4.1 The clinical evaluation of the shoulder

Diagnosis depends upon three lines of enquiry, all of which should concur for the case to be proven. The first line of enquiry is the history. Using questions and answers we develop a short list of two or three possible pathologies. This is then subject to rigorous analysis against known facts. Occasionally the inquisition will trigger a red flag (the crescendo pain of calcific tendinitis), or it leads into an area where mistakes in diagnosis can lead to tragic events (the missed secondary tumour in the humeral metaphysis). However, we must remember that patients are human, they forget, dissemble, and sometimes lie. So ask the same question in two different ways (for instance, ‘have you had any illnesses?’ followed by ‘what tablets are you on?’) and if the answers don’t match you discard them or dig deeper.

The second line of enquiry is to examine the shoulder in a logical stepwise manner. But remember:

Fortunately pathology from the shoulder tends to fall into one of four areas: the stiff shoulder, the wobbly shoulder, pain on reach (the painful arc), and the remnants. Examination will at least get you into one of these four areas, and the first three have a specific forensic investigation that will prove the case.

So we come to the third line of investigation, and the most powerful, the forensics. In our case, radiology, ultrasound, magnetic resonance imaging (MRI), and arthroscopy. Rarely blood tests will be required. Stiff shoulders merit a radiograph; wobbly shoulders merit examination under anaesthetic and arthroscopy; and pain on reach merits an ultrasound. Forensics trumps the history and the examination.

Our problem is that we do not have unlimited time in outpatients. For this reason the hip surgeon goes to the forensics first, the radiograph of the hip, and then asks the patient about their symptoms. The shoulder surgeon has been hampered by the lack of forensics, but portable ultrasound can be performed rapidly in the clinic, and can give a firm diagnosis on those with pain on reach, and radiographs will sort out the stiff shoulders. Finally shoulder arthroscopy has come of age so that most shoulder conditions cannot only be identified but can also be treated arthroscopically.

Age is key to shoulder pathology. A useful aphorism is that ‘all patients below the age of 40 have instability until proven otherwise’, for instability is a condition of teens to thirties. Rotator cuff disease is a degenerative disease that starts to give pain on reach in the forties, tears of the cuff in the late fifties to sixties, and cuff arthropathy in the eighties (thus the aphorism ‘Grey hair equals cuff tear). The Japanese call contracture (frozen shoulder) ‘50-year-old shoulder’ for a reason, and if the letter states that the patient is 70 and has had a hip replacement then it is more likely that they have arthritis in the shoulder rather than a contracted (frozen) shoulder.

Dr Watson was a poor doctor for Holmes had to admonish him: ‘Observe my dear Watson, don’t just look!’ Facts can be deduced as the patient enters the room, before a word is said or a hand shaken. Do they look biologically the same age as their chronology, younger or older? How are they dressed, for patients with stiffness or loss of reach can’t pull sweaters over their heads, so will have clothes that button or zip up? How are they holding the shoulder? How protective are they? Is their neck held stiffly or moving normally? Remember the aphorism ‘Grey hair equals cuff tear’. With increasing experience you may note subtle signs such as the oven burns from syringomyelia, the bossed clavicles of glenoid dysplasia, or the absent facial expression of the patient with fascioscapulohumeral dystrophy.

Introduce yourself whilst cautiously shaking their hand, and at the same time note whether they have the shoulder shrug of the patient with a massive cuff tear, the stiff shoulder of arthritis, Dupuytren’s palmar contracture so often associated with contracted (frozen) shoulder, the engulfing hand of acromegaly, the rheumatoid hand of the rheumatoid shoulder, a weak grip, a strong grip, a tentative protective grip, a stiff shoulder, or a mobile shoulder.

The problem with shoulders is that a history of true shoulder pain (pain felt over deltoid insertion), that has come on insidiously, is made worse by shoulder movement, that radiates down the radial border of the forearm, and that awakens the patient at night could come from virtually any patient with any disorder of the shoulder. Such a history would fit with a rotator cuff problem, a contracture (frozen shoulder), a calcific deposit, arthritis, or even instability. Even worse, since the majority of these problems are soft tissue problems, they won’t show up on a radiograph. Quel horreur, what can we do? The answer is that the shoulder surgeon relies more upon the objective physical signs and provocative tests of the examination, and these guide him to the correct investigation. The history should not be dismissed, but it can be performed rapidly. As Cyriax said ‘with the shoulder the history matters little; it is the examination that counts’.

The first purpose of the interview is to ascertain whether the pain is from the shoulder or referred from another source. True shoulder pain originates from the shoulder and radiates to the muscles of the arm, around the insertion of deltoid. Indeed many patients will say, ‘It’s not my shoulder doctor, it’s my arm’, and will vigorously rub the deltoid insertion when asked to show where the pain is. When severe, the pain will radiate down the radial border of the forearm to the wrist, occasionally to the thenar eminence. The pain may radiate into the supraspinatus fossa, beneath trapezius, but pain more central to this, or along the medial border of the scapula is far more likely to be referred from the neck. Shoulder pain is made worse by shoulder movement.

