1 What are the cardinal signs of joint inflammation?

The same as for inflammation in general: tumor, dolor, calor, rubor—all originally described by the Roman encyclopedist Celsus in the first century A.D. One hundred years later, the Greek Galen (personal physician to Marcus Aurelius) added functio laesa (i.e., the dysfunction of the organ involved). Virchow reiterated this concept in 1858. Note that these signs of inflammation can apply not only to the joint per se but also to the tendons, ligaments, bursa, or muscles controlling the joint.

2 What are tendons? What is tendinitis?

Tendons attach muscle to bone, thus transmitting muscular force across joints. They are often covered in tenosynovium, a sheath of connective tissue and synovium. Tendinitis is the general term for disorders of the tendon, including inflammation of the tenosynovium (tenosynovitis) and tears of either bone attachment (enthesis) or the tendon’s body.

3 How are disorders of tendons differentiated from joint problems?

By paying attention to the pain. Tendinous disorders cause pain only on (1) passive stretch of the tendon at its extreme range of motion and (2) active joint motion (i.e., requiring muscle contraction). Conversely, passive joint motion produces no pain.

4 What are ligaments? What are the findings of a ligament injury?

Ligaments attach bone to bone. Injuries present in different ways, based on their degree. Tenderness over the ligament, and pain upon ligament stretching, are the most common manifestations. Abnormal joint motion and gapping with stretching require instead a significant disruption of the ligament. Finally, ecchymoses over the site usually indicate severe injury.

5 What are bursae? How do you identify bursitis?

Bursae are fluid-filled synovial sacs that facilitate the movement of articulating structures. They can be found over bony prominences and between adjoining muscles with different directions of contraction. Their inflammation (bursitis) presents with tenderness and/or fluctuance in the periarticular area, but not in the joint per se.

6 Describe joint swelling (tumor)

Swelling is any increase from normal in the joint volume as a result of (1) bony enlargement (often due to osteophytes), (2) synovial proliferation (i.e., synovitis), or (3) intra-articular fluid. Palpation usually allows the examiner to separate these three conditions, insofar as bony enlargement is firm and synovial proliferation is also firm (although palpatory findings may range from indistinct joint margins to sponginess), whereas intra-articular fluid is instead fluctuant.

7 What is the significance of joint tenderness (dolor)?

It is another sign of joint pathology. Normal joints can be palpated with significant force without eliciting any pain. Hence, tenderness (ranging from mild discomfort to severe pain) is always abnormal. This also can limit joint motility, thus forming the basis of Galen’s “functio laesa.”

8 What is the significance of articular warmth and erythema (calor and rubor)?

They indicate pathology, too. Normal joints should be cooler than the surroundings and not red.

9 What is crepitus?

It is palpable crunching throughout the range of motion of either a joint or a tendon. This may originate from irregularities in the cartilage, bone-on-bone articulation, or tendon per se.

10 What is the significance of joint cracking or popping?

No significance, unless accompanied by pain. Sensation of passive joint cracking is common, probably due to tendon or ligament slippage over a bony prominence. This is different from the audible “pop” that can be induced by actively “cracking a joint,” which is instead due to sudden release of nitrogen gas from the synovial fluid under the negative pressure of joint distraction.

11 What are the main patterns of joint involvement?

Note that polyarticular involvement can be symmetric (with one side of the body mirroring the other [i.e., same joints, or rows of joints, on both extremities]) or asymmetric (involving different joints in different extremities).

12 How do you measure range of motion (ROM)?

With a goniometer—always comparing one side to the other.

13 What are the findings of joint hypermobility?

Note that joint hypermobility can be benign or associated with Ehlers-Danlos.

14 What is the anatomy of the shoulder?

It results from the confluence of three bones (humerus, clavicle, and scapula) and four joints (glenohumeral, acromioclavicular, sternoclavicular, and scapulothoracic). Everything is kept in place by various static and dynamic stabilizers: the “static” being labrum, capsule, and three ligaments (acromioclavicular, coracoclavicular, and coracoacromial); the “dynamic” being the scapular stabilizers (trapezius, rhomboid, and teres major) plus two muscles: rotator cuff and deltoid.

15 Describe the muscles and tendons of the shoulder

16 What are the shoulder’s movements? How do you test its ROM?

The shoulder can actively abduct, adduct, externally and internally rotate, flex, and extend. It has the largest ROM of any joint, since it provides mobility not only to the girdle but also to the hand. ROM is tested as follows:

If active ROM elicits pain, evaluate the same movements through passive ROM. To provide your patient with adequate support (and thus ensure maximal relaxation), gently rest one hand on his/her shoulder while using your other hand to move the humerus through the same ROM as previously discussed. Look for pain and crepitus. Pain and limitation on active, but not passive, ROM indicate muscular or tendinous problems. Crepitus suggests instead degenerative joint disease.

17 What areas of the shoulder girdle should be palpated?

As a mnemonic for structures to palpate, use Really Great and Beautiful ACtresses (Rotator cuff, Glenohumeral joint, Bicipital tendon, Acromioclavicular joint).

18 Can history identify the cause of a shoulder ailment?

Yes. For instance, recurrent subluxation in young individuals usually indicates multidirectional instability; constant shoulder pain and decreased ROM in diabetics classically reflect adhesive capsulitis; pain and weakness in workers whose jobs require recurrent overhead action suggest rotator cuff pathology; shoulder pain after a fall on an outstretched arm argues for acromioclavicular (AC) lesions.

19 What is the general approach to the shoulder exam?

Always expose both shoulders (and watch while the patient removes the shirt). Then carry out a systematic exam: inspect, palpate, assess ROM, measure strength, evaluate neurologically, and perform special shoulder tests. Also, examine the cervical spine and upper extremity.

1. Inspect for scars, color, edema, deformities, muscle atrophy, asymmetry, and guarding.

2. Palpate for pain or point tenderness (the presence of either narrows the exam):

Bony and soft-tissue structures, such as coracoid process, acromioclavicular joint, greater tubercle

Subdeltoid and subacromial bursae

Supraspinatus muscle and its insertion (anteriorly, with arm externally rotated and flexed)

Infraspinatus muscle (with arm hyperextended)

Major muscle groups and biceps tendon

Sternum and sternoclavicular joint

3. Assess active and passive ROM, especially in regard to elicited pain and reduced movement.

4. Determine muscle strength. This is an essential part of the exam, and comparing side to side may help you locate the area of concern. Always carry it out with and without resistance. To isolate the various muscles, use the following maneuvers:

Supraspinatus: arm forward 90   degrees in the scapular plane and forearm pronated (thumbs down, “empty can” maneuver). Drooping of this position suggests full-thickness rotator cuff tears.

Subscapularis is tested by internal rotation. Arm is rotated internally with the dorsum against the buttock. Actively lift the hand from the buttocks against resistance.

External rotators, teres minor, and infraspinatus are primarily tested by external rotation (arm on the side and in 90   degrees of abduction).

Deltoids are primarily assessed by abduction.

Biceps is primarily tested by elbow flexion and supination.

20 What is the shoulder pad sign?

A sign of bilateral shoulder effusions. Very typical of amyloidosis.

21 What are the most common musculoskeletal causes of shoulder pain?

Hence the mnemonic, “Basically I Test Religiously For Damaged Objects.”

22 What are the origins of referred shoulder pain?

Various. Shoulder (or scapular) pain can originate from many internal organs, including the myocardium (angina and infarction), hepatobiliary system (cholecystitis), and diaphragm (subphrenic abscess). It also may originate from cervical spine and neurovascular entrapment. For example, burning and tingling in the deltoid area may result from irritation of nerve roots, especially C5 and C6. Hence, any patients with shoulder pain who also have C-spine symptoms should have a brief neck exam (with and without resistance) to exclude referred disease.

23 In addition to history, how else do you identify referred shoulder pain?

By its being typically nondescript, poorly localized, and not reproducible on shoulder exam.

24 What is shoulder synovitis? How do you diagnose it?

Shoulder synovitis is inflammation of the joint. Diagnosis is made by detecting “fullness” just below the clavicle, medial to the deltoid, and clearly visible when compared to the other side. On palpation, there is “bogginess” over the anterior surface of the joint, coinciding with the fullness.

25 What is acromioclavicular (AC) arthritis? How do you diagnose it?

It is arthritis of the AC joint, a structure that is minimally mobile but still prone to inflammation. This, in turn, may lead to rotator cuff irritation through the downward protrusion of bony spurs into the tendon. Pain of AC arthritis is initially vague, localized to the joint, and possibly radiated to the shoulder, anterior chest, and neck. With time, it may become associated with crepitus and swelling. Pain can be elicited by direct compression of the joint, or by stress maneuvers. These involve (1) cross-body adduction of the arm behind the back (which produces pain in the AC joint at the end of adduction); (2) movement of the arm across the chest (so that the hand touches the opposite shoulder); and (3) cross-arm maneuver (the arm is forward flexed and then adducted across the body). These tests are positive when they elicit pain in the AC joint.

26 What is AC separation?

A disruption of the AC joint, usually traumatic. When compared to the unaffected side, the area is swollen, deformed, and painful upon compression or stress maneuvers (such as moving the arm across the chest). In fact, the patient usually keeps the arm very still.

27 What is bicipital (or biceps) tendinitis?

Inflammation of the long head tendon. This can be sudden (from a direct injury) or gradual. The latter is usually the result of shoulder overuse and thus typical of “overhead” athletes: baseball pitchers, racquet players, swimmers, and rowers/kayakers. As the arm is passed into excessive abduction and external rotation, the long head tendon suffers repetitive injury and eventual wear-and-tear. Most commonly, though, the tendon becomes inflamed because of other shoulder problems, such as rotator cuff disease, impingement, instability, or labral tears.

28 What are the symptoms/findings of bicipital tendinitis?

Achy anterior shoulder pain, worsened by overhead activity, lifting of heavy objects, and elevated pushing/pulling. Rest is usually beneficial, whereas flexion of the elbow against resistance is detrimental. Pain is vague, though at times it may become localized to the anterior humerus. On exam, there is point tenderness over the bicipital groove, which is the area where the long tendon is anatomically exposed. This lies 3   inches below the anterior acromion and may be best localized by holding the arm in 10   degrees of external rotation. Pain also can be elicited by passive abduction of the arm in a painful arc maneuver (see question 41), which is typical of impingement syndrome, although at times it also may be positive in patients with isolated biceps tendinitis.

29 Which specific maneuvers can reproduce the pain of bicipital tendinitis?

Maneuvers that resist the normal function of the biceps—supination and flexion of the forearm:

30 What is the “Popeye” sign?

A sign of rupture of the long head of the biceps tendon. The patient reports a sudden, painful, and audible snap, associated with (1) retraction of the biceps belly toward the elbow and (2) bulging over the anterior upper arm—as in the cartoon character “Popeye.” In the elderly, this may occasionally result from trauma. Otherwise, it is usually due to long-standing tendinitis. Hence, it is preceded by a long history of shoulder pain, quickly resolving with a painful snap.

31 What is shoulder impingement?

A concept first introduced by Neer in 1972 to describe mechanical impingement of the rotator cuff tendon. This runs above the humeral head and glenoid, and below the acromial process, coracoacromial ligament, and acromioclavicular joint. Recurrent friction causes bursitis, tendinitis, and ultimately, tendon degeneration and tearing.

32 What is the cause of shoulder impingement?

Mechanical wear and tear. True tear of the cuff is actually a problem of older subjects, whereas rotator cuff disease and impingement tend to affect primarily laborers (whose job requires repetitive and protracted overhead activity) or young athletes (whose sport also involves repetitive overhead motions, such as throwing, swimming, volleyball, and tennis and other racquet-playing activities). Raising the arm over the shoulder forces the humerus against the edge of the acromion. Usually, there is enough room between the acromion and rotator cuff to allow the tendons to slide easily underneath the bone while the arm is being elevated. Recurrent arm-raising, however, eventually creates impingement (i.e., friction on the subacromial bursa and the distal part of the tendon). With time, this causes irritation and swelling of the bursa (bursitis), further narrowing the space between the acromion and rotator cuff. As a result, impingement on the tendon becomes more severe, which is risky since its blood supply is limited. Hence, the resulting tendinitis and, ultimately, the degenerative damage. Bony spurs of the AC joint (which sits directly above bursa and rotator cuff tendons) may further narrow the subacromial space, and so can abnormal acromial morphology (such as a hooked acromion).

33 How do you diagnose rotator cuff tendinitis?

By carefully examining the shoulder and by knowing the function of the four rotator cuff muscles (i.e., abduction, external rotation, and internal rotation).

