Internal Derangements of Joints: Upper and Lower Limbs

Rotator Cuff Disease

The commonest cause of rotator cuff tendon tears is external impingement, occurring mostly in patients over the age of 40 years. Acute injuries are uncommon in the younger population, except in athletes. Impingement of the rotator cuff tendons occurs between the humeral head and coracoacromial arch during abduction of the upper arm. Initially there is reversible oedema and haemorrhage in the tendons, which may lead to tendinopathy and eventually failure of the tendon. The subacromial space may be reduced by bony abnormalities such as ACJ osteophytes and abnormalities of the shape of the acromion. Secondary impingement may occur through abnormal coordination of the rotator cuff muscles and abnormal scapulothoracic movement.

The impingement phenomenon is associated with the development of subacromial bursitis and acromial bone spur formation. This further limits the subacromial space and aggravates the impingement process.

Tendinopathy is defined as tendon injury on a cellular level that is most commonly age related and degenerative in nature but may also occur following trauma in younger individuals. The connective tissue that binds and organises the collagen bundles of the tendon undergoes microscopic tearing that leads to activation of inflammatory mediators and disorganised tendon healing. The tendon often thickens and may show features of delamination, mucoid degeneration, and eventually partial tearing on imaging. Calcific tendinopathy is characterised by intrasubstance deposition of calcium hydroxyapatite crystals of unknown aetiology. The calcific deposits may be asymptomatic but can become painful when they produce focal tendon swelling that may contribute to external impingement. Release of calcium from the tendon into the overlying SAB can produce an acute inflammatory bursal reaction.

Rotator cuff tendon tears are defined as partial or full thickness. A partial-thickness tear (PTT) involves either the articular surface (commonest) or the bursal surface (less common), but does not extend all the way through the tendon. A full-thickness tear (FTT) extends from the articular surface to the bursal surface and creates an abnormal communication between the GHJ and SAB. The term ‘full thickness’ only indicates that the tear extends through the full thickness of the tendon; it does not imply the tear extends from the anterior edge of the tendon to the posterior edge. However, as the tear size increases, the whole tendon may become torn (anterior to posterior), creating a large tear with medial tendon retraction. The supraspinatus is most commonly affected, but tears may progress to involve both infraspinatus and subscapularis. A cuff tear in short axis measuring 5 cm or more, or involving at least two of the tendons of the cuff, is referred to as a massive tear.

Tears of the LHB pulley and subscapularis tendon may lead to medial subluxation of the LHB tendon from the bicipital groove. The LHB may also show features of tendinopathy or may eventually rupture.

Radiography is useful for demonstrating bony abnormalities of the ACJ and acromion and excluding associated GHJ arthrosis ( Fig. 39.1 ). Marked narrowing of the subacromial space is a specific but insensitive sign of a full-thickness rotator cuff tear ( Fig. 39.2 ). Magnetic resonance imaging and US directly visualise the rotator cuff tendons. Both techniques are capable of diagnosing tendinopathy ( Fig. 39.3 ) and have nearly 100% accuracy rates for FTTs of the rotator cuff. MR arthrography is not usually indicated for primary rotator cuff disease. The most important features that help determine management include the following:

• size and shape of cuff tear

• location of cuff tear

• presence of associated rotator cuff muscle atrophy

• dislocation or rupture of the LHB tendon

• bony abnormalities of the coracoacromial arch

• secondary arthrosis of the GHJ.

The primary sign of a rotator cuff FTT is a focal deficiency of the tendon ( Figs 39.4 and 39.5 ). This nearly always occurs at the tendon insertion on the tuberosity. The margins of the tear are best delineated when there is fluid within the tendon defect. Secondary signs of an FTT include the presence of fluid in both the GHJ and SAB, and flattening or concavity of the subacromial fat plane. FTTs can be described according to their shape. Typical tear configurations are crescentic, ‘ U ,’ or ‘ L ’ shaped.

PTTs are less reliably demonstrated by both MRI and US, and it may be difficult to differentiate tendinopathy from partial tears. Focal clefts, tears, or tendon thinning affecting the articular margin of the footprint of the tuberosity are most common ( Figs 39.6 and 39.7 ). Tendon thickening is not always present. It is important not to mistake magic angle artefact on short echo time (TE) MR sequences or anisotropy on US as evidence of tendinopathy.