Alarm bells should ring in patients whose pain radiates into the hand, for this is the pattern of referred pain from the C6 and C7 nerve roots. Similarly, beware of the patient whose pain radiates to the ulnar side of the forearm, the axilla or the chest, for this is the radiation from the thoracic outlet, the lower trunks of the brachial plexus (C8, T1), or the C8 and T1 roots. In patients with such radiation, always suspect a neurological cause for their pain and perform a careful neurological examination.

Referred pain from the viscera (gall bladder to right shoulder and myocardium to left shoulder) is mentioned in every textbook, but search as I may I have yet to see such a case in a shoulder clinic, despite being responsible for the secondary care of 400 000 patients and the tertiary care of 3 million people for the last two decades.

Pain coming from the acromioclavicular joint and the sternoclavicular joints are better localized than glenohumeral joint pain. Patients will point to the acromioclavicular joint when that is the cause. Pain from the sternoclavicular joint is well localized and radiates out along the subcutaneous border of the clavicle.

Enquiries should be made into the generic qualities of the pain: the onset event, duration, severity, radiation, exacerbating features, and what treatments have been attempted so far and to what effect? But lots of pathologies share the same features of pain in the shoulder, so it is only really worth seeking those factors that are specific to certain pathologies. The nature of pain is rarely discriminatory in the shoulder.

The majority of patients will present with pain and can then be placed into one of three categories: stiff shoulders (arthritis and contracted (frozen) shoulder), wobbly shoulders (instability), and loss of reach (pinching, partial and full thickness tears of the rotator cuff), so we need two additional lines of questioning about stiffness and instability.

Stiffness limits function. Yet it is extraordinary how patients can adapt to stiffness in one shoulder. Neer showed how most activities can be performed as long as you have 150 degrees of flexion, 40 degrees of external rotation, and internal rotation to L2. The Stanmore functional triangle has been described as the ability to reach the mouth, the opposite axilla, and wipe the bottom. Less movement than this severely compromises the ability to maintain independent living. There are five main causes of stiffness.

You, of course, will take the axillary radiograph and make the diagnosis.

As you can see all you need to make the accurate diagnosis in stiffness is a radiograph, in two planes, and to interpret it correctly.

At last we come to an area where the history is discriminatory. If the patient says their shoulder came out, it came out. This history can be pursued vigorously. Describe the first dislocation, how and when? Was this traumatic or atraumatic? Was it transient or locked out? Did it go back spontaneously, with a little help from bystanders, at hospital, under sedation, or under general anaesthetic? Was it secure afterwards, were they protective, did it redislocate, how, when, how many times, how was it then put back in?

Strangely, patients have little concept of the direction of dislocation, to be honest it is so painful they don’t care, but if radiographs were taken with it dislocated this is helpful, as is the presence of a Hill–Sachs or reversed Hill–Sachs lesion at the time of the consultation.

Of course there is a group of patients with symptomatic subluxation, and atraumatic transient dislocation, for whom diagnosis can be difficult. Always suspect this as a cause of shoulder pain in anyone less than 40 years of age.

Some patients will helpfully show you they can dislocate the shoulder. Beware; this is a red flag situation. They may just have marked joint laxity with posterior positional dislocation, in which case they gently sublux on raising the internally rotated adducted shoulder and then get a clunk of relocation as the shoulder is abducted. But if they dislocate with the elbow at the side and a huge grin on the face, beware—this is a Polar III, muscle-induced dislocation that will be resistant to any surgical adventure. The history and examination for muscle patterning and Polar III instability is complex and will be described in detail in Chapter 4.7.

Finally, one of the joys of being a shoulder specialist is that patients will turn up outside the three boxes of stiff shoulders, wobbly shoulders, and loss of reach. These are the remnants, but no less important for being so. These cases are the neurological conditions: the winging scapulae, thoracic outlet syndromes, neuralgic amyotrophy, and a variety of nerve palsies. Then the curios: the Sprengel’s shoulder, obstetric plexus palsies, glenoid dysplasias, muscular dystrophies, as well as disorders of the acromioclavicular and sternoclavicular joints. Finally come the nasties, for tumours do occur around the shoulder, primary tumours being rare, but the proximal humerus is a common site for secondary tumours. Thus the patient may present with weakness, loss of function, swelling, wasting, noises, and winging.

Weakness can only come from three things: rupture of a tendon (common), muscle weakness (myopathy, extremely rare), or failure of motor enervation (nerve palsy, rare).

Weakness from a rotator cuff tear is common. The patient complains of inability to reach and will often say that they have to assist the arm, by holding the forearm with the opposite unaffected hand. Commonly the patient will have to assist to brush the hair, to wash, to brush the teeth, and to reach forwards. They will adapt and use tricks such as holding the elbow to the side whilst lifting, and will lean right forwards almost touching the floor to dress and undress. Wasting will be apparent. Usually the weakness is accompanied by pain.

The isolated rupture of long head of biceps occurs with a sudden painful event, is associated with bruising down the course of biceps (rotator cuff tears rarely bruise), and the patient notices a change in shape of biceps to the ‘Popeye muscle’. This is painful when it occurs, but the pain settles within a few days, so the patient may present with weakness of elbow flexion and supination (using a screwdriver), although this is uncommon because the short head of biceps is intact. Weakness is more commonly seen in the rarer rupture of the distal tendon of insertion into the radial tuberosity.