Note that given the anatomic closeness of the long head tendon of the biceps (which passes down the bicipital groove in a fibrous sheath between the subscapularis and supraspinatus tendons), patients with rotator cuff disease also may have biceps tendinitis (see questions 27 and 28).

34 What is the “drop arm” test?

A good way to identify rotator cuff pathology. Ask patient to raise the extended arms to a complete overhead abduction. Those with rotator cuff tear will be unable to smoothly bring the arms down to the sides from their abducted position. In fact, they may even display a cogwheel effect.

35 What are the symptoms of shoulder impingement?

The initial one is pain—aching and gradual (acute and tearing suggest instead a rotator cuff tear), centered around the anterior-superior-lateral aspect of the shoulder, and occasionally referred to the deltoid region. Pain interferes with sleep (especially when the patient rolls onto the affected shoulder) and is exacerbated by lateral or anterior raising of the arm and by forward flexion and internal rotation of the humerus (as if trying to reach into a back pocket). Pain worsens with time, and the joint may become stiff, causing “catching” sensations upon lowering of the arm. Weakness and inability to raise the arm suggest instead a rotator cuff tear.

36 How do you examine for shoulder impingement?

(1) By palpating the subacromial space (which elicits pain in patients with bursitis/tendinitis), and (2) by assessing the shoulder girdle muscles, especially during external/internal rotation and abduction. Supraspinatus problems can be identified by the empty can test, also described by Jobe, and so named because the patient’s position is similar to that assumed when emptying a can. To carry this out, have the patients (1) abduct the shoulder to 90   degrees and forward flex it at 30   degrees and (2) fully rotate the upper extremity (so that the thumbs are pointing toward the floor). While they do so, instruct them to forward flex the shoulder while you are applying resistance from behind. Patients with supraspinatus tendinitis or partial injury to the tendon will experience pain. Those with a partial- or full-thickness tear will be instead unable to achieve any forward flexion.

37 Are there any special maneuvers that can be used for testing impingement?

The Neer (impingement) test and the Hawkins-Kennedy test. Both cause the supraspinatus tendons to rub against the acromion, thus eliciting pain in cases of impingement. Still, beware that it is usually very difficult to clinically identify the location of the problem, that is, to separate bursitis from tendinitis or even partial rotator cuff tears (which is why God created magnetic resonance imaging [MRI]). One possible exception is the diagnostic subacromial bursa injection: local anesthetic and steroids injected into the bursa will relieve bursitis but not tendinitis nor partial rotator cuff tear.

38 How do you perform the Neer (impingement) test?

The patient’s forearm is internally rotated, so that the thumb points downward. While standing behind the patient, place one hand on the patient’s scapula and with the other hand grasp the forearm and forward flex it, eventually positioning the patient’s hand over the head. Forced elevation and internal rotation of the arm cause the greater tuberosity of the humerus to compress the subacromial bursa. This, in turn, squeezes the supraspinatus tendon against the acromion, causing pain in cases of impingement. The test also can differentiate AC arthritis from subacromial bursitis (Fig. 21-1).

Figure 21-1 Impingement test.

(From Mellion MB: Office Sports Medicine, 2nd ed. Philadelphia, Hanley & Belfus, 1998.)

39 How do you perform the Hawkins-Kennedy test?

Hold up the patient’s arm to 90   degrees of forward flexion (i.e., to the shoulder level) and 90   degrees of elbow flexion. Then, forcefully internally rotate the arm to 90   degrees (i.e., thumb pointed down). This causes the greater tuberosity of the humerus to compress the subacromial bursa, and the supraspinatus tendon to impinge against the coracoacromial ligament—thus eliciting pain (“impingement sign”). Hawkins is more sensitive than Neer in detecting subtle degrees of impingement.

40 How else can one elicit pain in supraspinatus tendinitis?

Have the patient hold the elbow against the side and force it into external rotation against resistance.

41 What is the “painful arc” sign?

A painful arc of motion, a useful test for evaluating a painful shoulder. Arms are down at the patient’s side, and then abducted to 180   degrees above the head (rotating hands as necessary to complete the arc). The maneuver should be smooth and painless. Impingement disease (such as supraspinatus tendinitis or partial rotator cuff tear) will produce pain with elevation of the arm above the shoulder level (i.e., in an arc between 40 and 120   degrees). There will be no pain before 40   degrees and no pain after 120   degrees. Glenohumeral arthritis instead produces pain throughout the arc.

42 What are rotator cuff injuries?

They are a spectrum of diseases (ranging from acute reversible tendinitis to massive tears of the supraspinatus, infraspinatus, and subscapularis) that are common causes of shoulder pain. Although seen in all ages, they usually present after the fourth decade, with peak at 55–85.

43 What are the causes of rotator cuff tear?

Most are the end-result of chronic tendineal degeneration, usually from repetitive friction against the overlying coracoacromial arch. This may be due to recurrent overhand motions (as in baseball pitching), but also to more lowly and routine daily activities, such as cleaning windows, washing and waxing cars, or painting. Once the tendons are weakened, excessive force will tear them. This may occur when trying to catch a heavy falling object, trying to lift a big load with the arm extended, or simply falling directly onto the shoulder.

44 What are the symptoms of rotator cuff tear?

The most common is pain, anterolateral and superior, usually referred to the deltoid insertion, and worsened by holding the arm in an overhead or forward flexed position. The next most common is weakness and decreased range of motion. In cases of complete tear, there also is inability to raise the arm. Finally, there may be articular clicking, catching, or crepitus.

45 What are the findings of a complete rotator cuff tear?

The patient cannot actively abduct the arm from 0   degrees. If the arm is passively abducted above 90   degrees, there will be inability to hold it up and further abduct to 180   degrees. If the arm is passively lowered below 90   degrees, it will fall to the side (drop arm test). Finally, with the elbow against the side, there will be inability to externally rotate the arm.

46 What is glenohumeral (shoulder) dislocation?

A problem as old as mankind (Egyptian tomb murals from 3000 B.C. depict reduction techniques, while Hippocrates fully described them) because the shoulder, being the most mobile joint in the body, is also the one more likely to dislocate. Anterior dislocations are the most frequent (95%), followed by posterior (4%) and inferior (0.5%).

47 What are the causes of dislocation?

The most common is a traumatic force that overcomes the stability of the joint. Anterior shoulder dislocations usually result from abduction, extension, and external rotation (typical, for example, of the preparation for a volleyball spike). Falls on an outstretched hand also are common, especially in older subjects, and so are seizures. Whatever the cause, the resulting blow overcomes the resistance provided by the glenohumeral capsule, the labrum, and the rotator cuff muscles, forcing the humeral head out of the glenohumeral joint and rupturing or detaching the anterior capsule. The labrum itself also may tear.

48 What is the presentation of dislocation?

The typical is posttraumatic shoulder pain and decreased range of motion. In an anterior dislocation, the arm is held in slight abduction and external rotation, the shoulder is “squared off” with loss of deltoid contour, and the humeral head is anteriorly palpable (just beneath the clavicle, in the subcoracoid region). There also will be inability to touch the opposite shoulder, plus resistance to abduction and internal rotation. Given the risk of impingement of the neurovascular bundle, one should always check (and compare) radial pulses and also evaluate the axillary nerve. This can be done by testing pinprick sensation in the “regimental badge” area of the deltoid and through palpable contraction of the same muscle during attempted abduction.

49 How do you test for glenohumeral instability?

It depends on the type of instability: anterior versus inferior.

50 How do you test for anterior shoulder instability?

Through the apprehension and Jobe’s relocation tests. Start with “apprehension” (Fig. 21-2). To perform it, ask patients to lie supine, with the affected shoulder just off the examining table. Grasp the elbow with one hand, and gently bring the arm to 90-degree abduction and 90-degree external rotation. Then push with your other hand on the posterior aspect of the humeral head, from back to front. Anterior shoulder instability will give a feeling that the arm is about to pop out of the joint. At the same time, patients will experience pain, apprehension, and guarding. In the original series of Rowe and Zarins, all 60 cases of anterior shoulder instability had a positive apprehension test. If the patient experiences pain and/or apprehension, move on to the second part of the maneuver: the Jobe’s relocation test. This is performed in the same position, but this time by pushing on the anterior aspect of the humeral head, from front to back, as if relocating a glenohumeral joint that had been partially dislocated by the apprehension test. Patients with primary impingement will have no change in pain, whereas those with anterior instability (subluxation) and secondary impingement will have relief of pain and/or apprehension. When relying primarily on relief of apprehension, the relocation test has sensitivity for anterior instability of 68%; specificity, 100%; positive predictive value, 100%; negative predictive value, 78%; and accuracy, 85%.

Figure 21-2 Apprehension test.

(From Mellion MB: Office Sports Medicine, 2nd ed. Philadelphia, Hanley & Belfus, 1998.)

51 How do you test for inferior shoulder instability?

Through the sulcus sign. Allow the arms to rest on the patient’s side, then pull them down. Compare shoulders. Any asymmetric anterior dimpling suggests inferior shoulder instability.

52 How do you diagnose multidirectional instability?

By the presence of both inferior instability (positive sulcus sign) and anterior instability (positive apprehension and Jobe’s relocation tests).

53 How do you test for glenoid labral tears?

Through the O’Brien and anterior slide tests.

54 How do you perform the O’Brien test?

The patient stands, with arm flexed to 90   degrees and elbow in full extension. Then (s)he adducts the arm to 10–15   degrees medial to the sagittal plane of the body, and internally rotates it, so that the thumb points down. The examiner stands behind the patient applying a downward force to the arm. With the arm in the same position, patient is then asked to supinate the palm (thumb pointing up), and the maneuver is repeated (i.e., the examiner again applies a downward force to the arm). The test is positive if it elicits pain with the thumb pointed down and relieves it with the thumb pointing up.

55 How do you perform the anterior slide test?

The patient is standing or sitting, with hands on hips, and thumbs pointing posteriorly. The examiner stands behind the patient and places one hand on the elbow and the other on the posterior aspect of the top of the shoulder, with the index finger extending over the anterior aspect of the acromion at the glenohumeral joint. Then the examiner applies a force to the elbow and upper arm that is directed forward and slightly superiorly. The patient is asked to push back against this force. The test is positive if it elicits pain and/or pops and clicks in the shoulder. It has sensitivity of 78.4% and specificity of 91.5%. Hence, it is useful but not sufficient.

56 What is adhesive capsulitis?

A painful shoulder condition often referred to as frozen shoulder. This may follow an injury, or more commonly a wrist fracture that caused the arm to remain immobilized for several weeks, possibly triggering an autoimmune process, and eventually leading to severe loss of motion.

57 What is the mechanism of adhesive capsulitis?

Inflammation, which “glues” the capsule and surrounding structures into a frozen shoulder.

58 What are the symptoms of adhesive capsulitis?

The most common is shoulder pain, causing a reduced range of motion, both on active and passive movements. Pain and tightness may occur at night and often interfere with activities of daily living, like getting dressed, combing hair, or reaching across a table.

59 How is the diagnosis made?

By history and physical exam. A crucial finding that helps differentiate a frozen shoulder from a rotator cuff tear is the limitation of ROM both on active and passive movements. Conversely, a rotator cuff tear limits active, but not passive movements.

60 What are the elbow’s movements? Range of motion?

The elbow flexes to 150   degrees (allowing us to touch the shoulder with the thumb). It also extends to 0   degrees. Finally, it provides motion to the forearm, making it pronate and supinate to 80   degrees.

61 Is the elbow varus or valgus?

Valgus. With the elbow fully extended, the normal angle is indeed in valgus (cubitus valgus). Fractures, however (especially in children), may cause a varus (gunstock) deformity.

62 What do valgus and varus mean?

This is a very confusing terminology. In orthopedics, valgus indicates an outward angulation of the “distal segment” of a bone or joint, so that it is “twisted away” (i.e., away from the body, or midline of the limb). Conversely, varus indicates its inward angulation (so that it is now twisted toward the body, or midline of the limb). Note that both terms always refer to the direction in which the distal segment of the joint (or bone) is pointing. In fact, when referred to as a bone, the bone itself is considered to be the distal segment of the joint. Hence, a varus or valgus deformity of the forearm refers to the arm/forearm joint (the elbow) and not to the wrist. Having said that, a normal elbow is in valgus, because with the joint fully extended (and the palms facing upward) the distal segment of the forearm will point away from the body (or midline of the limb). If you think this is confusing, wait until you see how it applies to the knee exam (see question 213).

