Upper Extremity

(1)

Orthopaedics, Trauma and Plastic Surgery, University Hospital Leipzig, Leipzig, Germany

2.1 History

2.1.1 Localization and Nature of Complaint

Pain	Localization	Circumscribed/radiating
	Character	Numb/sharp/drilling/throbbing/burning/cramp-like
	Situation	During certain movements, under load/at rest, at night
Swelling	Location/extent
Deformity	Location/kind	Altered posture, deformity
Movement disorder	Location/kind/direction	Limitation of movement/locking/stiffness, walking distance
Sensory disorder	Location	Paresthesia/numbness/tingling/pins and needles
Motor disorder	Location/degree (extent)	Muscular atrophy
	Location/degree (M5–M0*)	Weakness/paralysis/spasticity
		Shoulder/elbow/wrist/finger Flexion/extension/abduction/abduction

*Janda’s muscle strength test:

Level 5: Full movement, normal strength

Level 4: Movement possible against some resistance

Level 3: Movement possible against gravity

Level 2: Movement possible with aid, but not against gravity

Level 1: Only some muscle twitching

Level 0: No muscle twitching

2.1.2 Time Correlations

Beginning and course	Congenital/acquired (age/point in time)
	Acute/chronic
	Slowly/stably progressive
	Occurrence in flares with or without symptom-free intervals
	During the day/at night

2.1.3 Concomitant Circumstances

Accident	Yes/no
Location	Leisure/workplace
Mechanism of injury	Kind	Fall/working overhead/lifting a load/heavy lifting/accident
	Triggering event	No triggering event/fall/bending/rising from a squatting position Height/weight/load/persons involved
	Motor vehicle accident	Type of vehicles involved/direction/speed, angle of impact, lateral, head-on or rear-end collision, head impact/headrest/safety belts
Preexisting conditions	Family medical history
	Degenerative/bacteria/rheumatic inflammatory	No/if yes: local/systemic
	Bacterial infection/viral infection
	Traumatic/tumor
	Malformations
Common symptoms	Fever, weight loss (time period of weight loss), fatigue, nocturnal sweating	Yes/no

2.1.4 Existing Treatment/Past Treatment

Medication	Medication/dose/duration of intake	Localized/systemic
	Relief	Yes/no
Physical therapy	Application	Forms/duration/frequency
	Relief	Yes/no
Orthopedic aids	Walking stick/crutches Basques/bandage Brace/cast	Yes/no
Operations	Time/site/type/success

2.2 Shoulder

2.2.1 Systematic Examination

Local findings

Shoulder position/relief	Physiological/pathological (right/left)	Shoulder on equal level/elevated shoulder Protraction of the scapula Prominent acromioclavicular/sternoclavicular joint
Swelling/redness/hyperthermia	No; if present, then:	Localization/extent/scope
Hematoma/abrasion/open wound/scab	No; if present, then:	Localization/extent/scope
Scarring	No; if present then:	Localization/extent (soft/rough/displaced)
Muscles	Supraspinatus muscle/infraspinatus muscle/deltoid muscle/pectoral muscle	Highly developed/wasted/shortened Atrophy (significant?), muscle tone increase or decrease (right/left)
Mobility shoulder	Anteversion/retroversion Abduction/adduction External rotation/internal rotation (in neutral position, at 90° of abduction) Aprons and neck grip	−−/−−/−− degrees (passive/active, right/left)
Crepitation	No; if so:	Fine/coarse (left/right)
Shoulder pain	Motion pain (active/passive) Neer’s impingement test Tenderness, subacromially, at the greater tuberosity, at the bicipital groove, at the coracoid	None; if yes: positive (right/left)
Rotator cuff	Painful arc Jobe test Pain during motion against resistance (external rotation, internal rotation, abduction, adduction) Outside rotation lag sign Internal rotation lag sign Belly press	Pain yes/no (right/left)
Biceps tendon	Yergason test Palm-up test	Pain yes/no (right/left)
Glenohumeral guidance	Apprehension test Posterior apprehension test Sulcus sign	Positive yes/no (right/left)
Clavicle/acromioclavicular joint	Piano key phenomenon Finger pointing test Cross-body test (horizontal displaceability) AP displaceability	Pain yes/no (right/left)
Arm length	Lateral edge of the acromion–ulnar styloid process	–cm (right/left)
Amputation stump length	Lateral edge of the acromion—end of the amputated arm (stump)	–cm (right/left)

Neurology

Reflexes	Biceps tendon (C5) Triceps tendon (C7) Brachioradialis (C6)	Right/left Vigorous/decreased/absent/supernormal (hyperreflexic)
Sensory examination	Dermatome (segment assignable/not exactly assignable) (right/left)	Hypesthesia/paresthesia/dysesthesia
Motor function examination	Shoulder elevation (C3–C5) Shoulder abduction (C5/C6) Elbow flexion (C5/C6) Elbow extension (C7) Pronation (C6–Th1) Supination (C5/C6) Wrist extension (C6/7) Wrist flexion (C6–Th1) Wrist drop (N. radialis) Hand of benediction (N. medianus) Ulnar claw (N. ulnaris)	Right/left intact/impaired function (M0–M1–M2–M3–M4–M5)

Circulation

Arteries	A. axillaris A. radialis	Fully/barely/not palpable (right/left)
Veins	Venous stasis	Present/absent (right/left)
Capillary pulse	Fingertips	Visible/invisible

2.2.2 Leading Symptoms of the Shoulder

The leading symptoms of the shoulder are summarized in Table 2.1.