Isolated ruptures of pectoralis major are subtler. There is a painful event in a 20-year-old man, who is a weightlifter or frequent gym user, who may or may not be on ‘health food supplements’ that may or may not contain nandrolone or some other androgenic steroid. There is a change of shape of the anterior axillary fold accompanied by bruising. There is weakness of pectoralis major.

Axillary nerve palsy is rare. It occurs after anteroinferior and inferior dislocations of the shoulder. There is decreased sensibility of the badge area of skin and weakness and wasting of deltoid. Muscle fasciculation may be seen. The injury is often a neurapraxia, but the nerve can be completely ruptured and require grafting.

Suprascapular nerve palsy is usually insidious in onset, presenting as a severe burning pain over the upper scapula accompanied by rapid wasting of infraspinatus (and supraspinatus although that is less obvious as it is covered by the healthy trapezius). It mimics cuff tear but the wasting is much more severe than seen with rotator cuff tears and has a more rapid onset. There is weakness and fatigue on reach.

Injuries to the long thoracic nerve and to the spinal accessory nerve lead to loss of scapula control and winging. Patients often complain that the ‘shoulder blade sticks out’. It may press awkwardly against the seatback when seated on a chair. Partners and family members note the cosmetic asymmetry of the shoulder blade. There is a loss of the shoulder fulcrum and lifting is weak and limited.

Fascioscapulohumeral dystrophy (FSHD) is the rarest of the causes of shoulder weakness. Patients usually present from late teens through to late twenties with shoulder girdle weakness particularly in abduction and flexion. The facial muscles are weak leading to a loss of facial expression, and that weird symptom, inability to whistle! Strangely the deltoid muscle is often preserved leading to a ‘Superman’ appearance. The key to diagnosis lies in the affected chromosome 4q35.

Occasionally patients complain of swelling. A swollen sternoclavicular joint is often noted by a perimenopausal female looking in the mirror. Swelling of the medial clavicle can occur in SAPHO (synovitis, acne, pustulosis, hyperostosis, and osteitis) syndrome or Garre’s sclerosing osteomyelitis. The patient may notice a swelling over the acromioclavicular joint with the ‘Geyser’ sign where fluid herniates out of the top of the joint from a communication with a massive cuff tear. The massive bursal fluid swelling of cuff tear arthropathy disturbs the patient with this condition. Remember that tumours both benign and malignant occur around the shoulder.

Deformity may be a presenting complaint, usually in children and adolescents. The deformity of congenital pseudarthrosis of the clavicle, the bossed clavicle of primary glenoid dysplasia, the elevated scapula of Sprengel’s shoulder, the ‘waiter’s tip position’ of Erb’s palsy. The absent pectorals of Poland’s anomaly and the dimples of posterior positional dislocation are all infrequent findings in the shoulder clinic.

The examination is more revealing than the history. Most pathology will fall into one of three boxes: the stiff shoulder, the wobbly shoulder, and pain on reach (the cuff). Examination should be tailored to the pathology suggested by the history. For instance, if the history points towards a wobbly shoulder then the time available to you should be used for instability tests, rather than the more esoteric eponymous tests of the rotator cuff. In the real world time is limited.

A plethora of eponymous clinical signs have sprung up over the last two decades. However, few have weathered the tests of specificity and sensitivity to gain mandatory use in the examination. Beware that clinical signs can be confounded, particularly by stiffness. Thus the belly press sign, an enormously important sign of subscapularis dysfunction, can be confounded by stiffness into internal rotation, producing a false positive belly press sign. Inspection and palpation are common to all stems, but should not take long.

Stand back and look at the profile of both shoulder girdles from the front. Is there asymmetry? Is one shoulder lower than the other? Is the posture slouched (common with thoracic outlet problems), are the scapulae protracted (gunslingers posture)? Is there asymmetry of deltoid bulk that is more pronounced than dominance should allow? Look from the side. Is the biceps’ shape altered? Look from the back. Is there wasting of infraspinatus (rotator cuff tear or suprascapular nerve entrapment)? Is there any winging? Pay attention to old surgical scars. Are the scars stretched as occurs with instability, or are there any striaie on the skin?

Pay careful attention to the humeral head. Is it elevated or more prominent than it should be, for this will suggest a tear of the cuff? If, like Sherlock Holmes, you are observing rather than just looking, inspection will take a matter of seconds.

The sternoclavicular and acromioclavicular joints are subcutaneous, and if the history has suggested that they are culpable, then they are easy to palpate. However, the glenohumeral joint line cannot be reached because the acromion covers the posterosuperior aspect, the coracoacromial ligament covers the anterosuperior aspect, and the conjoined tendon covers the anterior joint line. This only leaves the posterior joint line that lies beneath both deltoid and infraspinatus rendering palpation of the joint line impractical. Yet the greater tuberosity can be palpated easily. Since this is the site of most cuff pathology you may detect tenderness and even a ‘sulcus and eminence’ of the tear itself. Unless there is a lump or bump don’t spend too much time palpating. But do place a hand on the shoulder as you move it for soft crepitus and catching may be felt from the cuff, squeaking from an arthritic joint surface, or even a clunk of subluxation or relocation in unstable shoulders.