63 How do you detect swelling of the elbow?

It depends. Mild swelling can be appreciated as a filling in of the groove between the olecranon and lateral epicondyle. Conversely, moderate to severe swelling causes loss of bony margins on palpation.

64 What is the most common finding of an abnormal elbow?

A flexion contracture. This is the first abnormality to develop and one that often becomes permanent. A common sequela of fracture, elbow flexion contracture also may occur in subjects who have to keep their elbow flexed for long periods, like long-distance truck drivers.

65 What is “tennis elbow” (lateral epicondylitis)?

The most common elbow injury: 10   times more frequent than medial epicondylitis (i.e., “golfer’s elbow”), and occurring in 50% of tennis players. The mechanism is overuse wear-and-tear of the proximal attachment of the extensor/supinator muscles of the forearm, typically affecting a 30- to 50-year-old recreational athlete. It usually responds to rest and conservative measures.

66 Other than tennis, does anything else cause tennis elbow?

Any activity that requires repetitive contraction of the wrist extensors. This includes hammering nails, picking up heavy buckets, or pruning shrubs. The repeated hyperextension required by these movements eventually results in enthesitis of the wrist extensors (i.e., inflammation of the enthesis, that is, the site of tendinous attachment to the bone—actually a more degenerative than inflammatory process. Hence an enthesopathy). With time, this leads to tendineal microtears, subsequent fibrosis, and, ultimately, tissue failure.

67 What is the presentation of tennis elbow?

The classic one is lateral elbow pain, aching, gradual, at times nocturnal, but typically worsened by hyperextension of the wrist. Pain may eventually spread down the forearm, possibly reaching the back of the middle and ring fingers. Forearm muscles also may feel tight and sore. Activities of daily living (like picking up a cup of coffee or a gallon of milk) often precipitate it. Diagnosis is made by demonstrating point tenderness over the lateral epicondyle, elicited by grasping and worsened by forced hyperextension of the wrist or by supination against resistance. Flexion or pronation is instead normal (see Golfer’s Elbow). Range of motion is normal too, although there may be a weakened grip on the affected side. A helpful maneuver is the chair raise test, where the patient stands behind a chair and attempts to raise it by placing the hands on top of the chair back, and then lifting. This typically elicits pain over the lateral elbow.

68 What is “golfer’s elbow” (medial epicondylitis)?

An overuse injury to the proximal attachment of the flexor/pronator muscles of the forearm, commonly seen in the dominant elbow of a golfer. Its mechanism is similar to that of lateral epicondylitis, but less common since wrist flexors are stronger and less likely overstressed (see Fig. 21-3).

Figure 21-3 Testing for lateral epicondylitis (left) and medial epicondylitis (right).

(From Mellion MB: Office Sports Medicine, 2nd ed. Philadelphia, Hanley & Belfus, 1998.)

69 What is the cause of golfer’s elbow?

Overuse tendinopathy (i.e., the same cause of its more lateral counterpart, “tennis elbow”). This results not only from recurrent swinging of a golf club, but also from any racquet sport that requires repeated flexion at the wrist and pronation. Hence, medial epicondylitis can affect tennis players who hit their forehand with heavy topspin (or serve poorly), bowlers, archers, weight lifters, various throwers, lumberjacks (who chop wood with axes or run chain saws), and any individual who frequently uses screwdrivers or hammers. Repetitive stress at the musculotendinous junction (and at its insertion over the medial epicondyle) eventually leads to acute tendinitis or chronic tendinosis, tendineal microtears, fibrosis, and tissue failure. One half of golfer’s elbows also develop ulnar compressive neuropathy, in or around the medial epicondylar groove.

70 What is the presentation of golfer’s elbow?

Very similar to that of cubital tunnel syndrome. Athletes usually complain of aching pain over the medial epicondyle, triggered by the acceleration phase of throwing. Nonathletes report discomfort even while shaking someone’s hand. With more advanced disease, there also may be grip weakness. Diagnosis is made by demonstrating point tenderness over the medial epicondyle, worsened by forced flexion of the wrist against resistance. There also may be pain with resisted forearm pronation, and in more protracted cases, with resisted elbow flexion. Yet, ROM of the elbow and wrist is usually normal. Tinel’s sign should be tested over the ulnar nerve, just to rule out ulnar neuropathy. In fact, ulnar symptoms can occur in 25–50% of patients, with occasional/constant numbness and/or tingling radiating down into fourth and fifth fingers.

71 How frequent is ulnar nerve entrapment at the elbow?

Very frequent. In fact, most ulnar nerve entrapments do indeed occur at the elbow (i.e., in the cubital tunnel, which is located on the medial side of it—hence, the term, cubital tunnel syndrome). This is the second most common compressive neuropathy after carpal tunnel syndrome, affecting men 3–8   times more often than women.

72 What are the causes of cubital tunnel syndrome?

Various. Swelling of the elbow joint, bony spurs, constricting fascial bands, or trauma to the ulnar notch have all been implicated. Work also may be a factor, especially when causing repetitive elbow flexion and extension (such as pulling levers, reaching out, or lifting) or protracted direct pressure on the joint (like leaning on the elbow while sitting at a desk, or during a long drive). The ulnar nerve also can be damaged from a direct blow to the cubital tunnel. Still, a clear-cut relationship with occupational activities is not well defined.

73 What is the presentation of cubital tunnel syndrome?

Similar to that of medial epicondylitis (golfer’s elbow), ranging from a vague discomfort at the elbow to frank hypersensitivity, intermittent at first and more constant as time goes by. Exam reveals pain and tenderness in the cubital tunnel, which may radiate proximally or distally. There also may be sensory changes in the distribution of the nerve, involving the ulnar side of the forearm and extending into the fourth and fifth fingers. Paresthesias also are common, especially after protracted resting upon, or flexion of, the elbow (as when sleeping or talking on the phone). Tinel’s sign can occur over the medial epicondylar groove, but only in 25% of asymptomatic patients. In later stages, there may be weakness of grip and pinch, plus loss of fine dexterity. Intrinsic muscle atrophy and clawing of the fifth finger (Wartenberg sign) are less common.

74 How do you diagnose cubital tunnel syndrome?

Through the elbow flexion test. This is carried out by asking the patient to flex the elbow past 90   degrees, supinate the forearm, and extend the wrist. The maneuver is positive if it reproduces discomfort or paresthesia within 60   seconds. Addition of shoulder abduction may further enhance its yield. Differential diagnosis of cubital tunnel syndrome includes other causes of paresthesias and weakness along the C8–T1 distribution, such as cervical disk disease/arthritis, thoracic outlet syndrome, or ulnar nerve impingement at the Guyon canal.

75 What is olecranon bursitis?

A common inflammation of the bursa overlying the olecranon. This is located over the posterior tip of the elbow, between the skin and proximal aspect of the ulna.

76 How does it present?

Suddenly if due to infection or acute trauma, gradually if due to chronic irritation. The hallmark is posterior elbow swelling, quite demarcated, and presenting as a goose egg over the olecranon. Swelling is fluctuant, often recurrent, and usually painless. Yet, it may be associated with point tenderness over the olecranon, worsened by full flexion or pressure, as when the patient leans on the elbow or rubs it against the table while writing. The area may be warm and red, especially with infection (fever). ROM is usually normal, even though pain at the posterior elbow may limit some functional activities (like writing) and prevent the end-range of elbow flexion.

77 What are the causes of olecranon bursitis?

Many. Given its superficial location, the most common is acute trauma (like falling onto a hard floor) or repetitive microtrauma (recurrent rubbing of the olecranon against a desktop during writing). Less common reasons include infection (via skin abrasion or hematogenous seeding—septic bursitis), inflammation as part of a systemic inflammatory process (rheumatoid arthritis [RA]), and crystal deposition (gout, pseudogout). The last two may present with focal inflammation at other sites.

78 Which finding differentiates infection from other causes of olecranon bursitis?

The definitive one, of course, is a positive gram stain or culture of the fluid aspirated from the bursa. Still, if erythema extends past the margins of the bursa, infection is the most likely cause.

79 How do you tell rheumatoid nodules from gouty tophi?

By palpation: rheumatoid nodules are rubbery (whereas tophi are firm) and either subcutaneous, subperiosteal, or intrabursal (whereas tophi are instead subcutaneous or intrabursal, but never subperiosteal). Still, biopsy or aspiration for monosodium urate crystals remains the test of choice. Note that both rheumatoid nodules and gouty tophi are quite common at the extensor surface of the elbow, as well as in other sites of chronic and repetitive pressure. Yet, only tophi may occasionally drain to the surface, so that urate can be recovered from an ulcer overlying the nodule.

80 What is the carpal tunnel?

A wrist channel, whose floor is formed by the carpal bones and the ceiling by the transverse carpal ligament. Through this tunnel flows the median nerve, bringing sensory fibers to the palmar surface of the first three fingers and to one half of the fourth finger. It also provides a motor branch to the thenar muscles, responsible for thumb opposition. Through the tunnel also pass the flexor tendons, providing the hand and fingers with movements that are crucial for grasping. In the tunnel, the median nerve rests on top of the tendons, just below the transverse carpal ligament.

81 What is carpal tunnel syndrome (CTS)?

An important cause of painful impairment of the hand. It is due to compression of the median nerve at the wrist, resulting in a constellation of typical signs and symptoms. It affects women three times more commonly than men, usually during the third to fifth decades.

82 What is the cause of CTS?

Any condition that narrows the carpal tunnel. A major one is trauma, especially repetitive microtrauma (such as the one of typing, or operating a jackhammer). Other causes simply swell the tissues delimiting the tunnel, through either inflammation or fluid retention. Among these are rheumatoid arthritis, pregnancy, hypothyroidism, and diabetes (the latter also may cause a direct neuropathy of the median nerve). Smoking, obesity, and caffeine often play a predisposing role.

83 What are the symptoms of CTS?

The earliest is paresthesia in the median nerve distribution: thumb, forefinger, middle finger, and one half of the ring finger, but typically not the small finger. The “asleep” sensation is then followed by pain, which may occur during gripping activities, such as sweeping, hammering, or driving. Eventually, pain occurs at rest, and even awakens the patient at night. Hand-shaking (flick sign) can often provide relief. With time, pain and numbness may spread up the arm, into the shoulder, and even to the side of the neck. Eventually, the patient develops weakness (and ultimately atrophy) of the thenar muscles, making thumb opposition increasingly difficult. This interferes with grasping, including driving, holding a phone, or picking up a newspaper.

84 What is the physical exam of CTS?

Once the appropriate history is obtained, two maneuvers are typically carried out: Tinel’s sign and Phalen’s sign (first described by the American orthopedist George S. Phalen, 1911–1998) (see Fig. 21-4).

Figure 21-4 Tinel’s sign (left) and Phalen’s sign (right).

(From the American Society for Surgery of the Hand: The Hand: Examination and Diagnosis, 3rd ed. New York, Churchill Livingstone, 1990.)

85 How do you elicit Tinel’s sign?

By asking the patient to hyperextend the wrist while you tap over the median nerve (i.e., over the carpal tunnel) with either a forefinger or the reflex hammer. The test is positive when it reproduces the symptoms (i.e., a tingling sensation along the distribution of the median nerve).

86 How do you elicit Phalen’s sign?

By having the patient juxtapose the dorsal surfaces of the hands while holding the wrists in hyperflexion for 60   seconds (or less in case symptoms were to occur sooner). This will increase the intratunnel pressure, thus reproducing the tingling. Note that in Phalen’s original definition of CTS, diagnosis was established by one or more of three bedside findings: (1) sensory changes of the hand restricted to the median nerve distribution, (2) a positive Tinel’s, and (3) a positive Phalen’s. Yet, many traditional findings, including Phalen’s, Tinel’s, and the flick sign have low sensitivity and limited or no value. Hence, electrodiagnosis has become so crucial that some third-party payers would now not even compensate claims without it. Nerve conduction studies have good sensitivity and superb specificity (49–84% and 95–99%, respectively).

87 How do you elicit the flick sign?

By asking patients what they do with their hands and wrists when symptoms occur. The response is positive when the patient demonstrates a flicking motion of hands and wrists—as if shaking down a thermometer. Although initially promising, the flick test also has shown limited utility.

88 How valuable is physical exam in confirming the diagnosis?

Not too valuable. Since the classic signs only occur in one half of the cases, other maneuvers have been suggested, such as: (1) assessing sensory loss in the distribution of the median nerve; (2) looking for atrophy of the thenar eminence (which, however, occurs only in long-standing and neglected cases, plus also may result from cervical radiculopathies and polyneuropathies); and (3) testing the strength of the abductor pollicis brevis muscle. Findings most helpful in predicting the electrodiagnosis of CTS (which is the gold standard) are: (1) classic or probable Katz hand diagram results (i.e., tingling that primarily involves the thumb and index and long fingers as opposed to the little finger); (2) hypalgesia in the median nerve territory; and (3) thumb abduction weakness.