Table 2.1

Leading symptoms of the shoulder

History	Pain	Local findings, functional tests	Sensory function disorder	Motor function disorder	Points to
Mostly patients older than 40 years, acute or subacute disorder	After lifting a heavy load or a fall, sudden shoulder pain or spontaneous pain at night, increasingly during the day	Weakening of the rotation and abduction (up to pseudoparalysis), positive painful arc, local tenderness, painful movement against resistance	None	None	Rotator cuff tear
Mostly middle-aged women, chronic to subacute shoulder pain	Pain at the proximal humerus	Local tenderness to pressure at the proximal humerus, possibly limiting the mobility	None	None	Calcifying tendinitis
Lesion of the rotator cuff or the biceps tendon, calcifying tendinitis (often primarily unknown), dysfunction	Guarding posture	Restriction of abduction, external rotation, and grip into the neck. Localized tenderness	None	None	Secondary frozen shoulder
Women (40–60 years). Phase alternating between pain and restriction of movement	Relatively acute pain, especially at night. Pain subsides, whereas mobility decreases	(Steadily increasing) painful limitation of movement	None	None	Primary frozen shoulder (stages 1–2)
Recurrent shoulder dislocation after primary traumatic shoulder dislocation	Pain in dislocation may be less with more frequent dislocations	Positive anterior apprehension test. Positive sulcus sign. Perhaps positive posterior Gerber	None	None	Post-traumatic recurrent shoulder dislocation
Humeral fracture, pressure injury at the upper arm	Only in trauma	Weakened grip	In the hand: hypesthesia at the thenar eminence, palm, and palmar side of the radial 3 1/2 fingers	Hand of benediction	Injury to the median nerve in the upper arm
Humeral shaft fracture. Shoulder crutch. Sleeping on a park bench. Weakness in the arm and hand	Only if trauma	Free passive mobility, active dorsiflexion not possible in the wrist	Hypesthesia radial/posterior to 2 1/2 fingers	Drop wrist	Damage to the radial nerve in the upper arm
Usually first presentation in childhood with a prominent shoulder topography, hypoplastic craniofacial bones, and progenia	None	Shoulders can be folded across his chest downward	None	None	Dysostosis cleidocranialis

Fig. 2.1

(a, b) Shoulder symmetrical (a), elevated shoulder left (b)

Fig. 2.2

Ruptured biceps tendon (long tendon): by actively flexing the arm in the elbow against the examiner’s resistance, the muscle belly of the biceps muscle is distally displaced

Fig. 2.3

(a, b) Shoulder function can be tested by asking the patient to hold onto his/her neck or by acting as if they are binding an apron behind their back. These are combined movements. Holding onto the neck tests abduction and external rotation. If abduction is intact, the elbow is held above the head. If abduction is limited, the elbow is often only held below the head. Binding an apron tests retroversion and internal rotation

Fig. 2.4

To prevent the scapula from also moving, the shoulder is fixed when testing range of motion. For this, abduction/adduction, anteversion/retroversion, and internal/external rotation of the shoulder are performed. The movement can be performed either actively by the patient or passively by the examiner. When testing anteversion/retroversion in the shoulder (a, b), normal range of motion is 150–170/0/40°

Fig. 2.5

(a, b) Testing abduction/adduction in the shoulder joint (a, b) Range of motion: 90/0/40°. Some examiners include abduction beyond 90° with movement of the scapula and simultaneous external rotation of the arm (normal ROM for abduction up to 180°)

Fig. 2.6

(a, b) Testing external and internal rotation of the shoulder joint from the neutral position (a, b). Some examiners additionally examine rotation from a starting position of 90° abduction

Fig. 2.7

Testing the painful arc in the shoulder: to determine subacromial stenosis, especially in cases of a supraspinatus tendon rupture, as well as a rotator cuff tear, the arm is abducted. The test is positive when during active abduction or adduction; pain is elicited between 40° (a) and 120° (b). Pain should decrease beyond 120° abduction, because the major tubercle has then exited the acromial roof. If pain is reported beyond 120° abduction, and further abduction exacerbates the pain, it is a strong indication for damage to the acromioclavicular joint

Fig. 2.8

Neer’s impingement test: this test examines painful subacromial stenosis. The examiner fixes the scapula with one hand, while the other arm is used to elevate, adduct, and internally rotate the patient’s arm. This causes the major tubercle to come in contact with the acromion. If subacromial inflammation is present, the test is painful

Fig. 2.9

Jobe test: this test examines shoulder function and impingement of the supraspinatus tendon. The patient holds the arm in 90° abduction and 30° anteversion. The elbow is stretched. The arm is internally rotated and the thumb points to the floor. Now the patient is asked to further abduct the arm in the shoulder against the examiner’s resistance. If pain is elicited and muscle weakness is present when compared to the opposite side, the test is positive and indicates a lesion of the posterosuperior part of the supraspinatus tendon. If the test is painful in external rotation, this indicates a lesion to the anterior parts of the supraspinatus tendon

Fig. 2.10

Testing for tenderness at the shoulder joint: acromioclavicular joint (I), subacromial (II), coracoid process (III), major tubercle (IV), intertubercular sulcus (V)

Fig. 2.11

(a, b, c) Testing active movement against resistance: pain is possible under abduction (a), external rotation (b), and internal rotation (c). The supraspinatus muscle serves as the starter of the shoulder abduction from the neutral position. To test this, the patient is asked to abduct the arm from the neutral position, i.e., 0° abduction (a), against the examiner’s resistance. If this is not possible or weaker than the opposite side, it is an indication for a supraspinatus tendon lesion. From 40° abduction onward, the deltoid muscle assists in abduction. Pain during external rotation against resistance (b) indicates a lesion of the external rotators (infraspinatus and teres minor muscles). With the arm pressed to the trunk and the elbow flexed to 90°, the external rotation in the shoulder is performed against resistance. To prevent assistance of the deltoid muscle, external rotation can be tested in a 90° abducted and 30° horizontally flexed shoulder. Pain during internal rotation against resistance (c) indicates a lesion of the internal rotators (subscapularis muscle, pectoralis major muscle—these muscles do not form part of the rotator cuff). With the arm fixed to the trunk and the elbow flexed to 90°, internal rotation in the shoulder against the examiner’s resistance is tested. If pain is reported, this indicates a subscapularis lesion