Calcific tendinopathy can be visualised on radiographs as discrete amorphous deposits of calcium density. On US they are echogenic and may or may not cast acoustic shadowing ( Fig. 39.8 ). Small deposits of calcium may be difficult to detect on MRI, as both the calcification and surrounding tendon are of low signal intensity (SI).

Glenohumeral Joint Instability

The GHJ is an inherently unstable joint. Injury or abnormality of the static stabilisers renders the joint susceptible to recurrent dislocation and further injury. Chronic GHJ instability may lead to secondary arthrosis if untreated. Imaging is used to document the extent of internal derangement in order to determine the therapeutic options.

Instability of the GHJ may be dependent on three factors, referred to as the Bayley triangle:

• traumatic structural

• atraumatic structural

• habitual non-structural (abnormal muscle patterning)

A combination of these factors may be present in any one patient, but trauma is the commonest cause of instability. Anteroinferior dislocation is the commonest presentation. Posterior dislocation is frequently encountered following epileptic seizures. Inferior dislocation is rare.

Radiography is the primary imaging technique to confirm GHJ dislocation and establish joint congruity following reduction. Antero­posterior (AP) and axial views or a modified caudal angled axial are most appropriate. MRI, MR arthrography, or CT arthrography are used in the non-acute setting to assess the static stabilisers.

Anterior GHJ dislocation causes tearing and detachment of the anteroinferior glenoid labrum, known as a Bankart lesion. The location of the labral tear is described according to clockface terminology: 12 o'clock represents the biceps anchor and 3 o'clock is anterior at the equator of the glenoid. Fluid SI or contrast medium extending between the glenoid and labrum is the primary sign of a labral tear ( Fig. 39.9 ). The labrum may become displaced, and it is important to assess the position of the labrum with respect to the face of the glenoid.

More severe injury may be associated with a bony injury of the glenoid rim, usually called a bony Bankart lesion ( Fig. 39.10 ). Non-enhanced CT may occasionally be preferred to assess the size of the bony defect of the glenoid. There is usually associated impaction injury on the posterosuperior aspect of the humeral head called a Hill–Sachs defect ( Figs 39.11 and 39.12 ).

In posterior dislocation, the location of labral and humeral injury is opposite to anterior dislocation; such dislocations are termed reverse Bankart lesions and reverse Hill–Sachs defects.

Injury to the joint capsule and glenohumeral ligaments is common. The anterior band of IGHL is the most important joint stabiliser. It may be torn at the humeral insertion or less commonly from its origin on the glenoid. Imaging with the arm in ab duction and e xternal r otation (ABER imaging) is sometimes used to assess the integrity of the liga­ment, to identify the degree of labral displacement and loss of joint congruity.

The most important features that help determine management include:

• Location and extent of labral defect using clockface terminology.

• Pattern of labral displacement.

• Presence of bony glenoid rim defects.

• Associated GHJ ligament deficiency.

• Glenoid version.

• Secondary arthrosis of the GHJ.

• Size, depth and position of the Hill–Sachs defect.

Until recently, a large or deep Hill–Sachs defect was referred to as an engaging lesion, which could lever on the anterior glenoid margin in abduction and external rotation and precipitate a recurrent dislocation. The amount of glenoid bone loss as part of a Bankart injury would also influence this risk. A new concept, termed ‘glenoid track’, has been developed. There are normal zones of contact between the glenoid and the humeral head during various shoulder movements shown to involve about 83% of the glenoid width. The relative size of the Hill–Sachs defect and amount of glenoid bone loss provide a means to predict the risk of recurrent dislocation and help determine surgical management. Configurations considered ‘off-track’ are likely to require additional correction of the osseous problems as opposed to simply addressing the labral injury alone ( Fig. 39.13 ).