89 Who was Tinel?

Jules Tinel (1879–1952) was another product of the superb French medicine of the turn of the century. The son of a medical family, Tinel studied with Troisier, Dejerine, Landouzy, and Netter. Convinced by Dejerine to go into neurology, he eventually became chair at the Salpêtrière in Paris. After serving in World War I, he focused on psychosomatic medicine. During WWII, he took a very active role in the French resistance, for which he was imprisoned and even lost his son, Jacques, killed by the Nazis in the death camp of Dora in Neuhausen. After the war, he worked in the Boucicaut Hospital, until his death of heart failure in 1952.

90 What is the piano key sign?

A sign of rheumatoid arthritis of the wrist, typically due to a synovitis that is stretching ulnar-carpal ligaments and causing dorsal dislocation of the distal prominence of the ulnar head (caput ulnae syndrome). Because of its dorsal subluxation, the ulnar styloid can be pressed volarly on examination, giving the feel of a piano key being pressed down—hence, the name. To elicit it, first stabilize the distal radius with one hand, then grasp the head of the ulna between the thumb and index finger of your other hand. Evaluate freedom of motion, and look for pain or crepitus. Pressing the ulnar head will elicit the piano key sign.

91 What is a common cause of pain on the radial side of the wrist?

De Quervain’s tendinitis. This is a hand-and-wrist disorder caused by entrapment tenosynovitis of the two thumb muscles’ tendons (abductor pollicis longus and extensor pollicis brevis) as they travel through a retinaculum tunnel near the end of the radius. Thickening of the tendons from either acute or repetitive trauma restrains their gliding through the tendon sheath, thus causing the problem. This sort of friction tendinitis is very frequent in day care workers and new mothers, as a result of awkward hand positions while caring for infants (such as repetitive lifting of babies as they grow heavier). Patients present with aching pain on the thumb side of the wrist and at the base of the thumb, usually noticed when forming a fist, grasping, gripping, or turning the wrist. There also may be swelling over the thumb side of the wrist, point tenderness, and at times crepitation and “triggering” (i.e., catching or snapping when moving the thumb—hence, the term “snapping thumb syndrome”). Because of pain and swelling, there also may be difficulties in moving the wrist and thumb, including opposition. Thus the inability to “pinch.” Finally, extrinsic compression of radial branches by the swollen tendon sheath may cause paresthesias on the back of the thumb and index finger. Pain can be elicited by the Finkelstein test.

92 How do you diagnose de Quervain’s tendinitis?

Through the Finkelstein test, first described by the American surgeon Harry Finkelstein (1865–1939). This is performed by placing the thumb into the palm, closing the fingers around it, and moving the hand in ulnar deviation. Stretching of the involved tendon(s) will reproduce the pain.

93 Who was de Quervain?

Fritz de Quervain (1868–1940) was a Huguenot Swiss, who studied in Bern, trained with Kocher and Langhans, and later on became chair of surgery, dean, and rector at the University of Bern. He retired on the eve of WWII and eventually died of acute pancreatitis in 1940. A prolific writer with a keen interest in thyroid diseases, de Quervain was responsible for introducing iodized table salt in the treatment of goiter, a common problem in mountainous Switzerland. He also was a strong proponent of a general approach to the patient rather than an artificial division into specialties. Finally, he was one of the first clinicians to understand that many cases of postoperative pneumonia were in reality pulmonary infarcts. He reported his tendinitis in 1895, as case series of five patients with tender and thickened first dorsal compartments at the wrist.

 94 What is the “intersection” syndrome?

A painful wrist condition that can affect individuals who do repeated wrist actions. Patients present with pain on top of their forearm, about 3   inches proximally to the wrist. This also is the site where the two thumb muscles cross over (i.e., intersect) the two wrist tendons of the extensor carpi radialis longus and extensor carpi radialis brevis, both responsible for extending the wrist. Friction tenosynovitis of the wrist tendons eventually interferes with their smooth gliding in the tendon sheath, causing swelling and redness at the intersection point and a pain that can spread either up along the edge of the forearm or down into the thumb. Crepitus may be present.

 95 How do you differentiate de Quervain’s tendinitis from an intersection syndrome?

Both involve inflammation of the wrist tendons, but the pain has different location: in intersection syndrome, it is over the wrist, at the intersection point , whereas in de Quervain’s tenosynovitis is instead over the hand (i.e., in the de Quervain’s tunnel [along the edge of the wrist and near the end of the radius]). The Finkelstein’s test is positive in de Quervain, but negative in intersection.

 96 What causes the intersection syndrome?

Overuse of the wrist extensor tendons. This causes the tendons to rub against the thumb muscles, as if they were a violin bow, until, like overused strings, they eventually develop friction tendinitis. Predisposing activities are those that make the wrist curl down (and in) toward the thumb. Hence, intersection syndrome is very common in downhill skiers (who have to plant their ski poles deep in powder snow) and also in practitioners of racket sports, weight lifting, canoeing, and rowing. More lowly activities, such as raking leaves against a hard ground or shoveling snow, also can produce stress on the wrist extensor tendons, and thus the syndrome.

 97 What is a wrist ganglion? How is identified?

Ganglions are benign and often asymptomatic fluid-filled cysts, closely associated with an underlying joint or tendon sheath, and usually connected to it by a stalk. They are the most common soft tissue tumors of the hands and wrists and are not occupationally related. They affect women three times more often than men, usually during the second and fifth decades. They tend to be solitary, rarely exceeding 2  cm in diameter. Although generally asymptomatic, they may present with pain, paresthesias, weakness, and limitation of motion. They can involve almost any joint of the hands and wrists, although their most common forms are: (1) the dorsal wrist ganglions (60–70%), (2) the volar wrist ganglions (20%), and (3) the distal interphalangeal ganglions of the flexor tendon sheath (10–12%). The cysts are smooth walled, translucent, and white. They have a fluctuant swelling that moves with the involved tendon and a mucinous content that is rich in hyaluronic acid, albumin, globulin, and glucosamine.

 98 What is the cause?

Unknown, although repetitive injuries (like playing tennis or golf) may have a predisposing effect. According to one theory, wrist ganglions are formed whenever wear-and-tear of a joint or tendon sheath allows fluid to escape into a cyst. This also would explain why ganglions have a stalk. Over time, the cyst grows large, since fluid can only enter it but not exit it (one-way valve).

 99 What are the typical wrist findings of rheumatoid arthritis?

An early finding is swelling of the extensor carpi ulnaris tendon. Later findings include protrusion and instability of the distal ulna, due to laxity of the radial ulnar ligaments. Finally, in more advanced disease the carpal rows sublux toward the dorsal side, causing a bayonet deformity.

100 What is Guyon’s canal syndrome?

It is a compression neuropathy that affects the ulnar nerve as it travels through a wrist tunnel called the Guyon’s canal. Note that the ulnar nerve can be compressed either at the wrist (in the Guyon’s canal) or at the elbow (in the epicondylar groove). Given its more superficial position at the elbow, the most common site of injury is indeed repetitive elbow pressure, such as leaning on it while working or driving. Compression in Guyon’s canal requires instead repetitive pressure on the palm, often because of excessive wrist and hand twisting. Heavy gripping can do it, too, as in the case of cyclists or weight lifters, but also jackhammer operators and patients on crutches. Finally, fracture of the hamate bone can cause Guyon’s canal syndrome in golfers who club the ground instead of the golf ball, or baseball players during batting.

101 What is the anatomy of the Guyon’s canal?

The floor is formed by two bones (pisiform and hamate), and the ceiling is provided by the ligament between them. Both the ulnar nerve and artery run through the canal. After emerging from under it, the nerve divides into a sensory branch (that supplies the fourth and fifth fingers) and a motor branch (that supplies instead the interosseous muscles, the adductors pollicis, and the deep head of the flexor pollicis brevis). Note that the hamate bone provides the medial side of Guyon’s canal. This includes a small hook-shaped spur (the hook of hamate) that serves as attachment for several wrist ligaments. Ulnar compression in the canal is usually caused by either arthritis of the hook or its fracture. Still, this entrapment is much less common than that of CTS. Occasionally, both conditions may coexist.

102 What are the symptoms of ulnar compression?

The earliest is paresthesias, affecting the fifth finger and the ulnar half of the fourth. As in CTS, symptoms usually occur during the early morning hours, often awakening the patient. There also may be difficulty in opening jars or turning doorknobs, and in opposing the thumb. Later findings include frank pain, followed by atrophy and weakness of the interosseous muscles. Ultimately, there may be clawing of the fourth and fifth fingers with severe intrinsic muscle wasting.

103 What are the symptoms of median nerve compression?

Pain and numbness along the thumb, index and middle fingers, and radial half of the ring finger.

104 What is the nerve supply of the hand?

See Figure 21-5.

Figure 21-5 Cutaneous innervation from the median nerve (white area), ulnar nerve (light shading), and radial nerve (dark shading).

(From Concannon MJ: Common Hand Problems in Primary Care. Philadelphia, Hanley & Belfus, 1999.)

105 How can you differentiate ostheoarthritis from rheumatoid arthritis (RA)?

By the pattern of involvement in the small joints of the hand.

106 Describe the typical deformities of rheumatoid arthritis

107 What is a trigger finger?

The most common entrapment tendinitis, 20   times more frequent than de Quervain’s. It is a painful condition characterized by locking of the affected finger in flexion (Fig. 21-6). This is usually due to tenosynovitis of the flexor tendon to the digit (hence, its term of flexor tendinitis) resulting in palpable swelling of the tendon itself, often nodular. Alternatively, it may be due to inflammation and swelling of the sheath surrounding the tendon. Either way, the tendon becomes unable to glide smoothly through the sheath. Hence, whenever the patient forces the finger to bend, there may be a painful snap as the tendon passes through the thickened portion of the sheath into its final flexed position. Then, given its inability to glide back into the sheath, the tendon will stay flexed. With more vigorous attempts, either by increased force from the finger extensors or by application of an external force (such as use of the other hand), the finger will eventually extend, usually with another (and often painful) snap as the tendon passes back through the thickened portion of the sheath—like a trigger being pulled and released. Yet, in more severe cases the finger will remain locked. Women are more affected than men, especially musicians, writers, gardeners, and hobbyists, since all these occupations require repetitive gripping actions. Treatment varies, depending on the severity of the condition, ranging from rest, to medications, to surgery.

Figure 21-6 In trigger finger, the fibrous flexor sheath surrounding the flexor tendon is thickened. Fibers of the flexor tendon bunch up into a nodule that is sometimes palpable. This nodule has difficulty in sliding through the fibrous flexor sheath during movements of the finger.

(From Mehta AJ: Common Musculoskeletal Problems. Philadelphia, Hanley & Belfus, 1997.)

108 What are the physical findings of a trigger finger?

There is usually tendineal tenderness over the palmar side of the MCP joint. There also may be a palpable nodule and a palpable (and painful) click upon the finger’s flexion/extension at the MCP.

109 What other typical deformities can be seen in the hand?

Figure 21-7 Mallet finger. The extensor tendon is usually torn near its insertion. Occasionally, a small ligament of the distal phalanx is avulsed by the tendon. The DIP joint cannot be actively extended.

(From Mellion MB: Office Sports Medicine, 2nd ed. Philadelphia, Hanley & Belfus, 1998.)

110 What are Heberden’s nodes?

They are painless nodules on the distal interphalangeal joints (Fig. 21-8). These may involve one or more fingers, but typically spare the thumb. The overlying skin is normal, and the nodes are hard, 2–3   mm in diameter, not interfering with fingers’ movement, twin in presentation, and typically located on the lateral and medial dorsal surface of the DIP (if affecting the PIP, the nodes are instead called Bouchard’s). Both reflect localized osteoarthritis. Hence, they are more common in the elderly. Involvement of a single joint is more prevalent in men, whereas multiple involvement is more frequent in women, where the condition is usually postmenopausal and hereditary.

Figure 21-8 Patients with degenerative joint disease of the hands can present with Heberden’s nodes (arrows). These nodules represent osteophytes at the DIP joint.

(From Concannon MJ: Common Hand Problems in Primary Care. Philadelphia, Hanley & Belfus, 1999.)