Fig. 2.12

Yergason test: the patient flexes the elbow to 90° and pronates the lower arm. The patient attempts to supinate the arm and further flex the arm in the elbow against the examiner’s resistance. The test is positive if pain is felt in the intertubercular sulcus (the long head of the biceps tendon)

Fig. 2.13

Palm-up test: the arm is lifted against resistance in 90° elevation with supination of the stretched elbow. The test is positive if pain is felt at the intertubercular sulcus

Fig. 2.14

(a, b) External rotation lag sign: the examiner maximally rotates the patient’s shoulder in an external direction. The patient’s arm is fixed to the trunk and flexed at the elbow. The patient is asked to hold this position (a). If the patient cannot hold the position, the external rotation lag sign is positive and indicates an infraspinatus or teres minor lesion. Once the examiner releases the patient’s arm, the patient’s arm spontaneously swings back inward (b) (in this example, this is simulated)

Fig. 2.15

(a, b) Internal rotation lag sign: the patient’s hand is led behind his back and lifted to maximally internally rotate the shoulder. The patient is asked to hold this position (a). In cases of a subscapularis muscle lesion, releasing the patient’s hand leads to a spontaneous return to the starting position (external rotation) and the hand moves down against the back (b) (simulated here)

Fig. 2.16

Belly-press test (Napoleon sign): the patient presses the flexed lower arm against the abdomen and tries to hold the elbow at the same level (a). If the subscapularis tendon is ruptured, the elbow dorsally sinks down and the hand is flexed (b) (simulated here). Even if the test is inconspicuous, a subscapularis rupture is still possible

Fig. 2.17

Anterior apprehension test: following anterior shoulder dislocation, anterior shoulder instability can occur. The examiner abducts the arm to 90°, flexes the arm in the elbow, and rotates the arm externally. Simultaneously, the examiner presses onto the humerus head from behind. In cases of anterior instability, this causes muscular resistance. The patient reports pain and fear that the shoulder may dislocate

Fig. 2.18

Posterior apprehension test: posterior shoulder stability can be tested by applying pressure to the humerus in a dorsal direction with the shoulder in 90° anteversion. Reporting pain and a dislocation tendency indicate posterior shoulder instability. The posterior apprehension test is positive

Fig. 2.19

Sulcus sign: the examiner pulls the patients hanging arm down. If inferior instability exists, a dimple is visible under the lateral acromion (a, b)

Fig. 2.20

Horizontal adduction test (cross-body test): in shoulder pathologies (e.g., arthrosis), pain in the shoulder can be provoked by adduction of the arm that is held in 90° anteversion

Fig. 2.21

Finger spreading test: the patient is asked where the pain is located. If pain is present in the shoulder, the patient will report a specific site and point his finger to the shoulder (positive finger pointing test)

Fig. 2.22

(a, b) Piano key phenomenon: in clavicular instability, the clavicle can be pressed down like a piano key

Fig. 2.23

Testing the anterior–posterior mobility of the clavicle in the acromioclavicular joint

Fig. 2.24

Peripheral sensory innervation at the trunk and the upper extremity (anterior and posterior view). 1 N. cutaneus brachii lateralis (N.axillaris); 2 N. cutaneus brachii posterior (N. radialis); 3 N. cutaeus antebrachii posterior (N. radialis); 4 N. cutaneous brachii medialis; 5 N. cutaneus antebrachii lateralis (N. musculocutaneus); 6 N. cutaneus antebrachii medialis (Plexus brachialis); 7 Ramus superficialis n. radialis; 8 Ramus superficialis n. ulnaris; 9 R. palmaris n. mediani; 10 N. medianus; 11 N. ulnaris; 12 N. radialis

2.2.3 Disorders

Common clinical disorders

Habitual Dislocation of the Shoulder

Glenohumeral instability that is accompanied by recurring atraumatic dislocations of the shoulder. One distinguishes among anterior, inferior (most common), and posterior dislocation. The inferior dislocation is often accompanied by an anterior or posterior dislocation. Dislocation in one direction is known as unidirectional; dislocations in multiple directions are known as multidirectional. Dislocations are often preceded by subluxations. One also distinguishes between random and paralytic dislocations.

Etiology: atraumatic origin (no history of accident). Generalized capsule and ligament laxity. Congenital malformations of the humeral head, joint cup, and the ligaments. Paralytic dislocations occur in the context of shoulder muscle paralysis.
History: habitual dislocation of the shoulder is almost always mentioned when taking patient history. Often, the patient already has a history of subluxations since childhood. Often, subluxations are not noticed. Also, dislocations and subluxations in adolescence and early adulthood during sport are common. The dislocation can mostly be easily repositioned. Both shoulders can be affected. Recurrent dislocation is common. Random dislocations often present in childhood (then mostly posterior). Psychological aspects are often important to consider.
Examination: patients mostly present with non-dislocated shoulders Fig. 2.1. A lateral indentation in the shoulder and a guarding posture can be difficult to spot. Depending on the dislocation direction, the stability test can be positive (anterior shoulder apprehension test, Fig. 2.17; sulcus sign, Fig. 2.19; positive posterior apprehension test, Fig. 2.18). A palpable snapping of the tissue can occur. Often the joints show hypermobility.
Diagnostics: X-ray of the shoulder in two planes and special targeted imaging (looking specifically at the bones), CT (with angiography), MRI, ultrasound (muscles, ligaments, labrum).
DD: to be clearly differentiated from traumatic and post-traumatic recurrent shoulder dislocation.