The examination for stiffness precedes all else, for if the joint is stiff no further examination is required—the patient needs a radiograph of the shoulder. Stiffness confounds the tests of rotator cuff dysfunction and so must precede them. Finally if the opposite of stiffness, excessive motion, is discovered then more attention must be placed on instability testing.

Ask the patient to move the shoulder himself or herself—this is active motion. Using a single finger to guide and nudge the patient’s arm into flexion will save you a great deal of time with verbal instruction. Patients do not understand instructions such as ‘flex or abduct your shoulder’. Place your other hand over the shoulder as the patient moves so that you will detect the rhythm between scapulothoracic and glenohumeral motion, detect translation of the humeral head, and finally detect crepitus, creaking and clunking. This means you have to examine one shoulder at a time, starting obviously with the normal side.

See if there is a restriction in active movement (that is, the range that the patient can comfortably initiate and sustain), and then the passive movement (the limit to which you can move the shoulder when pain is abolished). Four movements will be assessed, forward elevation, external rotation, internal rotation, and cross body adduction. By convention zero degrees is the anatomical position with the arm to the side and the antecubital fossa pointing forwards.

Note the level at which active movement ceases. Now rather than cause the patient increasing pain by forcing the shoulder passively further up, ask the patient to stoop forward (the bow test of Kolbel) for this often eases their pain and allows you to assess their passive range without hurting them (Figure 4.1.1). With the arm supported by you in this position of maximum elevation, ask them to stand, and finally now ask them to lower the arm, whilst you pay particular attention to how the scapula moves. You will see, in patients with rotator cuff disease, that they lock the glenohumeral joint during descent through their painful arc, leading to pseudo-winging.

If despite stooping the patient forward the shoulder will not move further, then we have a block to passive motion, true stiffness. Always note the quality of the end point of this movement. A leathery block to movement suggests a contracture. A firm bony end point is caused by osteophyte impingement in arthritis. An open end point—in other words, you know that the joint will move further but you dare not move it any more because of inordinate pain—is a red flag, it means either that there is a tumour or that the patient is exaggerating their symptoms.

Assess rotation both actively and passively. Beware for the shoulder is designed to position the hand accurately in space. Patients with little external rotation will cheat and abduct the arm in order to get the hand into position. (Remember that in every good detective story a few false clues are thrown in to see how clever you really are.) Keep the patient’s elbow locked to the side when testing external rotation (Figure 4.1.2). Patients with rotator cuff disease have near normal external rotation, but painful restriction of internal rotation. Patients with frozen shoulder and arthritis have passive restriction of both external rotation and internal rotation. Internal rotation is measured by the vertebral level at which the thumb rests at maximum internal rotation reach. If the patient has marked restriction of elbow flexion (for instance, in rheumatoid disease) then vertebral level is not an accurate method of measurement.

If significant passive stiffness is discovered then no further examination is required. A radiograph is mandatory and this will be normal in contracture and abnormal in arthritis, massive end-stage cuff tear, and locked posterior dislocation. Remember that stiffness may nullify further testing by producing false positive results.

To understand the clinical signs associated with rotator cuff disease you must first understand the anatomy and pathology of the rotator cuff. Most important is Professor Olivier Gagey’s concept of the fibrous skeleton of the cuff. The supraspinatus tendon comes from the centre of its muscle belly and migrates to the anterior edge of the tendon footprint of insertion. This central oblique tendon is extremely strong and acts as a ‘firebreak’ to tears. The majority of tears start just behind this tendon insertion leading to the typical posterosuperior cuff tear. This concept is expanded in Chapters 4.2 and 4.3.

This is the classic painful arc (Figure 4.1.3). Movement into the first 70 degrees of flexion is easy and pain free, but then as the footprint of the supraspinatus passes under the acromion, from 70–120 degrees, there is impingement between the surfaces and pain, and motion slows. As the footprint clears the under surface of the acromion, from 120 degrees to top pain eases and motion speeds up once more (Table 4.1.1).

Neer’s test is to inject some local anaesthetic into the bursa, bathing the bursal side of the footprint of cuff insertion. This abolishes the impingement and the normal pattern of movement is restored.

The arm is elevated in the scapula plane to 90 degrees. Now the elbow is flexed to a right angle and the arm is internally, and then externally rotated (Figure 4.1.4). Pain is seen to occur on internal rotation as the footprint of supraspinatus impinges against the anterior acromion. The sensitivity and specificity for Hawkins sign is 75%. It is one of the most useful tests of the posterosuperior cuff. Beware that passive limitation of internal rotation nullifies this test.

The arm is brought up in the scapula plane with the elbow extended and the arm fully internally rotated such that the thumb points to the ground (the Australians call this the ‘empty tinny test’ for it is the position in which you test that your can of beer is finally empty) (Figure 4.1.5). The patient is asked to hold this position against resistance from the examiner. If there is damage to the supraspinatus insertion then pain will register with the patient. If there is a tear of supraspinatus the arm will be weak. The accuracy of Jobe’s sign is 58%. It is another good test.