111 Who were Heberden and Bouchard?

112 What are Haygarth’s nodes?

Nodes very different from Heberden’s and Bouchard’s, since they are not degenerative but inflammatory. Hence, they present with other signs of inflammation, such as flushing of the overlying skin, increased temperature, thickening of the joint capsule, fluid in the cavity (in part responsible for their fusiform swelling), and limitation of movement. Contrary to Heberden’s, Haygarth’s nodes can be painful and tender. They are typical of RA, affecting proximal PIP joints rather than DIP (which RA never involves). Thus, they resemble more Bouchard’s than Heberden’s. Subcutaneous nodules are very common in RA, having been found on the extensor surfaces of upper extremities (primarily the elbows, but also fingers), knees, ankles, and occiput. Yet, they are not exclusive of RA, but can occur in other rheumatic disorders, like lupus, sarcoid, rheumatic fever, syphilis, tuberous xanthomatosis, and granuloma annulare.

113 Who was Haygarth?

John Haygarth (1740–1827) was an English physician from the city of Bath. A Cambridge graduate with a penchant for epidemiology, he eventually set out to study the diseases of the ancient city of Chester, including the value of isolation in infectious diseases and the usefulness of smallpox as a method of immunization. His eponymous work on rheumatism and rheumatic fever was eventually published in 1798, upon his return to Bath.

114 What are tophi?

They are deposits of uric acid (tophus is Latin for a calcareous deposit from springs, tufa). These can occur over the ears, feet, and hands of gouty patients. In the hands, they are pathognomonic of the disease (Fig. 21-9), even though they often get confused for rheumatoid nodules.

Figure 21-9 A, Gouty tophus deposition on the volar aspect of the long finger (arrow). This patient has severe gouty arthritis with multiple tophaceous deposits. B, Large tophus over the metacarpophalangeal joint of the dorsal long finger (arrow).

(From Concannon MJ: Common Hand Problems in Primary Care. Philadelphia, Hanley & Belfus, 1999.)

115 What are Janeway’s lesions?

They are small, flat, nontender, erythematous, or hemorrhagic macules of palms or soles. Like Osler’s nodes (which are instead swollen, tender, raised, pea-sized nodules of finger pads, palms, and soles), Janeway lesions are seen in bacterial endocarditis. In fact, before the introduction of antibiotics they occurred in 40–90% of endocarditis patients, but nowadays only 10–23% of cases have them. They also can be seen in SLE, bacteremia without endocarditis, gonococcal sepsis, and marantic endocarditis. They represent either septic emboli or sterile vasculitis, triggered by immune complexes.

116 Who was Janeway?

Edward G. Janeway (1841–1911) was a student of Austin Flint, whom he followed to Bellevue Hospital Medical College in New York, where he established himself as one of the first full-time consultants in American medicine. He had an interest in public service, eventually becoming Health Commissioner for New York and founder of its first Infectious Disease Hospital.

117 What is the Pachuco mark?

It is a cross-like tattoo (made with dots rather than lines), which during the 1970s used to be very common over the anatomic snuffbox of intravenous drug abusers (the snuffbox is the hollow space on the radial aspect of the wrist that can be seen when the thumb is fully extended). There it provided a sort of identification card for the drug-dealing world, easily visible upon handshaking. “Pachuco” is actually a Spanish-American term, possibly an alteration of payuco (yokel, rustic). The expression has been variously used to identify a Mexican-American youth or teenager, especially one who dresses in flamboyant clothes and belongs to a neighborhood gang.

118 What is the shape of the hand in acromegaly?

Spade-like. Due to enlargement of the distal parts of the body—acromegaly’s defining feature.

119 What is arachnodactyly?

It is the spider-like fingers of patients with Marfan’s. Described in 1896 by the homonymous Frenchman in a 5-year-old patient, the term arachnodactyly was actually coined 6 years later by Achard. The fingers are thin and long, resembling “the bent legs of a spider.” To test for it, use the Marfan’s thumb sign: ask patients to open their hands and cross their thumbs over their palms as far as possible; then ask them to fold the fingers across the thumb and make a fist. The test is positive if any part of the thumb sticks out beyond the ulnar surface of the fist. The sign is typical of Marfan’s, but also can occur in other conditions of joints’ hypermobility, like Ehlers-Danlos.

120 Who was Marfan?

Antoine B. Marfan (1858–1942) was a French pediatrician. The son of a provincial medical practitioner, Marfan contributed to several areas of medicine, including the astute observation that tuberculosis acquired before age 15 seems to provide a unique resilience to patients (which inspired Calmette to develop his bacillus Calmette-Guérin [BCG] vaccine). Very active in public health and service, Dr. Marfan also had a passion for literature and arts, enjoying concert music and trips to Italy, where he was particularly fond of Venetian paintings. Among his many friends was Emile Broca, of whom he wrote a biography. Upon his death, he left most of his fortune to the Society for the Preservation of Infants against Tuberculosis, which he had helped to create.

121 What is a short fourth metacarpophalangeal bone?

An unusually short and inwardly dimpled fourth knuckle. This is usually seen in patients with pseudohypoparathyroidism and Turner’s syndrome, but even in 10% of normal individuals.

122 What is the significance of calluses and abrasions on the dorsal aspect of the fingers?

They are an important clue to bulimia, due to trauma by the teeth during the induction of vomiting.

123 What is the anatomy of the first carpometacarpal (CMC) joint?

The first CMC is the basal joint of the thumb, the one that articulates its metacarpal bone to the trapezium of the wrist. It is a small joint for man, but a giant one for mankind, since it allowed our ancestors to oppose their thumb, which they then used to grasp objects and create “tools,” which they then used to whack other fellow hominids, thus taking the first and fundamental step in the evolution of our species—one that eventually gave us the name of Homo faber (i.e., the one who creates). Or whacks.

124 What is CMC squaring?

It is God’s answer to the evolution of the thumb. And since God has a sense of humor, She or He eventually thumbed Her or His nose at us by creating osteoarthritis (degenerative joint disease [DJD]). Carpometacarpal (CMC) squaring is an often-overlooked deformity of the base of the thumb, typical of DJD of the first CMC joint—a common problem, especially among women. The dominant hand is the one most affected, with onset typically after age 40. Initially, the thumb appears unremarkable, but as the disease progresses the CMC subluxes dorsally, starting to protrude proximally to the snuff box (thus creating a CMC squaring, or mushroom deformity). With time, the CMC becomes even more subluxated and stiff, and as a result the thumb metacarpal joint becomes fixed in adduction (i.e., tucked into the palm). As this happens, the only way for patients to lift the thumb off their palms (so that they can grasp) is by hyperextending the MCP joint itself. Eventually, this becomes so painful that the thumb remains frozen into a swan-neck deformity.

125 What is the presentation of CMC squaring?

The hallmark is pain, first on activity and then even at rest. It is localized at the base of the thumb and usually moderate in intensity, even though at times it may be incapacitating. Tenderness on palpation, crepitus on rotation, and joint limitations in fine motor skills also are typical. Grasp and proximal thumb-index pinching may be limited, and so are activities of daily living that rely on these movements, like using scissors, opening jars, or operating a can opener.

126 What is a sausage digit?

It is the inflammation of a whole digit, giving it a diffusely swollen appearance. A sausage-shaped swelling of a toe or finger (i.e., dactylitis, from the Greek daktulos, finger) can be quite painful. When unassociated with trauma, it is usually caused by tenosynovitis, and often periostitis as well as arthritis. It is frequently seen in seronegative arthritis, typically psoriatic, but also sarcoid–related. In psoriasis, it is often associated with pitting of the fingernails (see Chapter 3, questions 20–22.

127 What is a telescoped digit?

A finger that on exam can be moved in and out like a telescope. A telescoped digit (usually the PIP) reflects extreme joint destruction.

128 Describe the Bunnell-Littler test

It is a test for patients with difficulty flexing the PIP joint, since it can differentiate interosseous tightness from capsular contraction. To carry it out, ask patients to hold the MCP joint in a few degrees of extension, and then flex their PIP joint. If unable to do so, have them place the MCP in flexion, and then reattempt PIP flexion. Those with capsular contraction will not flex the PIP at all, whereas those with interosseous tightness will flex it by using the second maneuver (Fig. 21-10).

Figure 21-10 Bunnell-Littler test. A, To distinguish between intrinsic muscle tightness and joint contracture, the metacarpophalangeal joint is extended. B, The proximal interphalangeal joint is then moved into flexion.

(From Shankar K, Nayak N, Dowdell BC: Commonly used clinical tests and gait abnormalities. Phys Med Rehabil State Art Rev 10:631–652, 1996.)

129 What is a stiff hand syndrome?

It is thickening of the hands’ skin, which becomes waxy and tightened. Also called diabetic hand syndrome (or diabetic cheiroarthropathy, from the Greek kheir, hand), this eventually causes limitation of finger movement, with varying degrees of fixed flexion of the PIP joints. As a result, patients become unable to fully extend fingers or press their palms flat together (prayer sign). It is exclusively seen in protracted type 1 or type 2 diabetes, often paralleling microvascular injury.

130 What is a paronychia? A felon?

131 Can the fingers provide a clue to a patient’s sexual orientation?

Maybe. In a recent Nature study, researchers from Berkeley suggested that the length of the index and ring fingers might indeed statistically predict sexual orientation. According to their theory, womb exposure to high levels of androgens would shorten the index fingers of males, causing them to become a little smaller than the ring fingers. Women would have instead indices that are either longer or, at least, equal to their ring fingers. Researchers carried out their study by going to street fairs in San Francisco and persuading more than 700 fairgoers to have copies of their hands made on portable photocopying machines. They also inquired about family histories and sexual orientations. By doing so, they discovered that gay men have indices even shorter than those of straight men. And, more interestingly, that gay men also have a much greater number of older brothers. And so their theory speculates that womb exposure to even higher levels of androgens (as in cases of many preceding male siblings) would paradoxically induce a gay sexual orientation. This hypermasculinization would be the reason why, according to the same researchers, gay men often have longer genitalia and subtle differences in brain structure. It would also explain the finger pattern of gay women, which is very similar to that of straight men (i.e., indices shorter than ring fingers), similarly related to high womb exposure to androgens. What is really interesting, though, is that the role of the middle finger hasn’t yet been clarified. Maybe in a future study. On a partially related note, Romans-of-old also believed in connections between fertility and fingers—especially the fourth finger of the left hand, which they thought linked to the heart through a unique nerve. That is why they used to “chain” it at time of marriage by putting a ring around it, as a sign of enslavement of both heart and passions. And inside that ring they engraved the words: “Ubi Tu Gaia, Ego Gaius; Ubi Ego Gaius, Tu Gaia” (When you are happy, I am happy; and when I am happy, you are happy”). In other words, reciprocal tolerance is key to a successful marriage—good advice for all times.

132 How do you assess the cervical spine?

By inspecting for deformities and abnormal posture. Also by palpating for tenderness over the spinous processes, trapezius, scaleni, and sternomastoids.

133 How do you evaluate its ROM?

By asking patients to lift the head back (extension), touch chin to chest (flexion), chin to each shoulder (rotation), and finally touch each ear to the corresponding shoulder, but without raising the shoulder (lateral bending).

134 How do you diagnose temporomandibular joint (TMJ) arthritis?

By palpating the tragus of the ear and then inserting your index finger in the auditory canal while the patient is opening and closing the mouth. This allows you to assess for crepitus, as well as joint swelling and smoothness of articular motion. Finally, watch the mandibular tract during mouth opening: normally it is directed downward. Any jaw deviation to one side would reflect instead an abnormal TMJ.

135 What is torticollis?

An involuntary rotation of the head to one side. Due to spasm of the cervical musculature.

136 What is occipital neuralgia? What are its findings?

Occipital neuralgia results from impingement of the occipital nerve as it exits the skull at the occipital notch. Its symptom is pain, radiating from the occiput to the vertex of the head. It can be reproduced by pressure over the exit point of the occipital nerve.

137 What is spinal stenosis? How is it classified?

It is a narrowing of the spinal canal, nerve root canals, or intervertebral foramina. Due to degenerative changes of the spine (spondylosis, osteophytes, facet hypertrophy), disks (bulging, herniation), or ligamentum flavum (hypertrophy). It usually affects the cervical or lumbar segments (rarely the thoracic), eventually causing compression of spinal cord or terminal filaments in the caudal sac (cauda equina). It is common, affecting 5/1000 Americans older than 50.