Neuralgic Shoulder Amyotrophy

Acute, intense shoulder pain in the shoulder–arm region. Motor and sensory function loss manifests themselves as a consequence, especially in the upper arm plexus (C5/6).

Etiology: unknown.
History: sudden intense pain in the shoulder that radiates into the arm, mostly with a diffuse character. After a few days, the arm hangs flaccid and inwardly rotated. Paralysis is followed by muscular atrophy.
Examination: no movement limitation in the cervical spine! Shoulder abduction is completely paralytic (Fig. 2.5) as well as external rotation (Fig. 2.6). Scapula alata is common (Fig. 1.24). Sensory loss over the deltoid muscle and the radial under arm is rare (Fig. 1.11).
Diagnostics: X-ray of the cervical spine in two planes and semi-oblique (to rule out degenerative alterations, bone destruction); X-ray of the shoulder in two planes. Neurological consultation.
DD: radicular cervical compression syndrome; carpal tunnel syndrome, ulnar nerve compression, impingement syndrome, backpack paresis.

Scapula Alata (“Winged Scapula”)

Unilateral elevation of the scapula from the chest wall.

Etiology: long thoracic nerve injury and the resulting weakness of the anterior serrated muscles. Mostly idiopathic. Also possibly elicited by pressure injury (“backpack paresis”) or trauma. Rarely leads to complete paralysis. Perioperative positioning damage or during casting is also possible. Neuralgic shoulder amyotrophy, inflammation, and progressive muscular atrophy should also be considered.
History: “winging” of the scapula, often primarily a cosmetic concern (in neuralgic shoulder amyotrophy also a history of acute-onset shoulder pain).
Examination: when the hands are supported and pressed against the wall or when doing a push-up, the tendency of the scapula to flare out becomes visible immediately (Fig. 1.24).
Diagnostics: X-ray of the shoulder in two planes (rule out pathological changes to the bone).
DD: Sprengel deformity, exostosis, paresis of the accessory nerve (in this case, the scapula is lateralized and the shoulder is tilted), progressive muscular dystrophy (fascioscapular type), neuralgic shoulder amyotrophy (plexus neuritis).

Snapping Scapula Syndrome (Scapulocostal Syndrome)

Snapping sensation during movement of the scapula.

Etiology: incorrect posture, tense muscles, bursitis, costal hump in scoliosis, form alteration of the scapula (callus, exostosis), tumors.
History: snapping sensation behind the scapula. Can also be consciously elicited.
Examination: palpation of the scapula with the hand. When the scapula is moved, the “snapping” can be palpated, sometimes also heard. Tenderness to pressure and increased muscle tone over the medial scapular ridge.
Diagnostics: X-ray of the shoulder in two planes (to rule out pathological changes to the bone).
DD: all etiologically relevant disorders.

Subscapularis Tendinitis

Degenerative alteration of the of the subscapular muscle tendon, its gliding surface, and its insertion site.

Etiology: multifactorial. Nutritional problems, paradox arterial ischemia in athletes caused by heightened metabolism under stress (e.g., rigorous exercise program); degenerative.
History: mostly young patients. Pain elicited by sudden tension in stretched muscles (tennis, javelin). Also seen as load-induced pain in women between 40 and 60.
Examination: tenderness over the minor tuberculum. Positive painful arc, positive Jobe test, and positive Neer’s impingement test (Figs. 2.7, 2.8, and 2.9). Pain at inward rotation against resistance (Fig. 2.11).
Diagnostics: X-ray imaging of the shoulder in two planes (to rule out pathological bony alterations); ultrasound (rule out rotatory cuff rupture and biceps injury).
DD: primary and secondary impingement syndrome.

Primary Frozen Shoulder

Reversible stiffness of the shoulder joint occurring in three characteristic phases. Accompanied by a transient shrinking of the capsule, which subsides in the late stadia of the disorder. The duration of the stadia is between 4 and 6 months, the whole course of disease between 12 and 18 months. Less common than the secondary frozen shoulder.

Etiology: not fully known. A local immune reaction with a genetic predisposition is being discussed. Often patients present with a history of cervical syndrome, myocardial infarction, mastectomy, hemiplegia, Pancoast tumor, and medication (barbiturates).
History: commonly presents between 40 and 60 years of age, especially in women. Often affects the nondominant arm.
- Stage 1 (painful phase): increasing pain, especially at night and when working with the arms over the head. Lying on the affected shoulder is not possible. Almost unnoticed, mild functional disorder.
- Stage 2 (stiffening phase): subsiding pain (only present during sudden movement). Increasing stiffness of the shoulder. Clear functional impairment in everyday use and in work.
- Stage 3 (thawing phase): further subsiding of pain. Without special treatment, movement function is slowly restored.
Examination:
- Stage 1 (painful phase): movement is initially not impaired and pain is only felt in some movements.
- Stage 2 (stiffening phase): clear muscular atrophy. Abduction is only possible with outer rotation of the scapula. Pain at the end of a movement during passive testing of impaired mobility.
- Stage 3 (thawing phase): mobility returns to an almost physiological condition (Figs. 2.4, 2.5, and 2.6).
Diagnostics: X-ray of the shoulder in two planes (to rule out pathological changes to bone, tendinitis calcarea), ultrasound (to rule out subacromial bursitis); arthrography (to prove capsule shrinkage).
DD: secondary frozen shoulder, trauma, and upper arm plexus paresis.

Secondary Frozen Shoulder

Painful movement impairment of the shoulder due to an external cause or a different disorder of the shoulder. In contrast to primary frozen shoulder, the shrinkage of the capsule plays a minimal role. Much more common than primary frozen shoulder.