If either Neer’s, Hawkins’s or Jobe’s signs are positive then you should move straight to the ultrasound examination (Figure 4.1.6). The ultrasound will show you whether there is a tear, give you its exact position, and a measure of its dimension, it is worth a thousand eponymous tests. However, there are many other tests of the posterosuperior cuff and it is pertinent that you have heard of them.

These depend on weakness of a segment of the cuff. They are the modern equivalent of the ‘drop arm sign’. The drop arm sign was a particularly barbaric way of looking at a patient with a massive supraspinatus tear. The examiner elevated the arm to 120 degrees in the full knowledge that, without a functioning cuff, the patient will find it impossible to maintain this position. The examiner then let go and the arm dropped to the side! Patients were not as amused by this test as their examiners!

This demonstrates that there is a significant tear in supraspinatus. Like the drop arm sign this depends on placing the arm into a position that needs a strong supraspinatus and then letting go. The examiner takes the affected elbow and supports the weight of the upper arm with the shoulder in 90 degrees of scapular elevation. Now, using their other arm, the examiner externally rotates the forearm into full external rotation. Maintaining this position against gravity depends upon an intact supraspinatus. Now the examiner lets go of the forearm. If the cuff is intact this position can be maintained by the patient, but if the cuff is torn then the forearm will drop by about 30 degrees, the external rotation lag. In real life there are problems with the test. The examiner must understand exactly what they are doing, as must the patient. Pain may interfere with the test. Stiffness will render it null and void. There is difficulty between assessing how much movement is recoil and how much is lag. It is poorly reproducible. It has a specificity of 63% and a sensitivity of 80%. It has been superseded by portable ultrasound.

This is another lag sign. All military hornblowers must assume an identical position when blowing their horns. Otherwise they would look a mess! This position is with the hand at the lips and the elbow as high as it will go so that the arm, and forearm are parallel to the ground. This position can be maintained in the face of a torn rotator cuff. However, if the examiner now takes the hand, and fully externally rotates the forearm so that the forearm is now perpendicular to the ground we now have a position that can only be maintained with an intact cuff. Let go of the hand now and the forearm will drop, or lag, by 30 degrees. This test suffers from the same problems as the external rotation lag sign. It has been superseded by portable ultrasound.

Tears of the anterosuperior cuff (subscapularis and biceps) are less common than those of the posterosuperior cuff. These tears start around the biceps pulley and the superior part of the insertion of subscapularis into the lesser tuberosity. Subscapularis has a multipennate tendon of insertion into the lesser tuberosity.

This is the single most useful test of subscapularis function. The patient is asked to place the palm of the hand upon their abdomen. Now they are asked to keep the hand where it is and bring the elbow forward as far as it will go. If there is a complete tear of the subscapularis they will not be able to bring the elbow forwards. If they can pull the elbow forwards they are then asked to press the hand hard into the belly. If there is a partial tear of subscapularis they elbow will drop back (a lag sign) (Figure 4.1.7). Beware—if the shoulder is stiff a false belly press sign occurs, for instance, in patients with limited internal rotation from arthritis. Beware patients can cheat; in this case they flex the wrist pulling the elbow forwards, producing a false negative belly press sign. They must keep the wrist in a neutral position or the test is null and void. Finally, biceps problems can mimic subscapularis problems confounding the belly press sign.

This test is similar to the belly press sign, but is performed in more internal rotation. This means that the wrist must be placed on the small of the back, rather than on the abdomen. Now the patient is asked to actively increase the internal rotation by lifting the wrist away from the skin. The problem with this test is pain. Patients with cuff problems do not like placing the hand into internal rotation, and pain nullifies the test. Stiffness will also nullify the test.

This is a modification of the lift off test. The arm is placed with the wrist on the small of the back. The examiner now takes the wrist and pulls it 5cm away from the skin. With an intact subscapularis, and no pain or stiffness, the patient should be able to maintain this position. However, if subscapularis is torn then the wrist will drop (lag) back onto the skin of the small of the back. Once again it is difficult to discriminate between recoil and lag, and has the same problems of pain and stiffness.

There is not a good test for biceps! Biceps shape is important. All medical students know the ‘Popeye sign’ of a ruptured long head of biceps. However, you can have a complete intra-articular rupture of long head of biceps without a Popeye sign when the hypertrophied tendon jams in the sulcus, like a cork in a bottleneck. Between these two extremes the biceps can adopt subtle changes in shape.

This test is designed to isolate biceps by asking the patient to supinate the forearm against resistance. The examiner cradles the elbow with the shoulder held at about 40 degrees of scapular elevation. The examiner grips the patient’s wrist and pronates the forearm, asking the patient to resist (supinate) this force.

This is designed to detect a SLAP (superior labrum anteroposterior) tear. It is performed similarly to the Jobe test, but with the arm held at 20 degrees inside the neutral position (across the body) and at 90-degree elevation, and full internal rotation. The patient is then asked to resist the attempts of the examiner to push the arm towards the ground.

