitis
Calcic tendinitis of the rotator cuff is a painful
condition of the shoulder girdle and is a common clinical problem (Fig.9.13). The etiology
of calcic tendinitis is a matter of debate. The
pathogenesis of calcifying tendinitis includes
various stages of tendon degeneration, calcium
deposition, and calcium resorption. In the formative phase of calcium deposition, there may
be little or no pain. Typically, the resorptive
phase is more painful and clinically relevant,
related to the inammatory process of calcium
resorption.
History
In the resorptive phase, the patient may present with
an acute onset of severe shoulder pain that may
mimic a septic shoulder joint. In the formative
phase, the patient may present with more chronic
symptoms that mimic impingement syndrome.
Fig. 9.13 A calcium deposit is present in the supraspinatus tendon immediately medial to its attachment site on
the greater tuberosity in this true AP X-ray of the glenohumeral joint
222
E. Michaelson and B. Wiesel
Examination
Acute bursitis in the resorptive phase may lead to
fullness of the anterosuperior shoulder, but otherwise the inspection is typically unremarkable.
Typically, there is tenderness at the rotator cuff
insertion corresponding to the calcium deposition. There may be a loss of active motion secondary to pain, but passive motion and rotator
cuff strength testing, although painful, is generally intact. Impingement signs are often positive.
Dierential Diagnosis
The differential diagnosis includes rotator cuff
disease and adhesive capsulitis. Referred pain
from cardiac origin or other visceral organs and
radicular pain from the cervical spine should be
considered. Septic arthritis may need to be ruled
out in the acute, severely painful phase.
Imaging
The appearance of calcic tendinitis on radiographs varies depending on the phase of the disease. In the formative phase, the calcium deposit
is usually well circumscribed and easily identied. In the resorptive phase, the deposit may
appear uffy and less well dened. In addition to
the standard shoulder series, internal and external
rotational AP views can be helpful for identifying
more subtle deposits. Additional studies are not
usually indicated.
repetitive overhead throwing activities. A
thickened, contracted posterior capsule is a
hallmark of GIRD, leading to an anterior
humeral shift and the characteristic loss of
shoulder internal rotation compared to the
contralateral side. GIRD is a risk factor for
the development of symptomatic pathology,
especially internal impingement. Internal
impingement is abnormal contact between the
greater tuberosity or rotator cuff and the posterior glenoid or superior labrum in the
abducted and externally rotated shoulder
position. This impingement can be symptomatic, and it may lead to other attritional pathology including partial-thickness articular-sided
rotator cuff tears, posterior labral tears, or
SLAP tears (Fig.9.14).
History
Symptomatic patients with GIRD will localize
pain posteriorly and deep in the shoulder, worst
in the late cocking phase of the throwing motion.
Throwing athletes may also complain of
decreased velocity and loss of throwing control.
Patients will often have no pain at rest. Onset of
symptoms is generally insidious, without an
inciting event.
Treatment
Treatment generally involves pain management.
Noninvasive treatment options include antiinammatory medications and extra-corporeal
shock wave therapy. More invasive options include
corticosteroid injections and lavage therapy.
Surgical treatment is a last resort and involves
arthroscopic debridement of the calcium deposit.
The Throwing Shoulder:
Glenohumeral Internal Rotation
Decit andInternal Impingement
Glenohumeral internal rotation deficit (GIRD)
results from a physiologic adaptation in the
osseous structure and capsular balance to
Fig. 9.14 Patient participating in sleeper stretch, moving hand down towards the table to create shoulder
internal rotation and stretch the posterior shoulder
capsule