Etiology: primary and secondary impingement syndrome (rotator cuff lesion, calcific tendinitis of the shoulder, biceps lesions). Degenerative and inflammatory disease of the shoulder as well as cervically or abdominally radiating pain, fractures, and dislocation.
History: pain-relieving posture of the arm, leading to a limitation of external rotation (Fig. 2.6) and abduction (Fig. 2.5). During these movements (e.g., when combing one’s hair), the shoulder is typically elevated. Pain and movement impairment do not occur in the form of phases.
Examination: depending on the primary location of injury, local tenderness can present, e.g., subacromially, at the major or minor tubercle or over the sulcus intertubercularis. Movement, especially abduction (Fig. 2.5) and outer rotation (Fig. 2.6), is impaired (Fig. 2.3).
Diagnostics: X-ray of the shoulder in two planes (to rule out pathological changes to the bone), ultrasound, and eventually CT and MRI scans to show pathological changes in the rotatory cuff, biceps tendon, and the subacromial bursa.
DD: all etiologically relevant disorders. Primary frozen shoulder.

Pseudoarthrosis of the Clavicle (Acquired)

Nonunion of the bones involved in the clavicular joints.

Etiology: insufficient reposition or fixation during conservative treatment of a clavicular fracture (rare) or insufficient operative stabilization (e.g., with K-wires—common).
History: pseudoarthrosis should be considered if pain exists after more than 8 weeks following a clavicle fracture. Pain is elicited by load and at rest. Weakness and paresthesia are present. Blood perfusion problems are possible.
Examination: alterations to the surface are possible, localized tenderness, differing levels or protrusions are palpable. Abnormal mobility is possible with eventually a positive Adson test (Fig. 1.13). Piano key phenomenon possible (Fig. 2.22).
Diagnostics: X-ray of the clavicle a.p. (to prove pseudoarthrosis).
DD: costoclavicular syndrome.

Sternoclavicular Hyperostosis

Stiffening of the sternoclavicular joint due to ossification of the sternoclavicular ligaments and bone formation between the sternum, the clavicle, and the first rib.

Etiology: unknown.
History: mostly bilateral in patients between the ages of 30 and 50 years. Pain in the acromioclavicular joint.
Examination: local swelling and protrusion of the medial clavicular margin. Later local tenderness at the acromioclavicular joint.
Diagnostics: X-ray of the clavicle a. p. (to visualize the bony configuration of the clavicle).
DD: Tietze syndrome, sternoclavicular arthritis, sternoclavicular subluxation.

Impingement Syndrome (Supraspinatus Tendonitis)

Painful function impairment of the shoulder caused by contact in the subacromial soft tissue at the anterior ridge of the shoulder and/or the acromion, especially when spreading the arms. The lesions caused by this impingement can involve the rotator cuff, the subacromial bursa, and the long biceps tendon.

Primary impingement (outlet impingement): mechanical constriction around the joint surface of the supraspinatus tendon between the acromioclavicular joint, the anterior acromion, the coracoacromial tendon, and the coracoid process (so-called supraspinatus outlet).

Secondary impingement (non–outlet impingement): functional contraction of the subacromial space. Subacromial conflict situation caused by volume increase of the subacromial soft tissue and a high–riding shoulder (superior displacement of the humerus).

Etiology:
- Primary impingement: congenital form alteration of the anterior third of the acromion, caudal osteophytes at the acromioclavicular joint, and post-traumatic positional changes to the coracoid process.
- Secondary impingement: chronic subacromial bursitis, tendinitis calcarea, rotator cuff tear or the long biceps tendon, glenohumeral instability (habitual and traumatic shoulder dislocation), frozen shoulder, pseudoarthrosis of the major tubercle, and prostheses that are too deeply implanted.
History:
- Primary impingement:
  
  Stage I (edema and hemorrhage): pain during overhead work, mostly affects active patients under 25 years of age. Symptoms are reversible.
  
  Stage II (fibrosis and tendonitis): pain after strain to the joint, typically at the outer part of the proximal upper arm. Typically occurs from age 25–40. Symptoms are mostly reversible.
  
  Stage III (rotator cuff tear): movement-dependent chronic shoulder pain, nocturnal pain at rest, and pseudoparalysis. Symptoms are not reversible. The stages are not always easy to differentiate. It is important to rule out other causes of shoulder pain.
- Secondary impingement: shoulder pain, functional disorders, age, and course are determined by the cause of the pain.
Examination:
- Primary impingement: tenderness to pressure at the major tubercle and the minor tubercle, the intertubercular sulcus, the subacromial, and the coracoid process (Fig. 2.10). Active elevation is more painful than passive elevation. Positive Neer’s impingement test (Fig. 2.8). Crepitation. Positive painful arc (Fig. 2.7). Abduction against resistance painful (supraspinatus muscle) (Fig. 2.11). Positive Jobe test (Fig. 2.9). Also possible, painful external rotation against resistance (infraspinatus muscle) (Fig. 2.11). Alleviation is experienced in the subacromial local anesthesia test. Weakness in abduction and rotation against resistance if the rotatory cuff is torn. Active and passive movement limitations are possible.
- Secondary impingement: dependent on the differential diagnoses (chronic subacromial bursitis, tendinitis calcarea, rotator cuff tear, biceps tendon rupture, glenohumeral instability (habitual and traumatic shoulder dislocation), and frozen shoulder).

It is important to distinguish between primary and secondary impingement as this influences therapy. Primary impingement calls for conservative or surgical treatment, in some cases, requiring reconstruction of the rotator cuff. In secondary impingement, the cause for the impingement needs to be removed; otherwise, symptoms grow worse.

Diagnostics: X-ray of the shoulder in two planes (to visualize the bones and rule out other causes).

Bursitis Subacromialis

No independent disorder. Accompanies the chronic or acute stage of tendinitis calcarea as well as chronic polyarthritis and other disorders of the shoulder.