138 What are the findings of cervical stenosis?

The most typical are those of cervical radiculopathy, with or without myelopathy (i.e., spinal cord dysfunction). This usually involves the lower cervical spine (C5–T1), causing radiating arm pain, with numbness and paresthesias in the involved dermatomes. Occasionally, there may be associated weakness in the muscles supplied by the compressed root and changes in reflexes. Fine motor activities (like writing or typing) become difficult, too, and so does the ability to grip and let go of objects. If the upper cervical spine is affected, there also may be weakness and wasting of deltoid and shoulder muscles. In contrast to mechanical neck pain (which starts in the neck and may spread to the upper back or shoulder, but rarely extends below it), pain from cervical radiculopathy usually spreads farther down the arm. If stenosis is significant, the patient may not only develop finger numbness/tingling, but also signs and symptoms of myelopathy, such as clumsiness and difficulty walking (due to a spastic gait with loss of proprioception). In the most severe cases, there may be sphincter dysfunction, with loss of bowel and bladder control. On exam there will be “long-tract signs,” such as hyperreflexia and clonus. Knowledge of cervical nerves and their distribution is crucial for examining the hand, elbow, shoulder, and head.

139 List sensory distribution, reflexes, and motor innervation of cervical spinal roots

See Table 21-2.

140 What is the most common type of spinal deformity?

It is adolescent idiopathic scoliosis, a strongly familial condition of unknown etiology.

141 Describe the difference between scoliosis and kyphosis

142 How is scoliosis appreciated?

By running your finger down the patient’s vertebral spine. If scoliosis is present, the finger will follow the spine right and left along its primary and secondary curvatures.

143 What is Sprengel’s deformity?

A congenital elevation of the shoulder, described in 1891 by the German surgeon Otto Gerhard Karl Sprengel. It results from partial descent of the scapula and produces an asymmetric appearance of the shoulders and upper back. It can be associated with webbing of the neck.

144 What is the significance of tenderness over the spinous process(es)?

It suggests pathology of the vertebral body. It is demonstrated by striking your fist at each spinal level, or by firmly palpating over each spinous process. It is highly suggestive of underlying bony disease, such as compression fracture, infection, inflammation (as in seronegative spondyloarthropathy), or tumor.

145 How do you measure chest expansion?

Place a tape measure around the chest at the nipple line; ask the patient to first inhale to forced maximal inspiration and then exhale forcefully. The difference in circumference between maximal inspiration and expiration is the chest expansion, normally 5  cm (see Chapter 13, questions 60, 61, 152, and 153).

146 What is winging of the scapula? How is it demonstrated?

“Winging” refers to protrusion of the scapula from the chest wall. This can be accentuated by having the patient place both hands on a wall and then push outward.

147 What are the causes of scapular winging?

Seven muscles attach the scapula to the chest wall and help maintain its control. Of these, the serratus anterior and the trapezius are the most important. A winging scapula is usually associated with partial or complete paralysis of the serratus anterior, secondary to palsy of the long thoracic nerve (strenuous sport/activity, direct trauma, surgical error, and infection). Less common causes include weakness or paralysis of the trapezius, and various muscular disorders, such as spinal muscular atrophy and muscular dystrophy.

148 What are the consequences of scapular winging?

They are not merely aesthetic, since the compensatory muscular activity required to improve shoulder stability often leads to secondary pain and spasm, plus tendinitis around the shoulder.

149 What are the normal movements of the lumbar spine?

It can flex forward and laterally, and it can extend.

150 What is Schober’s test?

It is a bedside assessment of lumbar spine flexibility. It measures the degree of lumbar forward flexion, as the patient bends over while attempting to touch the toes (Fig. 21-11). It is carried out as follows: with the patient standing up straight, draw a line at the level of the posterior iliac spine. This corresponds to L5/S1 (i.e., the dimples of Venus, DV). Place a mark on the spine 5  cm below this line and another 10  cm above the line, so that the distance between the two is 15   cm. Then instruct the patient to touch his or her toes (i.e., to maximally flex forward the lumbar spine). If the increase in distance between the marks is <5   cm, the patient has reduced lumbar flexion—an early sign of ankylosing spondylitis in young individuals and degenerative disease in older ones.

Figure 21-11 Schober’s test.

(From Mellion MB, Walsh WM, Shelton GL: The Team Physician’s Handbook, 2nd ed. Philadelphia, Hanley & Belfus, 1997.)

151 How valid is Schober’s test?

It correlates with x-ray findings in measuring progressive loss of spinal motion. Hence, it allows for serial evaluation of progressive disease.

152 How can relative leg length be assessed?

Stand behind the patient, who, in turn, stands with the feet together and knees extended. Place your hands on the iliac crests. The relative height of each hand provides an assessment of relative leg length. Note, however, that this test is also influenced by scoliosis and relative pelvic tilt.

153 What are the symptoms of spinal (lumbar) stenosis?

The classic one is bilateral sciatalgia with neurogenic claudication (low back pain radiating down the lateral aspect of the leg, presenting at time with paresthesias).Since this is due to neurologic compression rather than arterial insufficiency (which causes instead true claudication), the pain will not be exacerbated by biking, uphill ambulation, or lumbar flexion. Instead it will be triggered by walking (especially downhill) and relieved by rest. It also is relieved by sitting, lying supine instead of prone, squatting, lumbar flexion, forward bending, but not standing. In fact, standing exacerbates it.

154 How are radicular symptoms reproduced in patients with spinal stenosis?

By asking the patient to either extend maximally the lumbar spine or flex it laterally.

155 What are the physical findings of spinal stenosis?

Very limited. Exam is usually normal and generally unhelpful. The Lasègue test is often negative. The most common findings are wide-based gait, abnormal Romberg, thigh pain following 30   seconds of lumbar extension, and neuromuscular abnormalities.

156 What is the stoop test?

A maneuver that helps separate neurogenic from vascular claudication. When pain occurs, patients with vascular claudication sit down to rest, whereas those with pseudoclaudication attempt to keep walking, either “stooping” or flexing the spine to relieve the stretch on the sciatic nerve.

157 What is the cauda equina syndrome?

A less common presentation of spinal stenosis. In addition to bilateral sciatica and lower extremity weakness, there is perineal/perianal anesthesia in 60–80% of patients, and bowel/bladder dysfunction in 90%. A cauda equina syndrome can be a surgical emergency.

158 What is the Lasègue test? How is it performed?

Lasègue is the straight-leg raising (SLR) test (Fig. 21-12), a maneuver aimed at detecting lumbosacral nerve root irritation/compression, as in patients with disk prolapse and sciatica. To carry it out:

Figure 21-12 Lasègue (straight-leg raise) test.

(From Shankar K, Nayak N, Dowdell BC: Commonly used clinical tests and gait abnormalities. Phys Med Rehabil State Art Rev 10:631–652, 1996.)

159 What is the significance of a positive straight-leg raising test?

It indicates nerve root impingement, usually by a herniated disk. It has high sensitivity (91%) but low specificity (26%), thus limiting its diagnostic accuracy. The “crossed” straight-leg raising test has instead low sensitivity (29%) but high specificity (88%). Hence, use them together.

160 What is the “crossed” straight-leg raising test?

The eliciting of pain on the affected side as a result of SLR testing on the unaffected side. It reflects severe root irritation. It has higher specificity for disk herniation than the standard SLR.

161 How do you perform the “reverse” straight-leg raising test?

With the patient lying prone, extend the leg at the hip and the knee. Ipsilateral pain in the anterior thigh would indicate upper lumbar root disease, a less common site of radiculopathy. The maneuver also is called the prone SLR test, or the femoral nerve stretch test, since it does put tension on the femoral nerve and its roots.

162 What is the “distracted” straight-leg raising test?

It is an SLR maneuver carried out while the patient is unaware of its being performed. To do so, have the patient sitting rather than recumbent. Then straighten the affected leg at the knee (i.e., do the SLR) while pretending to examine the foot for some unrelated reason—for example, during a Babinski maneuver, or sensory/motor testing, or pulse checking. Patients with organic pain will be positive on both standard and distracted SLR tests. Conversely, patients with nonorganic back pain (malingerers or psychosomatics) will only be positive on standard SLR.

163 How else can one separate organic from nonorganic back pain?

By the Waddell’s signs. In 1980, Waddell et al. reported eight signs (referred to as behavioral signs) that in a prospective study of 26 findings in 350 patient evaluations were consistently capable of identifying non-organic back pain (Table 21-3).

Table 21-3 Waddell’s Signs

* The predictive value is greatly improved when three or more positive signs are present.

(Adapted from Waddell G, McCulloch JA, Kummel E, et al: Nonorganic physical signs in low-back pain. Spine 5:117?125, 1980; and from Main CJ, Waddel G: Behavioral responses to examination: A reappraisal of the interpretation of nonorganic signs. Spine 23:2367?2371, 1998.)

164 Who was Lasègue?

Ernest-Charles Lasègue was a French internist (1816–1883), who, after contemplating a career in philosophy, got convinced by a mesmerizing lecture of Trousseau to become instead a physician. After struggling in medical school (he shared a room at the Latin Quarter with Claude Bernard, often wasting rent money on experimental guinea pigs and rabbits), Lasègue became Trousseau’s favorite student and close collaborator, eventually delivering in 1867 his eulogy—one of the finest in French language. He himself died at 67 of diabetic complications. A beloved teacher and prolific writer, Lasègue had a special interest in psychiatry, especially psychosomatic diseases. In fact, it was his desire to develop tests and maneuvers that could trap malingerers that eventually led to the discovery of the homonymous sign. As a person, Lasègue was witty, empathetic, and a strong supporter of arts and humanities (in defending a liberal education, he compared the time spent on humanities to the time spent by a soldier polishing his armor). Pierre Astruc relates how Lasègue discovered his homonymous sign:

Still, the sign did not appear in Lasègue’s Considération sur la sciatique. It was only years later that his pupil J.J. Forst put the sign on record.

165 What is low back pain?

A problem that afflicts two thirds of all adults at some point in their lives. In fact, it is the second most common complaint in ambulatory medicine, the third most expensive disorder in health care costs (after cancer and heart disease), and the number one cause of work-related disability in the United States. It also is the most common reason for emergency room evaluation. A precise pathoanatomic diagnosis, however, can only be found in one fifth of the cases.

166 What are the causes of low back pain?

Other than musculo-ligamentous injuries, the most common cause is age-related degenerative disease of intervertebral disks and facet processes (DJD), resulting in a nerve root syndrome. Spinal stenosis, spinal degeneration, and cauda equina syndrome are other possibilities.

167 What is a nerve root syndrome?

A painful radicular syndrome that can be due to nerve root impingement, but also simple inflammation or irritation (which explains why it may respond to conservative therapies without necessarily requiring surgical decompression). It is common, occurring in 1–10% of the population.

168 What are the causes of nerve impingement?

Various degenerative manifestations of the intervertebral disk. From mild to worse, these include bulging (where the annular fibers are still intact), protrusion, extrusion, and finally sequestration (where fragments of disk break off from the nucleus pulposus).

169 What is the most common site of disk herniation?

The L5–S1 interspace. Due to thinning of the posterior longitudinal ligament as it extends caudally.

170 What is sciatica?

Neuralgia of the sciatic nerve, usually due to lumbar disk disease.

171 In a nerve root syndrome, can you separate impingement from inflammation/irritation?

172 What are the physical findings of patients with low back pain?

They vary from patient to patient. Focus your exam on:

Table 21-4 Functional Muscle Testing

173 What are the physical findings of patients with a true herniated disk?

There may be no findings at all, except for a positive SLR test. Classic presentation, however, includes numbness in the dermatomes corresponding to the disk involved, with motor weakness and reflex loss. Note that herniated disks have different presentations depending on location:

174 What are musculoskeletal pain syndromes?

Syndromes that produce low back pain, like fibromyalgia and myofascial pain. The former is pain and tenderness on palpation of 11/18 localized areas (trigger points, one being in the low back), plus generalized stiffness, fatigue, and muscle ache. Myofascial pain is instead loss of ROM in the involved muscle groups plus tenderness over trigger points. Pain radiates along the distribution of a peripheral nerve and is relieved by stretching of the involved muscle group.

175 What are the other skeletal causes of low back pain?

176 What is the Trendelenburg’s sign?

A sign of weakness of the gluteus medius. This originates on the ilium (between the anterior and posterior gluteal lines), eventually terminating on the lateral surface of the greater trochanter. Its contraction pulls the two insertion sites toward one another, thus elevating the opposite side of the pelvis. This typically occurs when the subject stands on one leg: contraction of the gluteus medius of the weight-bearing limb prevents the pelvis from tipping toward the opposite (and unsupported) side, thus keeping it level. When the gluteus medium is weak, the contralateral hemipelvis tips down, the buttock sags, and the unsupported leg hangs lower (positive sign) (Fig. 21-13).

Figure 21-13 Trendelenburg’s sign.

