The pectoralis major (PM) is the largest muscle of the anterior chest wall and serves to adduct, flex, and internally rotate the humerus(1,2). The PM muscle is broken down into two main components or “heads” based upon muscle fiber origin: clavicular and sternal (Fig. 1).
PM injury results from direct trauma or indirect force overload. This commonly includes muscle overload during eccentric contraction with the humerus extended, as in performing the bench press maneuver(1,3–5).
This paper outlines the normal anatomy of the PM and the spectrum of PM injury on magnetic resonance imaging (MRI) and high-resolution ultrasound (HRUS). Advantages and disadvantages of these modalities in the setting of PM evaluation will be discussed. Important anatomical landmarks and imaging features are reviewed to aid the radiologist in diagnosing the type of PM injury and differentiating PM injury from other entities, such as infection or neoplasm. Operative and non-operative management of PM injury is also described.
The clavicular head is a single muscular segment arising anteriorly from the medial clavicle(2). It assists in forward elevation or flexion of the arm. The sternal head of the PM is more inferior and originates from the anterior surface of the manubrium, sternum, and first/second to sixth costal cartilages(2). The sternal head can have as many as seven individual segments. The lowest fibers originate from the fifth and sixth costal cartilage and fascia of the external oblique and transversalis abdominal muscles(6). Some authors describe it as the “abdominal segment” of the sternal head while others characterize it as a distinct third head(1,5,7). The sternal head assists in internal rotation of the humerus at the glenohumeral joint. It comprises a majority of the PM volume(2,6) (Fig. 2).
The clavicular and sternal heads form a common tendon that traverses anterior to the coracobrachialis and short head biceps brachii muscles and inserts onto the anterior surface of the humeral diaphysis, just lateral to the long head of the biceps brachii tendon (Fig. 3). The length of the tendon footprint on the humeral diaphysis measures approximately 4–6 cm in the craniocaudal dimension(8). The PM tendon has complex anatomy. There are distinct anterior and posterior layers, each measuring approximately 2 mm in thickness, which connect at the inferior margin in the shape of the letter “U”(2,4,9) (Fig. 4). The anterior tendon layer is comprised of the clavicular head and three to five most superior segments of the sternal head while the posterior layer is comprised of the two to three most inferior segments of the sternal head. In addition, the sternal segments twist as they course towards their insertion, with the lowest segments inserting most superiorly in the posterior layer(2,4).
MRI and US are well established as the two main imaging modalities for investigation of PM muscle pathology(5,10–12) (Fig. 5, Fig. 6, Fig. 7, Fig. 8, Fig. 9, Fig. 10, Fig. 11, Fig. 12, Fig. 13, Fig. 14, Fig. 15). However, it should be noted that some patients with suspected PM injury undergo initial radiographs, which may identify an osseous avulsion injury arising from the humeral insertion of the PM (Fig. 12).
MRI affords superior contrast resolution between the intermediate signal of muscle, hypointense signal of tendon, and the fluid signal hyperintensity that is associated with injury. The pathologic fluid signal is best depicted on fat saturated (FS) T2-weighted (T2-w) sequences, which are complemented by the anatomical detail better visualized on T1-weighted (T1-w) sequences. While sequence selection varies between institutions, most protocols typically contain axial, coronal, and sagittal fluid-sensitive sequences, such as T2-w FS, proton density (PD) FS, or short tau inversion recovery (STIR), as well as axial T1-w and coronal T1-w or PD sequences. Axial images are particularly useful in identifying the relationship between the PM tendon, biceps brachii and coracobrachialis muscle (Fig. 3). Occasionally, the axial images will be a smaller field of view to facilitate injury detection at the distal tendon insertion. Sagittal and coronal imaging planes help further characterize the extent and location of PM injury. This can include additional coronal oblique imaging in the plane of the PM muscle and tendon. Standard imaging time is approximately 45 minutes.