Tendinitis Calcarea (Calcifying Tendinitis)

Non-degenerative disorder with focal calcific deposits in the tendons of the rotator cuff. This is initially accompanied by decreased perfusion and cell–induced “chalky” calcific deposits in the inner tendon. The calcification can gradually increase. The calcification mostly resolves within some days under acute pain (acute stage).

Etiology: unknown, but certainly not degenerative.
History: Mostly affects middle-aged women. In the latent stage mostly clinically inconspicuous. In the chronic stage, chronic to acute pain.
- Acute stage: strong pain at day and at night, painful reduction in range of motion continuing for some days.
- Repair stage: decreasing pain; relapses are possible.
Examination: In the chronic stage, localized pain to pressure over the calcific deposit at the proximal upper arm. Reduction in range of motion is possible (Figs. 2.3, 2.4, 2.5, and 2.6). Positive Jobe test (Fig. 2.9). Positive Neer’s impingement test (Fig. 2.8).
- Acute stage: Shoulder often slightly swollen and warm, tenderness to pressure! Active and passive movement painfully limited.
- Repair stage: Receding tenderness, return to normal range of motion.
Diagnostics: X-ray of the shoulder in two planes, ultrasound (to visualize the calcific deposit; to rule out other causes).
DD: secondary impingement. In the acute stage: purulent omarthritis, arthritis urica of the shoulder, and pseudogout.

Congenital malformation and metabolic disorders

Sprengel Deformity (Congenital High Scapula)

Congenital high sitting scapula accompanied by a craniomedial displacement and external rotation of the scapula. Often combined with a decrease in size and a coarsening of the scapula.

Etiology: congenital, most likely a genetic etiology. Eventually also an exogenous etiology (embryopathy).
History: mostly only affects one side. More common in women than men. Mostly manifests in combination with other deformities (scoliosis, anomalies of the ribs, Klippel–Feil syndrome, spina bifida). Shortening of the levator scapulae muscle. High-standing shoulder blade.
Examination: the high-standing scapula is conspicuous when inspecting the patient from the back. If accompanied by Klippel–Feil syndrome, this impression is further emphasized by the webbed neck (pterygium colli). Range of motion is often not affected in the shoulder joint but limited at the scapulothoracic joint.
Diagnostics: X-ray of the scapula anterior–posterior and the cervical spine in two planes (to show high-standing scapula and rule out associated disorders of the cervical spine).

Cleidocranial Dysostosis

Rare. Systemic disorder involving delayed ossification leading to hypoplasia and aplasia especially of the skull and the clavicle.

Etiology: congenital, autosomal dominant.
History: the dominating clinical picture is the one-sided (mostly right-sided) or bilateral, partial, or total aplasia of the clavicles. A combined defect with shortening of the base of the skull, a hypoplasia of the facial skull, hypoplasia of the maxilla leading to prognathism, as well as aplasia of the symphysis and coxa vara is also possible.
Examination: in total aplasia, the shoulders can touch each other at the chest. In partial aplasia, a hypermobility of the shoulders exists.
Diagnostics: none.
DD: pycnodysostosis (or in combination with osteopetrosis, the so-called marble bone disease)

Gouty Arthritis of the Shoulder

Very rare in the shoulder! Inflammatory alterations of the shoulder joint, characterized by deposits of uric acid crystals in the shoulder joint and in the periarticular soft tissue. Manifests as acute arthritis or chronic arthropathy. The acute gout attack of the shoulder is known as omagra.

Etiology:
- Primary: purine metabolism disorder caused by a genetic defect, involving reduced renal excretion of uric acid or increased synthesis. Mostly induced by overeating.
- Secondary gout is seen in hematological disorders involving cell destruction or disorders involving renal function impairment.
History: presents in flares. Gout is similar to infectious arthritis during an attack, presenting with redness, swelling, loss of function, and severe pain. Mostly lasts days to weeks. After an acute attack, the symptom-free intervals tend to become shorter (in case of no treatment).
Examination: during a flare-up, massive swelling, redness, hyperthermia, protective stance, tenderness, and pain upon movement.
Diagnostics: X-ray of the shoulder in two planes (to rule out bony destruction, tendinitis calcarea). Blood tests: leukocytosis, slightly elevated erythrocyte sedimentation rate (ESR), elevated uric acid levels in plasma (hyperuricemia).
DD: omarthritis (acute rheumatic, unspecific, and specifically infectious), pseudogout, tendinitis calcarea (acute stage).

Pseudogout (Chondrocalcinosis)

Arthritis of the shoulder joint, caused by microcrystal deposits (calcium pyrophosphate crystals). The history and symptoms resemble gout. Chronic cases result in arthropathy.

Etiology: unknown. Metabolic disorder involving deposits of calcium pyrophosphate crystals in the synovial fluid and the joint capsule.
History: mostly older patients. Similar to gout, yet with a milder course of disease.
Examination: swelling, redness, hyperthermia, tenderness to pressure or movement.

Due to mild course of disease, pseudogout is often misdiagnosed as an arthritic irritation during active arthrosis.

Diagnostics: X-ray of the shoulder in two planes (analyzing the bones and ruling out pathological changes.) Arthrocentesis (polarized light microscopy).
DD: gout, rheumatoid arthritis, active arthrosis, infectious arthritis, specific omarthritis.

Degenerative disorders

Biceps Tendon Lesions

This includes all degenerative changes and rare traumatic changes to the biceps tendon and its supporting structures. One distinguishes among tendinopathy, tearing, and instability of the biceps tendon.

Tendinopathy of the biceps tendon

Degenerative changes to the biceps tendon. Rarely an isolated disorder, mostly occurs in combination with damage to the supraspinatus tendon and fibrosis of the subacromial bursa in the context of impingement syndrome (stage II).