Yergason only described his test in one patient, yet this test has been copied from textbook to textbook. Speed’s test also has a low sensitivity and specificity. These tests are fully covered in Chapter 4.4.

First some definitions are needed. Laxity is defined as ‘asymptomatic excessive translation’. This is to be differentiated from instability, which is defined as ‘excessive translation that causes symptoms in the conscious patient’.

Start with some general observations. Does the patient, like Abraham Lincoln, have the appearance of Marfan’s syndrome? Are they tall, thin, and have arachnodactyly? Do they have the rubbery skin of Ehlers–Danlos? More to the point, and more commonly, do they have striaei, one of the commonest markers of laxity? Do they have surgical scars that have stretched, another marker of laxity? A peculiar pit, or dimple, on the posterior aspect of the shoulder has recently been described as an association with posterior positional instability.

One of the dilemmas with examination of the unstable shoulder is that the patient will not let you! The art of examining the unstable shoulder is akin to horse whispering, you must first gain the trust of the patient. Like the abused horse the patient will have come across doctors before who have tried to dislocate their shoulder (the apprehension sign), have caused undue pain to their shoulder, and this shows in their eyes. Like the scared horse the whites of the patient’s eyes will be showing, never releasing their laser-like concentration on what nasty trick you are about to do to them. Moreover they will be resistant to any movement of their shoulder, for they know that they live on the knife-edge of dislocation, one of the most painful conditions that can occur to the human frame. Why else do you think that the inquisitors used the rack to torture confessions from their victims? This resistance to examination leads to another chicken-and–egg conundrum for any examination is greeted by intense protective muscle spasm. This complicates any examination for abnormal muscle couples around the shoulder.

The examination starts by gaining the patients trust, and you do this by examining the good shoulder first, and gently. More can be gained by looking at the asymptomatic shoulder than the protected shoulder. Most patients with dislocation have a pair of loose shoulders already. This is true even of most traumatic dislocations (as has been shown by Cheng Wallace (2007) in a study of 215 professional rugby players), but more so for atraumatic and posterior positional dislocation. So the first thing to look for is excessive mobility, and the second thing excessive translation and finally provocative testing (Box 4.1.1).

Laxity is a feature of youth! Stiffness is a feature of ageing. Children have been shown to have marked shoulder laxity. However, by the age of 18 (the commonest age for first-time dislocation) the extreme laxity of youth will have passed. The normal end point for external rotation is about 70 degrees. However external rotation of 85–95 degrees is clearly abnormal and this is termed ‘hyperlaxity’. It is a clear sign of shoulder laxity. The normal shoulder will internally rotate to T7 (the lower border of the scapula); anything more is a sign of laxity.

The Beighton score is a useful objective guide to laxity. Wrist hyperflexion counts for two points, little finger hyperextension at the metacarpophalngeal joint a further two, elbow recurvatum another two, knee recurvatum a further two, and the final two come from the ability to stoop forward so as to place the palms of the hands flat on the floor. This gives a total out of ten points.

This is a sign of excessive capacity or laxity of the inferior capsule. With the arm abducted to 90 degrees, the elbow fully flexed and the hand captured and not allowed to move from that position, the elbow is pushed upwards, abducting the arm as fully as it can go. The looser the inferior capsule, the higher the elbow will go (Figure 4.1.8).

Now is the time to stress the joint and see if translation is excessive. Of course this depends on what is normal and the examiner can only gain an appreciation of that with experience. Massive muscular men may show no apparent translation, whereas tiny, size zero girls may demonstrate a fair degree of translation for the same applied force. The amount of translation is graded by convention as 0 for nil, 1 for normal translation, 2 for translation to the glenoid rim, 3 for subluxation, and 4 for dislocation. We will try to translate the joint forwards (Rowe test), downwards (sulcus sign), and backwards (posterior jerk test).

This is the single most useful test of the unstable shoulder. The key is to unpack the capsule of the joint so that it is at its very loosest, for in that state abnormal translation can be shown, that can never be revealed when the capsule is in its tightest configuration. This means getting the standing patient to lean forwards some 40 degrees. Then the patient lets the arm hang down limply. In this unpacked position the surgeon grips the humeral head in one hand and steadies the socket by firmly holding the scapula and clavicle in the other hand. Now the surgeon applies forward (Figure 4.1.9) and then backward translation to the joint. The degree of translation is graded 0–4. Clearly the asymptomatic side must be tested first.

This test is analogous to the anterior drawer test of the knee. The test was first described by Gerber and Ganz in 1984; their description of the test is precise, but has been incorrectly copied into major textbooks. Like the Rowe test, the anterior drawer depends upon unpacking the capsule, positioning the shoulder with the capsule in its loosest configuration. The patient lies supine on the couch and the shoulder is held in the unpacked position of 70-degree flexion in the scapular plane, and neutral rotation. The patient’s forearm is gripped in the examiner’s axilla. One of the examiner’s arms stabilizes the scapula whilst the other drives the humeral head forward and backwards (posterior drawer test). This is a good test but the examiner needs three hands and the patient has to lie down. The Rowe test is easier and quicker. Many textbook editors describe the test being done with the patient seated, and the arm at the side. In this position the capsule is firmly packed and translation will be markedly inhibited confounding the test.