US provides a portable, more cost-effective, and faster alternative to MRI and affords superior spatial resolution. Although US is more user-dependent, studies have shown inter-observer reliability in detecting PM injury and adequate correlation with MRI and intraoperative findings(8,12). US assessment is conducted with a linear high-resolution transducer positioned transverse and longitudinal to the longitudinal axis of the PM muscle. The muscular clavicular and sternal segments are imaged from their origins to the common tendon insertion onto the humerus. Care is taken to identify the relationship of the PM tendon with respect to the regional anatomy. This includes following the bicipital groove in the transverse plane inferiorly to locate the PM tendon, which crosses superficial to the long head biceps brachii tendon and inserts on the lateral margin of the groove (Fig. 3). In addition, the short head biceps brachii muscle has been described as a useful anatomical landmark and can be followed from the coracoid process of the scapula inferiorly, superficial to which the PM tendon and myotendinous junction course.
Sometimes the symptoms of PM pathology can overlap with those occurring in the shoulder. Irrespective of modality, it is prudent to evaluate for primary and secondary signs of PM injury on imaging examinations that are otherwise tailored for the shoulder (Fig. 5).
PM tears occur almost exclusively in active men between 20–40 years of age(1,4,13,14). Approximately 75% of these injuries are related to sports activity with weight-lifting accounting for nearly 50% of the reported cases(3,4). PM tears often present clinically with sudden onset of pain and weakness during arm adduction(1,14). Chest wall and axillary hematoma formation and swelling is frequently encountered and can sometimes obfuscate medial retraction of the muscle(1,7).
The variation in muscle segment lengths in the PM is atypical compared to other muscles, which demonstrate more uniformity(2,6). While this maximizes power production, it predisposes the inferior segments of the sternal head to higher fiber excursion during 0° and 30° of humerus extension(6). Thus, the biomechanical model of failure is described as muscle overload during eccentric contraction with the humerus extended, as in performing the bench press maneuver(1,5). As a result, the inferior sternal head fibers are most commonly torn(2,10). The PM tendon is most commonly torn at the humeral insertion(13). The myotendinous junction is the second most common location of PM tears and has been documented to occur more frequently in those older than 30 years of age(15). With respect to tears involving the muscle proper, those involving the muscle origin from the sternal or clavicular head or intramuscular tears are less common than tears at the myotendinous junction.
The classification system developed by ElMaraghy and Deveraux is the most commonly used to describe tear of the PM and is based on the “U-shaped” orientation of the tendon (Fig. 6)(4). “Width” is characterized as the craniocaudal extent of the anterior and posterior layers(4). For example, a full width tear involves the entirety of the posterior or anterior layer. “Thickness” refers to the antero-posterior orientation of the fibers. A full thickness tear will therefore involve both the posterior and anterior layers. Tears are also characterized by the location: at the tendon insertion on the humerus, mid tendon substance, myotendinous junction, intra-muscular, or at the muscular origin. Tears at the humeral insertion can have associated avulsed osseous fragments; however, this is a rare injury location(13).
Muscle fiber and tendon disorganization, laxity and/or focal defect are characteristic imaging findings of acute PM tear (Fig. 7, Fig. 8, Fig. 9, Fig. 10). In the acute phase, this manifests as a focal T2 hyperintense or hypo/anechoic abnormality within the substance of the muscle or tendon on MRI and US, respectively.
Hematoma formation is a secondary sign of injury and can be within the muscle or tissues surrounding the torn tendon (Fig. 7, Fig. 8).
Acute hematoma demonstrates fluid signal on MRI and is predominately hypoechoic on US(12). In the subacute and chronic phases, hematoma can appear more organized and anechoic on US and, depending on chronicity, shows variable signal intensity on MRI(12).
Full-thickness tears at the distal humerus insertion result in nonvisualization of PM tendon fibers superficial to the long head biceps brachii tendon which may be anteriorly displaced(8,10) (Fig. 9). Care must be taken on image interpretation to accurately identify the anterior and posterior layers of the PM tendon so that full width partial thickness tears are not misdiagnosed as completely intact tendon (Fig. 10).