(From Goldstein B, Chavez F: Applied anatomy of the lower extremities. Phys Med Rehabil State Art Rev 10:601–630, 1996.)

177 How do you elicit it?

Stand behind the patient, and look at the dimples of Venus (i.e., the dimples over the sacroiliac joints). In a patient who is standing upright, with the feet together and weight evenly distributed between the legs, the two DV should be symmetric and at the same level (and so should the two iliac crests and the two buttocks). Then ask the patient to lift one foot off the ground and stand on only one leg, with the other flexed to 90   degrees. Ask him/her to maintain this stance for at least 30   seconds, so as to induce fatigue. In a normal subject, there should be an elevation of the unsupported hemipelvis and buttock (caused by contraction of the contralateral hip abductors, especially the gluteus medius). Sagging of the pelvis indicates a positive Trendelenburg’s.

178 What are the causes of a Trendelenburg’s sign?

In addition to intrinsic weakness of the muscle (from muscular dystrophy), a positive test suggests congenital dislocation of the hip, poliomyelitis, spinal nerve root lesions (paralyzing the superior gluteal nerve—hence, L5), or greater trochanter fracture (the distal insertion site of the gluteus medius).

179 What is a Trendelenburg’s gait?

A typical gait of gluteal muscle weakness (see Chapter 1, questions 75–80). While stepping from one leg to the other, the glutei are unable to hold up the pelvis, causing it to sag on the unsupported side. As a result, the “swinging” limb may become too low to clear the ground, causing the patient to compensate in one of two ways: (1) by leaning away from the unsupported side, trying to raise the swinging leg in the typical “waddling” fashion of progressive muscular dystrophy (so called because its gait resembles that of a duck), or (2) by stepping very high on the unsupported side, so that the swinging leg can clear the ground (“high steppage gait”).

180 What is Hoover’s test?

A bedside assessment of lower extremity strength, based on the principle that whenever a supine patient raises one leg, he or she involuntarily exerts counterpressure with the opposite heel. This response occurs even if that leg is paralyzed. Similarly, if the patient attempts to lift a paralyzed leg, he or she will exert counterpressure with the opposite (healthy) heel, regardless of whether any movement at all occurs in the paralyzed limb. This sign is absent in hysteria or malingering, but present in hemiplegia. Hence, it can separate true weakness from poor effort.

181 How is Hoover’s test carried out?

182 List sensory distribution, reflexes, and motor innervation of lumbar spinal roots syndromes

id=”p1920″/>See Table 21-5.

183 Where is the sacroiliac joint (SIJ)? What is its clinical importance?

The SIJ is located in the pelvis, between the sacrum and ilium, and is a common but frequently overlooked source of low back pain, both for the young (ankylosing spondylitis) and the old (DJD). This is not specific to any occupation or sport, but since its symptoms and findings can occur in other low-back pain situations (like herniated disks), diagnosing it is often difficult.

184 How do I locate the SIJ?

Sit behind a standing patient and place your fingers over the iliac crests. Your thumbs will naturally fall over the sacroiliac joints, where pressure can then be applied for SIJ tenderness.

185 What are the presenting symptoms of patients with SIJ disease?

The main one is a sharp or aching pain in the lower back, usually toward one side. Pain is frequently felt in the groin, often extending down the back of the thigh and occasionally even below the knee, eventually crossing anteriorly. Sacroiliac pain is alleviated by standing or walking, and worsened by sitting down for long drives or plane rides. Numbness, tingling, or weakness in the leg, knee, or foot is rare. In addition to sacroiliac pain and tenderness, there may be reduced motion in the lumbar spine (see Schober’s test, previously discussed).

186 What is the presentation of sacroiliitis?

Pain and tenderness over the SIJ joints, but no peripheral neurologic findings.

187 How do you assess sacroiliac joint tenderness?

There are several maneuvers that test/stress the SIJ, eliciting pain in patients with disease. The simplest one consists in applying pressure over the lateral pelvis in a patient lying on the side. Pain indicates SIJ tenderness. More dynamic maneuvers include Patrick’s, Gaenslen’s, and Yeoman’s tests. Gaenslen consists of maximally flexing one hip, while extending the other. To carry it out, ask the patient to lie supine, with one side of the pelvis off the examination table, and the contralateral leg flexed at hip and knee (held up by the examiner). Then extend the hip whose leg is lying below the edge of the table. This will stress both sacroiliac joints simultaneously, eliciting pain on the side being extended.

188 How many muscles control the hip?

Four groups of muscles: (1) the posterior (represented by the gluteus maximus and the hamstring, both responsible for moving back the thigh along the sagittal plane [i.e., extension]). Their counterparts are (2) the iliopsoas (an anterior muscle) and the rectus femoris (one of the quadriceps muscle, the largest anterior muscle). Both are responsible for lifting the thigh up (i.e., flexion). (3) The adductor muscles are instead located medially and are responsible for moving the thigh inward (i.e., adduction). (4) Finally, the abductor muscles are lateral and made up by the gluteus medius and minimus. They move the thigh outward (i.e., abduction).

189 What is the normal range of motion of the hip?

190 How many bursae does the hip have? Why are they important?

Three. All are important to know (and examine) since hip pain may be due to bursitis and not arthritis.

191 What hip structure can cause inguinal swelling?

The iliopsoas bursa. Its inflammation (a rather rare event) can cause anterior hip pain and a fluctuant inguinal mass between the iliopsoas and iliopectineal eminence (or “pelvic brim”). The snapping hip maneuver may identify patients with this condition: place your hand on the inguinal crease, while passively flexing, abducting, and externally rotating the hip. Then return the hip to a neutral position. A palpable snap during the last phase of the test suggests iliopsoas bursitis.

192 Which structures traverse the inguinal fossa?

From the lateral to the medial: nerve, artery, vein, emptiness, lymph node (all underneath the inguinal ligament). NAVEL is the mnemonic.

193 What are the causes of pain referred to the inguinal area? How do you identify it?

Pain referred to the inguinal area may originate in a lesion of the psoas muscle, such as an abscess or a hematoma. Its psoas origin is confirmed by eliciting pain through hip extension.

194 What is a trochanteric bursitis?

It is a painful inflammation of the homonymous bursa. This is a common cause of lateral hip pain, especially in older patients. Causes include acute trauma (from falls or tackles forcing the subject to land on the lateral hip region) or repetitive friction by the iliotibial band (which is an extension of the tensor fascia lata muscle). Runners may be especially at risk.

195 What are the symptoms of trochanteric bursitis?

The classic is lateral hip pain, even though the joint per se is intact. Pain radiates down the lateral aspect of the thigh (but contrary to sciatica, never all the way into the foot), worsening with internal and external rotation of the hip and pressure during sleep (as when lying in the lateral decubitus position); sometimes the pain even awakens the patient. On exam there is point tenderness over the greater trochanter and bursal swelling, even though this is often difficult to appreciate.

196 What is “log-rolling” of the hip?

A test that can separate pain of the hip “joint” from that of other structures. To perform it, roll the leg side to side while keeping it fully extended. Pain so elicited can only originate in the joint.

197 What is the FABER maneuver?

A screening maneuver for hip disease. The patient lies supine, while the affected hip is passively flexed, abducted, and externally rotated. Normally, the lateral leg should be able to lie flat on the examination table with the foot against the opposite knee. A positive test elicits anterior or posterior pain and indicates hip or sacroiliac joint involvement. In an athletic population, a positive FABER test has 88% sensitivity for intra-articular pathology.

198 How do you detect a flexion contracture of the hip?

By the Thomas test. This consists in asking supine patients to hold their uninvolved leg flexed against the chest (so to flatten the lumbar lordosis) while the examiner moves the symptomatic hip from full flexion to full extension. Inability to lay the affected thigh flat on the examining table (i.e., keeping it instead flexed) indicates a flexion contracture (or deformity). Conversely, a palpable deep click suggests a labral tear.

199 How should one approach a patient with hip pain?

By first localizing the pain, since anterior, lateral, and posterior pains have different etiologies.

200 How should one examine the hip of a patient complaining of pain?

By first observing the patient’s gait, which is going to be antalgic. Then by assessing range of motion of the hip (both active and passive), and carefully comparing the affected and normal side. Hip flexion; internal and external rotation; and flexion, abduction, and external rotation (FABER) should be tested, too. The most predictive finding for osteoarthritis (DJD) is a decreased range of motion—especially in internal rotation or abduction. For patients with restricted movement in one plane, the sensitivity for DJD is 100% and specificity is 42%; with restricted movement in three planes, the sensitivity is 54% and specificity 88%, with a likelihood ratio of 4.4. To ensure that the source of pain is not muscular, muscle strength also should be tested (by doing resisted hip flexion, adduction, abduction, external rotation, and extension). Specialized hip maneuvers should then be carried out. These include not only the Thomas test, FABER, and “snapping hip,” but also Ober’s test. In this test, the patient lies on the side while the examiner abducts and extends the affected hip before releasing the leg and allowing it to drop onto the examination table. Lateral hip pain or considerable tightness may indicate iliotibial band syndrome. Finally, evaluation of hip pain should include palpation of individual structures, like hip flexor muscles, greater trochanter, iliotibial band, and gluteus medius muscle—all maneuvers that can further localize the source of pain. Tenderness over anterior soft tissues would suggest a hip flexor muscle strain (or iliopsoas bursitis), whereas tenderness over the greater trochanter would indicate a trochanteric bursitis.

201 How common are knee disorders?

Very common. One of 10 adults reports knee symptoms, with pain accounting for 5% of all physicians’ visits, many resulting in diagnostic imaging or subspecialty referrals.

202 What are the main types of knee disorders?

(1) Patellofemoral, (2) ligamentous, and (3) meniscal. Basic understanding of knee anatomy and mechanism of injury is crucial for their identification.

203 Can history identify the site of injury?

Yes. A careful history (and physical exam) should first of all separate knee problems due to a systemic condition from those that represent instead a local musculoskeletal issue. For a local problem, history can then assist the clinician in determining whether this represents a patellofemoral disorder, or a more serious meniscal or ligamentous injury. In this regard, ask the patient to pinpoint the site of pain and assess its duration and impact on activity, the presence of “pops” at the time of injury, and any swelling—especially its timing in relation to trauma. For instance, a large effusion that occurs immediately after trauma would argue in favor of hemarthrosis, most commonly due to a ligamentous lesion (like the anterior cruciate). Delayed (or minimal) swelling would instead suggest a meniscal tear, especially if associated with locking. “Buckling” or “giving way,” whether in extension or flexion, would suggest knee instability, often due to ligamentous injury. Finally, pain going up steps, or in the anterior knee while sitting, would indicate patellofemoral dysfunction. Knowledge of the mechanism of injury (especially the direction of the force delivered to the knee) also is crucial.

204 What are the main mechanisms of injury?

They vary, depending on the type of force applied. A valgus stress (i.e., a force that pushes the knee medially, but its distal segment [the leg] laterally) usually strains the medial collateral ligament; conversely, a varus stress (i.e., a force pushing the knee laterally, but its distal segment [the leg] medially) strains instead the lateral collateral ligament. Hyperextension strains the anterior cruciate ligament, whereas twisting motions strain both ligaments and menisci.

205 What is the anatomy of the knee?

The knee is the largest joint in the body (in fact it is composed of two joints: the femorotibial and the patellofemoral). It articulates two femoral condyles with two tibial plateaus, in a modified hinge that relies on patella, ligaments, muscles, and tendons to achieve an extensive ROM.

206 How many ligaments support the knee?

Four, connecting the femur and tibia and thus providing dynamic stability to the joint. Two of them are external and two internal. The external (or extra-articular) ligaments are the medial collateral (MCL) and lateral collateral (LCL), which prevent the knee from moving too far from side-to-side. The MCL stretches from the medial femoral condyle to the medial tibia, whereas the LCL stretches from the lateral femoral condyle to the head of the fibula. The intra-articular ligaments are instead: (1) the posterior cruciate (PCL) in the front, running from the anterior portion of the femur to the posterior portion of the tibia, whereas in the back is (2) the anterior cruciate (ACL). These stabilize front-to-back motions of the tibia and femur, with the ACL preventing the tibia from sliding too far forward (hence, hyperextension of the knee), and the PCL doing the opposite (hence, preventing hyperflexion of the knee). Cruciate ligaments also aid in proprioception.