Some patients have really loose shoulders. These patients will dislocate in one direction and sublux in the opposite direction; they are thus classified as having multidirectional instability. These patients can be seen to sublux inferiorly by pulling down on the arm, when a dimple will appear between the acromion and the top of the humeral head, the so-called ‘sulcus sign’ (Figure 4.1.10).

Posterior instability is tested with the ‘posterior jerk test’. This test is poorly described in standard textbooks. The arm is elevated in adduction and internal rotation, and the humeral head will gradually slip off the back of the glenoid; this is usually pain free. With the shoulder thus dislocated the arm is taken from adduction to abduction and the humeral head will suddenly relocate with a jerk; this is usually associated with pain (Figure 4.1.11).

This is a crude test that mimics an anterior dislocation whilst the inquisitor observes the patient’s psychological resistance and physical protective instincts towards the thing they most dread, dislocation of their shoulder. By the twenty-first century doctors should use such barbaric tests sparingly! The diagnosis should already be clear from the history, or emergency department records, or radiographs. The diagnosis of recurrent anterior dislocation is seldom difficult (unlike posterior positional dislocation). If there is some difficulty then the Rowe test is far more revealing and does not hurt. For the sake of completeness we will describe the test. The shoulder is brought up into 90 degrees of abduction and then progressively externally rotated. The normal shoulder can be fully externally rotated until a firm passive end point is reached, and it will cause no pain. However, this same manoeuvre in a patient who has recurrent instability will cause extreme apprehension, then pain, and will finally dislocate. Clearly if examining the patient awake, in the clinic, the examiner should stop at the stage of apprehension but there are two further extensions of this test. If the patient is not looking sufficiently apprehensive then the shoulder is cranked into more external rotation, the crank test. If the patient is looking sufficiently apprehensive then pressure is applied to the humeral head to translate it back into socket, and the flood of relief visible on the patient’s face gives a positive relocation test, eponymously named after that kind Dr Jobe, the Jobe relocation test.

If examination has revealed that the shoulder is not stiff, that the tests of the rotator cuff are normal, and that there is no evidence of instability, radiographs and POC ultrasound are normal then you have a problem; you are also going to run over the twenty minutes allotted to each patient. Turn to the chapter on examination of the cervical spine for further details.

The acromioclavicular joint (ACJ) is subcutaneous, and therefore much easier to examine than the shoulder joint itself. It is rare for the ACJ to be the culprit if it is not tender along its anterior, superior, or posterior joint line. Instability can be seen if gross and the joint translates abnormally if it is unstable. Finally the joint can be stressed by torsion, elevating the shoulder into the high painful arc, or by compression (the scarf test), or ‘cross-over test’, or extension and adduction with resistance ‘the half nelson or resisted extension test’. O’Brien’s test described an active compression test with the upper limb flexed to horizontal at the shoulder with a little adduction. If the origin of the pain is in doubt, a small amount of lignocaine (1–2mL) can be injected directly into the ACJ and the tests repeated. The cross-over test and resisted extension test are most sensitive (77% and 72% respectively). O’Brien’s test was found to have low sensitivity (41%) but high specificity (95%). A positive finding on all three tests, however, conferred an accuracy of 93% and probably renders a diagnostic injection test unnecessary.

In the twenty-first-century rush to get scans, plain radiographs are often forgotten. This is a mistake. There are many things that are best seen on plain old-fashioned radiographs and these are fractures, calcific deposits, arthritis, tumours, and locked dislocations. All right you can see these on an MRI scan, but who has instant access to an MRI scanner in clinic? Besides, calcific deposits are far more difficult to see on MRI than on plain radiographs. A radiograph is the mandatory investigation for the stiff shoulder, and mandatory in any patient with a history of cancer (Box 4.1.2). The radiograph should be taken in the plane of the glenoid, which is 30 degrees to the sagittal plane of the body; this is the true AP of the shoulder.

Although cuff disease and instability are soft tissue diseases they may lead to secondary bone changes that can be seen on radiographs. Radiographs may show changes in the greater tuberosity in rotator cuff disease. These will range from irregularity of the bony footprint, sclerosis, pseudocysts, and eventually flattening of the tuberosity.

Changes may also occur at the anteroinferior acromion with sclerosis (sourcil sign) and spur formation within the footprint of the coracoacromial ligament. Less accurate is a reduction in the acromiohumeral distance, or a break in Shenton’s line of the shoulder.

Secondary changes in instability are the Hill–Sachs lesion (best seen on a Stryker notch view or West Point view) and bony Bankart lesions (best seen on an axillary or Bernageau view).

ACJ arthropathy is most readily confirmed with a plain radiograph of the joint. This requires the x-ray beam to be tilted 20–30 degrees in a caudal direction and the voltage reduced to ensure that the ACJ is not obscured by the base of the acromion or over-exposed (Zanca view).

Computed tomography (CT) scans are useful for surgical planning, particularly prior to fracture fixation and complex primary shoulder replacements. In continental Europe, CT is commonly used in the assessment of rotator cuff tears, particularly to assess fatty infiltration of the muscle belly (using the Goutallier classification) prior to surgery. CT arthrography can be used for rotator cuff disease and instability, but has been mainly superseded by MR arthrography (MRA).