Periosteal reaction can be detected on US in the setting of PM tendon injury (Fig. 10 D). MRI offers the additional benefit of detecting bone marrow edema which can be a secondary sign of injury (Fig. 11)(10). Radiography is beneficial in detecting periosteal reaction and osseous avulsion fracture (Fig. 12).
Findings of chronic PM injury include scar tissue formation, muscle atrophy, and tendon retraction (Fig. 13). A relative paucity of edema surrounding the PM tear is another characteristic of chronic injury.
PM strain manifests as less well-defined echogenicity and architecture on US and feathery fluid signal MRI abnormality without overt tear (Fig. 14).
In most instances, clinical history, patient demographics, and physical examination are adequate to diagnose the anterior chest wall findings as traumatic in etiology. However, infection and neoplasm are also possible and can present with similar symptoms and imaging findings. For example, a posttraumatic hematoma can appear similar to the more focal, circumscribed, or “mass-like” appearance of abscess or neoplasm (Fig. 15). This is particularly true for chronic PM tears, where the fiber disorganization may be less obvious with decreased edema and the propensity for chronic hematomas to have thicker walls. On post-contrast MRI, fibrous or scar tissue can enhance which may complicate the diagnosis. Axillary lymphadenopathy is rare in isolated traumatic muscle injury and if present, it should raise concern for infection or neoplasm.
Non-operative management of PM tears is recommended for partial tears, tears that exclusively involve the muscle belly, and contusion or strain. Initial management consists of rest, ice, analgesia, and immobilization of the adducted and internally rotated arm in a sling. Patients transition from passive to active range of motion and eventually to full resistance training from two weeks to four months post injury(16). Return to contact sports should not commence until 5–6 months after injury and, in some instances, certain training maneuvers like the bench press should be permanently avoided(16). Often, patients experience strength deficit and cosmetic defect with non-operative management(9,17). In the setting of low functional demand, patients with full-thickness tears may also undergo nonoperative management with satisfactory recovery to performing activities of daily living(18).
In 1980, Tietjen described a classification system for the management of PM injury based upon tear location and severity(19). This system was modified by Bak
Classification of pectoralis tear, modified by Bak
Grade | Location | ||||
---|---|---|---|---|---|
I | muscle contusion | A | muscle origin | D | tendon avulsion from humerus |
II | partial tear | B | muscle belly | E | Bony avulsion from tendon insertion |
III | complete tear | C | myotendinous junction | F | tendon intra-substance tear |
It is generally accepted that surgical repair produces higher patient satisfaction with better functional and cosmetic outcomes(1,3,6,9,17,21). Bone trough, suture anchor, and cortical button technique are all effective methods to repair the PM tendon(13,22–24). Further description of these techniques is beyond the scope of this article.
Patients are immobilized in a sling for six weeks following surgery. Passive range of motion begins after six weeks and at three months the patient should have full range of motion and can begin light resistance training(20). Return to full activity is achieved at six months postoperatively(17). High-weight, low repetition exercises that involve the PM, such as bench press, are discouraged indefinitely(20).
The timing of surgical intervention is important. Repair of an acute PM tear leads to better patient satisfaction and functional outcomes(3,25,26). After 6 weeks, a PM tear is generally considered to be chronic. Surgical management of chronic injuries can be more technically challenging and often requires a larger surgical field secondary to scar tissue formation and muscle retraction(4).
Artifact from surgical intervention and hardware is commonly visualized on post-operative MRI and US, (Fig. 10 A and Fig. 17).
Tear of the PM most commonly occurs in athletic males between the ages of 20–40 years. MRI and US are useful imaging modalities to diagnose PM injury. Recognition of regional anatomical landmarks and other etiologies of PM pathology results in the accurate description of injury which guides non-operative and surgical management.