Etiology: degenerative. Strong subacromial friction as a consequence of primary or secondary impingement and tearing of the rotatory cuff promote the development of degenerative changes to the tendon in the bicipital groove.
History: long overhead activity, Swimming, tennis, and golf. Pain in the anterior shoulder area.
Examination: localized tenderness to pressure in the bicipital groove (Fig. 2.10). Pain alleviation by means of an intertubercular local anesthesia test. Positive Yergason test (Fig. 2.12). Positive palm-up test (Fig. 2.13).
Diagnostics: X-ray of the shoulder in two planes (to rule out changes to the bone) and ultrasound (examining the rotator cuff, the biceps tendon, the subacromial bursa).

Biceps tendon rupture

Degenerative or traumatic rupture of the long head of the biceps tendon. Often occurs in combination with rotator cuff tear and impingement syndrome (stage III). The long head of the biceps tendon forms a functional unit with the rotator cuff. A loss of function of the long head causes an elevation of the humeral head.

Etiology: degenerative. Rarely traumatic.
History: Very rarely seen following trauma in young patients (traumatic rupture). Mostly seen in older patients following minor trauma or sudden strong contraction (degenerative rupture). Sharp pain in the proximal upper arm. Often preceded by shoulder pain, in some cases slowly increasing pain (creeping rupture). A distal displacement of the muscle is seen, combined with muscle weakness (often less pronounced in older patients).
Examination: localized hematoma (not always present), localized tenderness. During elbow flexion against resistance, the distal displacement of the muscle becomes visible (in contralateral comparison) (Fig. 2.2). In young patients, there is a clear reduction in strength during flexion; in older patients, this is often less pronounced.

Always look for associated injury to the rotatory cuff!

Diagnostics: X-ray of the shoulder in two planes (to rule out degenerative or destructive changes). Ultrasound (examining the rotatory cuff, the biceps tendon, the subacromial bursa).
DD: instability of the long head of the biceps tendon.

Instability of the long head of the biceps tendon

This disorder involves subluxation and dislocation.

Etiology: degenerative. Occurs in the context of rotatory cuff tearing that damages the coracohumeral ligament; also promoted by a preexisting flat bicipital groove.
History: pain in the anterior shoulder area. Snapping of the tendon. Overlap with symptoms of rotatory cuff tear is common.
Examination: localized tenderness in the bicipital groove (Fig. 2.10), positive Yergason test (Fig. 2.12), palpable tendon at abduction and outer rotation. Positive tests during rotator cuff rupture.

Often a large defect in the anterior rotator cuff is also present.

Diagnostics: X-ray of the shoulder in two planes (to rule out degenerative or destructive changes), ultrasound (examining the rotator cuff, the biceps tendon, the subacromial bursa).
DD: biceps tendon rupture.

Rotator Cuff Tear

Partial or complete tear of the tendons of the rotator muscles. Often occurs in combination with lesions of the long head of the biceps tendon.

Etiology: mostly degenerative changes, often creeping without any history of trauma. If there are preexisting degenerative changes, trauma can be the causal factor. Purely traumatic lesions are rare. They only occur in cases of severe trauma such as falling onto extended arms. In very rare cases of shoulder dislocation, an accompanying traumatic rupture occurs between the tendons of the supraspinatus muscle and the subscapularis muscle.
History: degenerative tears commonly occur after the age of 40. They can be induced by falling or sudden lifting of a heavy object (50 %). Initially a sudden severe pain is felt, followed by a loss of active mobility; a subcutaneous hematoma can also be seen after some days. Often no causal factor can be determined: in these cases, creeping pain, initially especially nocturnal pain, then also during the day is felt. If trauma (mostly in patients under 40) and interval tearing (older patients) are involved, acute shoulder pain is mostly present as well as a loss of function of the shoulder. In case of larger rupturing, a complete loss of function in the shoulder can occur.
Examination: fresh ruptures may present with hematoma, subacromial tenderness, and tenderness at the major tubercle and the coracoid process (Fig. 2.10). Palpable snapping and subacromial crepitation are possible, as well as a positive painful arc (Fig. 2.7) and positive drop arm test (the examiner performs a passive abduction of the patient’s arms and asks the patient to slowly adduct both arms; the test is positive when the arm cannot be slowly adducted but falls down). The passive mobility is normal; the active mobility is limited (Figs. 2.3, 2.4, 2.5, 2.6, and 2.7). Testing mobility against resistance induces pain and weak abduction (supraspinatus muscle) and/or abduction weakness (supraspinatus muscle), internal rotator weakness (subscapular muscle), and external rotator weakness (infraspinatus muscle, teres minor muscle) (Fig. 2.11). Furthermore, a positive internal rotation lag sign, external rotation lag sign, or Belly-press test (Fig. 2.16) may be seen (Figs. 2.14, 2.15, and 2.16). In cases with severe rupturing, the arm cannot be actively raised anymore (pseudoparalysis).
In older findings, secondary impairment of passive mobility (secondary frozen shoulder) and atrophy of the supraspinatus and infraspinatus muscles may be found.
Diagnostics: X-ray of the shoulder in two planes (to rule out bony alterations, shoulder elevation), ultrasound, (athropneumo) CT, and MRI (to visualize rotator cuff tear).

Acromioclavicular Arthrosis

Degenerative disorder of the acromioclavicular joint. Also seen in combination with rotator cuff tear.

Etiology: in old age, the primary form dominates. In younger patients, arthrosis is mostly post-traumatic, especially following fracture of the lateral clavicle with subsequent remaining instability. Also seen following infections.
History: pain at the shoulder (not in the upper arm!) reaching up to the neck. The pain arises following excessive loading and is exacerbated by overhead work or sports. Can also be clinically symptom-free.
Examination: localized tenderness to pressure at the acromioclavicular joint. Positive horizontal adduction test (Fig. 2.20). Positive finger pointing test (Fig. 2.21). Pain in the acromioclavicular joint is exacerbated by abduction beyond 120° (positive painful arc) as well as by adduction from a 90° anteversion position.
Diagnostics: X-ray of the shoulder in two planes (to visualize the degenerative changes at the acromioclavicular joint).
DD: rheumatoid arthritis, infectious arthritis.