Superior Labral Tears

Tears of the superior labrum and biceps anchor are commonly encountered injuries in overhead throwing athletes. Abnormal traction on the biceps anchor and superior labrum results in tears that usually extend posteriorly. They are often referred to as superior l abrum from a nterior to p osterior (SLAP) tears. MRI, MR arthrography or CT arthrography may assess the glenoid labrum.

Contrast medium or fluid SI extending into the substance of the labrum or through the chondro-labral junction is the primary sign of a SLAP tear ( Fig. 39.14 ). Tears may be localised to the posterosuperior labrum, or may be more extensive. There may be tear extension into the LHB tendon. There are many grades of SLAP tears described but the extent of the tear and the structures involved are the most important features.

The most important features that help determine management include:

• Extent of labral tear using clockface terminology.

• Involvement of biceps anchor and tendon.

• Presence of associated rotator cuff tears.

Tendons

Insertional tendinopathy around the elbow joint most commonly affects:

• common extensor origin: tennis elbow

• common flexor origin: golfer's elbow

• distal biceps tendon

The triceps and other tendons are rarely involved.

Tendinopathy of the common extensor and flexor tendons presents with localised pain over the distal humeral epicondyles. It is often a clinical diagnosis, although imaging may be performed in refractory cases to confirm the diagnosis and exclude a tear. US is frequently used to guide injection therapy.

The affected tendon is thickened and hyporeflective on US, with neovascularisation on Doppler imaging ( Fig. 39.18 ). High SI is demonstrated on fluid-sensitive MRI sequences ( Fig. 39.19 ). Tendon tears are demonstrated as focal areas of deficiency. In chronic cases, new bone formation may be seen on radiographs at the tendon enthesis. Calcific tendinopathy is much less common than in the rotator cuff of the shoulder.

The distal biceps tendon inserts on the tuberosity of the proximal radius. It does not have a tendon sheath, but surrounding connective tissue is known as a paratenon. It is surrounded near the insertion by the bicipitoradial bursa. Distal biceps tears are often clinically unrecognised, but may be amenable to surgery if diagnosed early. In the early stages the tendon is thickened and there may be an effusion in the bicipitoradial bursa ( Fig. 39.20 ). In complete rupture, the tendon retracts proximally. MRI and US may be used to confirm the diagnosis and locate the tendon end ( Figs 39.21 and 39.22 ).

Bone and Cartilage

The capitellum is the third most commonly affected site in osteochondritis dissecans (after the knee and ankle). It commonly affects teenagers and young adults. A focal osteochondral fragment or defect may be visualised on radiographs. Cross-sectional imaging with MRI, MR arthrography or CT arthrography is used to detect radiographically occult lesions and for grading osteochondral lesions (OCLs) ( Fig. 39.23 ). The osteochondral fragment may remain in situ or lie remotely within the elbow joint. Fluid SI at the base of the OCL on MRI, or contrast medium tracking around the fragment on arthrographic images, is a sign of an unstable lesion. Integrity of the overlying articular cartilage is a good sign of stability.

Reports should include:

• size and location of osteochondral defect;

• stability of the lesion and integrity of overlying cartilage; and

• presence of any remote intra-articular bodies.

Intra-articular bodies are also frequently encountered in OA of the elbow. They may be calcified, but non-calcified chondral bodies may also occur. CT is often utilised to assess the size and location of osteophytes before surgery, as well as identify small loose bodies. Chondral bodies are not visualised on radiographs or conventional CT. In some cases, pre- and post-arthrography CT may be performed ( Fig. 39.24 ). Conventional MRI is less sensitive for detection of small intra-articular bodies.

Ligaments

The collateral ligaments of the elbow may be torn as the result of an elbow dislocation and may require surgical repair. A coronoid process fracture is a sign of an unrecognised elbow dislocation. Chronic tears of the ulnar collateral ligament (UCL) are infrequently encountered in some throwing sports and in weightlifters.

In acute injuries, MRI shows the presence of soft-tissue oedema and haemorrhage around the affected ligament. MR arthrography may be preferred for diagnosis of chronic tears. Acute UCL tears often occur at the proximal origin on the medial humeral epicondyle ( Fig. 39.25 ). In chronic tears, the defect is usually at the insertion on the sublime tubercle of the ulna.