CT is a useful modality for examining the sternoclavicular joint.

In the clinic time is of the essence, so an abbreviated study is permitted, scanning in only three planes, as opposed to the 12 planes recommended in most radiological texts. An axial scan is first used to demonstrate the lesser tuberosity, subscapularis, biceps sulcus, and long head of biceps tendon. Secondly, an oblique coronal (or longitudinal) view is used to show the greater tuberosity and the supraspinatus. Finally, a saggittal oblique (transverse) view is used, demonstrating the greater tuberosity and supraspinatus tendon, rotator interval, and biceps. All findings are recorded in detail at the time. In each of the three planes a record is made of the articular appearance (normal, positive cartilage reflection sign, osteophytes), the bone (normal, irregular, calcification, fracture line), the collagen (normal, heterogeneous, hypertrophic), presence of a defect (rim-rent, cleft, delamination, focal absence, absent cuff), and the presence of an effusion (nil, effusion, flattening of bursa, bursal concavity). A firm diagnosis of the state of the rotator cuff and biceps is then recorded. A full thickness tear is diagnosed on sonography if the tendon is absent, or if there is a focal deficit. A combination of one or more indirect signs such as a bursal concavity, an effusion around the biceps, bony irregularity, or a positive cartilage reflection sign allow a judgement to be made by the surgeon of the presence of a supraspinatus tear.

MRI has revolutionized the field of imaging in the shoulder, because it can image the soft tissues. Unlike ultrasound, MRI can image through the bone, and it can image the bone, and it can image to depths of tissue that cannot be reached by high frequency ultrasound. It is therefore the imaging modality of choice for instability, as it will demonstrate labral abnormalities. Visualization of SLAP tears and Bankart tears are improved by MRA using gadolinium enhancement.

MRI is the imaging modality of choice for large rotator cuff tears where the degree of retraction under the acromion, and the degree of wasting and fatty infiltration of the muscle belly will determine whether the tear should be repaired, or whether repair is a forlorn hope. MRA is useful in demonstrating articular side partial tears.

MRI is not as good as CT for looking at bone yet it is the investigation of choice for avascular necrosis. MRI is the investigation of choice for lumps, masses, and tumours around the shoulder. MRI will demonstrate pathology that cannot be seen by ultrasound, such as labral cysts and ganglia.

However MRI is not without problems. The equipment is extremely expensive and far from portable! Patients do not like MRI. It is claustrophobic, noisy, and patient unfriendly. One-third of patients will not have a second MRI scan. It will demonstrate morphology, but not histology. It suffers from a phenomenon called the ‘magic angle effect’ that can produce false positive results. MRI is very bad at showing calcific deposits as these are dark, as is the tendon, so there is no contrast difference between the calcium and the tendon.

MRA suffers from the problem that it is invasive. Intra-articular injection of gadolinium is usually done under image intensifier control and local anaesthetic. This ramps up the degree of difficulty, often needing two radiology suites, careful timing, transfer from room to room, and the time of a skilled radiologist. On top of this patients do not like invasive diagnostic procedures.

Shoulder arthroscopy remains the gold standard forensic investigation for the shoulder. Not only can the inside of the glenohumeral joint be appreciated, but also the outside view of the rotator cuff from within the subacromial bursa. An essential preamble to arthroscopy is examination under anaesthetic.

This is a provocative test, being the shoulder equivalent of the Barlow and Ortolani tests of the hip, or the pivot shift in the knee. The arm is cradled by the examiner and brought into the unpacked position of 70-degree flexion in the scapula plain. The joint surfaces are compressed (loaded) and then a conscious effort is made to dislocate the shoulder, then to reduce it. The clunk of dislocation and relocation is quite distinctive.

The arthroscope is now introduced into the joint and a standard 12-point examination is conducted.

The 12-point examination is thorough and should confirm the diagnosis. More detail can be sought from textbooks such as Shoulder Arthroscopy by Bunker and Wallace, which is available free on the Internet at sites such as http://www.shoulderdoc.co.uk. These days arthroscopy is rarely used for diagnosis alone, it is used for treatment, releasing contracted shoulders, decompressing impinging shoulders, repairing rotator cuff tears, and stabilizing the unstable joint. All of these will be covered in the ensuing chapters in this section.

Surgeons only need to know two things: when to operate and how to operate. When to operate is what this chapter has been about. Knowing when to operate involves establishing the diagnosis and the severity of the disease. However, despite the advances in clinical examination and the profusion of forensic examinations (radiographs, CT, ultrasound, MRI, MRA, and arthroscopy) that are now available to us, the diagnosis can remain elusive. The surgeon must take in a vast amount of information, solve several simultaneous equations at once, discard the dissembling and lies, assemble the truths, seek concordance, check with forensics, and come to a solution. Nobody said this was easy; it is why surgeons are carefully chosen, continuously examined, trained for 20 years, and prefer coastal navigation to football. Higher-level reasoning has always, and will always be the most important distinctive characteristic of the consultant surgeon.

As to how to operate, that will be covered in the following chapters.