Omarthrosis

In primary omarthrosis, beyond the typical morphological changes to the cartilage and bone, an enlargement of the humerus head sets in and in some cases an erosion of the posterior margin of the glenoid cavity leading to dorsal subluxation of the humeral head. Moreover, an enlargement of the posterior ligaments is seen. Secondary omarthrosis develops on the basis of preceding injury.

Etiology: primary (cause unknown). Secondary after repositioned dorsal dislocation, preoperated instability, and in deformity or dislocation fractures that have not healed (more common). Also common in chronic polyarthritis, chondromatosis, and villonodular synovitis of the shoulder joint.
History: pain under load with alleviation at rest. Weakness and impaired mobility. Primary omarthrosis mostly presents after 60, mostly bilateral (otherwise mostly on the right side) and commonly in women. Can also lead to impingement in cases of chondromatosis.
Examination: atrophy of the shoulder muscles (supraspinatus, infraspinatus, deltoid), localized tenderness to pressure, pain during movement, grating sound, and crepitation. Active and passive mobility limited (especially external rotation and internal rotation (Figs. 2.4, 2.5, and 2.6)).
Diagnostics: X-ray of the shoulder in two planes (proof of omarthrosis, ruling out humeral head arthrosis and chondromatosis). Ultrasound.
DD: especially in the early stages, all etiologically relevant disorders, humeral head necrosis.

Rotator Cuff Arthropathy

Special form of omarthrosis. Late condition of a severe rotator cuff defect in combination with glenohumeral instability. Involves loss of cartilage, destruction of the subchondral plate, and arrosion at the acromion and at the acromioclavicular joint as well as at the coracoid process. Osteoporosis develops due to the severe immobility. The long head of the biceps tendon is mostly ruptured.

Etiology: nutritious and mechanical factors.
History: recurring subluxation. Increasing pain at rest and under load. Decreased muscle strength and mobility.
Examination: atrophy of the shoulder muscles (supraspinatus, infraspinatus, deltoid muscles), localized tenderness to pressure, pain during movement, crepitation, grating noise. Reduced range of motion during passive movement. The arm cannot be actively lifted (pseudoparalysis).
Diagnostics: X-ray of the shoulder in two planes (to visualize the damage at the joint), ultrasound (to visualize the rotator cuff rupture, to visualize the biceps tendon).
DD: primary or secondary omarthrosis, osteonecrosis of the humeral head.

Osteonecrosis of the Humeral Head

Cellular death of bone tissue due to recurring or longer interruption of blood supply to the tissue. Often inconspicuous in the early stages, osteoporosis can develop in later stages. Can lead to fracturing and to complete destruction of the humeral head and a disturbed joint congruency.

Etiology: traumatic (after fracturing and dislocation), alcohol abuse, steroids, infection, tumors, neuropathic (diabetes, syphilis, syringomyelia). Also aseptic bone necrosis in children.
History: pain during loading, in later stages, pain at rest. In neuropathic cases, pain is absent. Mobility decreased.
Examination: localized tenderness to pressure, pain during movement, impaired mobility.
Diagnostics: X-ray of the shoulder in two planes (examining the damage, to rule out omarthrosis), ultrasound (examining the rotator cuff and the biceps tendon), scintigraphy (showing a pathological metabolism in the humeral head).
DD: primary and secondary omarthrosis.

Inflammatory disorders

Nonspecific Inflammation

Purulent omarthritis (infectious arthritis)

Joint infection of the shoulder caused by microorganisms. The pathogen can be isolated from material in the joint. Mostly presents as monoarthritis. Also called septic arthritis.

Etiology:

Primary arthritis: infection via an open wound during surgery or during intra-articular injection. Secondary arthritis: hematogenous infection. In adults, mostly caused by staphylococcal, streptococcal, or Neisseria infection. In children, mostly caused by Haemophilus influenzae. Fungal infections are also possible. Patients more prone to infection include patients with a history of diabetes, alcohol abuse, tumors, HIV infection, and immunosuppressive therapy.
History: severe swelling of the shoulder and a severe functional impairment. Severe pain and fever.
Examination: swelling, redness, hyperthermia. Guarding. Tenderness to touch and pressure. In rheumatoid arthritis and immunosuppressive therapy, the physical findings can be less pronounced.
Diagnostics: X-ray of the shoulder in two planes (to rule out bone destruction), ultrasound (effusion), scintigraphy, blood tests (blood sedimentation rate, leukocytes, CRP elevated), and puncture.
DD: rheumatic omarthritis, active omarthrosis, gout, pseudogout, specific omarthritis.

Nonspecific sternoclavicular arthritis

Nonspecific chronic inflammation of the sternoclavicular joint without being able to isolate a pathogen.

Etiology: unknown. Especially common in women of middle age and postmenopausal (postmenopausal arthritis).
History: pain-free swelling of the sternoclavicular joint.
Examination: local swelling of the sternoclavicular joint. No redness, no hyperthermia, no tenderness to pressure.
Diagnostics: X-ray of the clavicle a.p. (to rule out any bony alterations). Ultrasound (soft tissue swelling), scintigraphy (increased accumulation of a tracer), blood tests (erythrocyte sedimentation rate, leukocytes, CRP slightly elevated), and arthropuncture can also be performed.
DD: Tietze syndrome, septic arthritis, arthritis in psoriasis, sternoclavicular hyperostosis, sternoclavicular subluxation.