207 What are the menisci?

Two semilunar fibrocartilaginous ligaments that wedge between the femur and tibia. Their function is (1) to spread the weight of the body over a larger area and (2) to help the ligaments stabilize the joint. If one can imagine the knee as a ball (femur) resting on a flat plate (tibia), the menisci work like a gasket, filling the space between the femoral condyles and tibial plateaus and thus distributing the weight. Without menisci, the concentration of force onto a small area of the tibial plate would quickly damage the cartilage and lead to arthritis. Thicker on the outside than the inside, they also convert the tibial surface into a shallow socket. And since a round ball in a socket is more stable than a round ball on a flat plate, they enhance the stability of the joint. The patellar tendon further stabilizes the joint by connecting anteriorly the quadriceps tendon to tibia and patella. Finally, note that the medial meniscus is attached at its most medial surface to the MCL. Conversely, the lateral meniscus does not have any attachment to the LCL. This is quite important for the knee exam (see question 240).

208 What are the primary muscles of the knee?

The quadriceps and the hamstring, which are, respectively, the primary extensor and flexor of the leg. The hamstring lies posteriorly in the thigh, whereas the quadriceps covers instead the anterior, lateral, and medial aspects of the knee. Part of its tendon includes the patella, which sits anteriorly to the two femoral condyles, smoothly gliding over the patellofemoral groove.

209 What is prepatellar bursitis?

An inflammation of the prepatellar bursa—a flat, round, superficial, and fluid-filled structure between the patella, patellar tendon, and skin. Prepatellar bursitis may be due to trauma (like a fall or a direct blow to the knee), although more commonly, it is the result of overuse, like repeated kneeling. Hence, it is frequent in roofers, plumbers, carpet-layers, housemaids, nuns, and overachieving White House interns. It also can be infectious, usually from a skin break, with Staphylococcus aureus being the main culprit. Symptoms include knee pain, swelling, redness, and difficulty ambulating. Exam reveals erythema, crepitation, and decreased knee flexion because of pain. There also is fluctuant edema over the lower pole of the patella. Finally, there also is an infrapatellar bursa (anserine) just below the knee. As with prepatellar bursa, this, too, can be affected by direct or repetitive trauma.

210 How do you examine the knee?

The same way you examine other joints: with a thorough, systematic, and repetitive routine. Always compare side to side, starting with the unaffected side. Inspect, palpate, test ROM, assess gait, measure girths, and finally carry out specific maneuvers for integrity of menisci and other knee ligaments.

211 What do you look for when inspecting the knee?

In a standing position, look for misalignments between the femur, tibia, and patella. In a supine position, look instead for scars, asymmetry, swelling, redness, or chronic deformities. Evaluate the patella, patellar tendon, medial and lateral joint lines, femur, tibia, and tibial tuberositas. Use important landmarks, like the tibial tuberosities and the two condyles (lateral and medial), both located on the anterior surface of the shin. Since knee problems often limit use of the affected leg, look for wasting of the quadriceps, hamstring, and calf muscles. Finally, watch the patient walk, looking again for misalignments but also for limping or pain.

212 What is the Q-angle (or “quadriceps angle”)?

It is not a Star Trek member of the “Continuum,” but the angle between the tibia and femur—and a great tool for identifying misalignment. To calculate it, draw two lines: (1) one from the tibial tuberositas to the mid-patella and (2) the other from the mid-patella to the anterior superior iliac spine. The normal angle is 15   degrees, although it is wider in women because of their larger pelvis. Wide Q-angles reflect genu valgus but also increased patellofemoral contact, thus predisposing to patellofemoral disease.

213 What are the most common types of knee misalignment?

“Genu varum” and “valgum.” Varum is an angulation of the knees away from each other. Valgum is instead an angulation of the knees toward each other. Both can be congenital or acquired. A less-common condition is windswept knees, where one knee is varum and the other valgum (see Fig. 21-14). If the use of these terms seems to contradict that of question 62, is because of their etymology, considering that in Latin valgum means “knock-kneed,” while varum means “bowlegged.” In other words, in a knock-kneed person, the femur is deviated inward in relation to the hip (and thus the term varum is correctly applied for the hip, since it refers to the distal segment being angled inward). Yet, in the same knock-kneed person, the opposite situation is found at the knee, with its distal segment (i.e., the tibia) now being deviated outward (so that the term valgum is indeed the one to use for the knee). Hence, it is correct for a knock-kneed deformity to be called both varum (at the hip/femur) and valgum (at the knee/tibia), although the common terminology is to refer to it as genu valgum. Conversely, in a varum deformity of the knee, the distal part of the leg below the knee is deviated inward, resulting in a bowlegged appearance. If this is confusing, just remember that “varum = inward” and “valgum = outward,” and that both terms always refer to the direction in which the distal part of the joint points. When the terminology specifies a bone rather than a joint, the bone is taken to be the distal segment of a joint. Thus, a varum deformity of the tibia refers to the femur/tibia joint (the knee) and not to the ankle.

Figure 21-14 Normal alignment and malalignment of the knee.

(From Staheli LT: Pediatric Orthopaedic Secrets. Philadelphia, Hanley & Belfus, 1998.)

214 Can osteoarthritis cause misalignment of the knee?

Yes. And since it usually affects the medial aspect of the joint, it causes primarily bowing.

215 How do you demonstrate patellar tracking?

Ask the patient to sit. Then extend the knee, while keeping your finger over the patellar midpoint. During extension, the patella should remain midline in the femoral groove. Any medial or lateral movement indicates knee misalignment. This, in turn, may predispose to patellofemoral disease.

216 What is patellofemoral syndrome (disease)?

A constellation of symptoms due to malposition of the knee, resulting in increased/misdirected mechanical forces on the undersurface of the patella. This can be due to unbalanced muscle pull, misalignment between joint surfaces, or excessive knee valgus (i.e., increased Q-angle) with increased lateral forces. All eventually affect the patellofemoral interface and cause the retropatellar cartilage to wear down (chondromalacia).

217 What are the symptoms and findings of patellofemoral disease?

The most common is knee pain, which is retropatellar and typically triggered by activities requiring knee flexion and forceful contraction of the quadriceps (like squatting or ascending/descending stairs). Pain also is exacerbated by sitting with the knee flexed for a protracted period, such as when driving the car or watching a movie. Hence, the terms “theater sign” and “movie-goer’s knee.” In fact, these patients often prefer to sit in an aisle seat, where they can keep the knee extended for longer periods. On exam, there may be tenderness along the facets of the patella, the tibial tuberositas, or the patellar tendon. Note that pain elicited lateral to the patella usually indicates pathology over the insertion of the iliotibial band; conversely, pain elicited medial to the patella (i.e., at the insertion of the medial hamstring) indicates anserine bursal tenderness.

218 What is anserine bursitis?

A common cause of anterior knee pain in athletes or patients. The pes anserine (goosefoot) bursa is located with its associated medial hamstring tendons along the proximomedial aspect of the tibia. In case of tight hamstrings, bursitis can ensue, although this also may be due to direct trauma. Pain along the medial aspect of the knee is the presenting complaint. On exam, there is tenderness over the bursa, which is located slightly distal to the tibial tuberositas and two finger breadths medial to it. Management is usually conservative.

219 How do you test for patellofemoral syndrome?

With the patient supine, slightly flex the leg to be tested, so that the quadriceps is relaxed. Then, gently push down on the patella with both thumbs, or try to palpate its undersurface. Pain on either of these maneuvers suggests chondromalacia. Now move the patella across the femur: medially, laterally, superiorly, and inferiorly. Crepitus or pain on passive motion also suggests patellofemoral disease. Finally, measure the Q-angle, since wider angles may predispose to it.

220 What is an extension lag of the knee?

The inability to actively extend a knee that can be passively extended by the examiner—another sign of patellofemoral disease. A flexion contracture is instead the inability to passively extend the knee, a common finding in intrinsic knee disease.

221 What is the patellar inhibition test (patellofemoral grinding test)?

It is patellar pain upon isometric contraction of the quadriceps—an important apprehension sign and another clue to patellofemoral disease. To elicit it, have the patient lie supine and with the leg extended. After applying some suprapatellar resistance (i.e., holding the patella in place with one hand), have the patient contract the quadriceps. This will press the inferior surface of the patella onto the femur, thus eliciting pain or crepitus in cases of chondromalacia.

222 What is the role of palpation?

Tenderness on palpation reflects different processes based on location:

223 How do you palpate the knee?

Ask patients to sit with the knees slightly flexed, since this prevents other stabilizing elements of the joint from interfering with the exam. Examine the tibial tuberosity, and then move along each side of the tibial plateau, up toward the medial and lateral femoral condyles. Feel the patella.

224 How do you evaluate the knee’s range of motion?

With a goniometer, and by comparing the affected to the unaffected side.

225 What is osteoarthritis of the knee?

A common event in large, weight-bearing, and synovial joints. One fourth of people between 55 and 64 show signs in their knees (gonarthrosis), while 23% have it in the hip (coxarthrosis). Prevalence reaches 39% and 23%, respectively, at ages 65–74, and totality at 75–79.

226 What is the mechanism of osteoarthritis?

Trauma, either direct or cumulative. The latter is typical of weight-bearing joints like the knee, and it is due to years of recurrent wear-and-tear. A healthy synovial joint normally allows a significant amount of motion along its extremely smooth articular surface. To do so, it relies on a synovial membrane, an articular (or hyaline) cartilage, an underlying (subchondral) bone, an overlying joint capsule, and plenty of synovial fluid. Osteoarthritis primarily affects the articular cartilage, eventually forming tears, first small and then large. With time, these lead to fragmentation into the joint, exposure of the underlying bone, formation of osteophytes, and cystic degeneration of the subchondral bone. Ultimately, the joint undergoes mechanical deformation, resulting in misalignment, instability, and further degeneration.

227 What are the symptoms of gonarthrosis?

The classic one is pain, insidious, ache-like, and typically worsened by activity/relieved by rest. With time, this becomes persistent and more debilitating. There also may be damage to ligaments or menisci. On exam, the joint may be warm, with crepitus, effusion, and reduced ROM. Gait is often antalgic. Note that gonarthrosis can involve the medial, central, or lateral compartment of the knee—individually or together. Yet, precise location is often difficult to determine on simple exam. Imaging can be much more accurate.

228 How do you detect knee effusions?

It depends on the amount. Large effusions can be detected by simple inspection or basic palpation. Inflammatory effusions (like those of infection, gout, or RA) are often associated with inflammation, and thus with warmth, redness, and painful movements. Smaller effusions are instead harder to detect, except for the bulge sign (or milking), which can identify <15   mL of intra-articular fluid but remain absent in larger effusions. Bulging is demonstrated by a two-step test:

229 What about intermediate-sized effusions?

They require either patellar ballottement or the fluid wave test.

230 What are the mechanisms of ligament injuries?

Note that given the forces involved, ligamentous tears are often associated with meniscal tears. It also is possible to tear more than one ligament at once, with the most common combination being MCL and ACL. Hence, always do a comprehensive exam.

231 What are the symptoms of ligamentous injuries?

Usually acute pain, swelling, and often a “pop” (reflecting the tearing of the ligament). After these subside, pain and instability can occur upon movements that require use of the damaged ligament—such as rotation, which now becomes unimpeded.

232 How does the function of cruciate ligaments relate to symptoms?

233 Which maneuvers test the anterior cruciate ligaments?

(1) Lachman’s test, (2) the anterior drawer test, and (3) the lateral pivot shift (or Macintosh) test.

234 How do you perform the Lachman maneuver?

Have the patient supine, with the knee flexed to 20–30   degrees, and heel on the table toward you. Stand on the patient’s side, and hold the femur with your left hand, just above the knee, firmly enough to prevent any movement of the upper leg but gently enough to allow for the hamstrings to relax. Then, use your right hand to pull the proximal tibia up toward you, while at the same time stabilizing the femur with your left hand. An intact ACL will limit the amount of distraction by providing a firm end-point. Now reverse your hand position, and repeat the maneuver on the other leg. Compare responses. The test is positive when the end-point is not discrete, or the tibia moves excessively forward (anterior subluxation). Note that Lachman requires a good grasp of the leg; hence, it may be difficult to perform when the patient has large legs or the physician has small hands. In this case, have the patient’s leg hang off the side of the table.

235 How do you perform the anterior drawer test?

Have the patient supine, hip flexed to 45   degrees, knee to 90   degrees, and foot/heel resting flat on the table. Stabilize the foot by sitting on its dorsum. Wrap your hands around the knee, with fingers embracing the medial and lateral insertion of the hamstrings and thumbs on the tibial tuberositas, along the medial and lateral joint line. Make sure that the hamstrings are relaxed, then quickly pull and push the proximal part of the leg, testing the degree of distraction of the tibia in relation to the femur. Do these maneuvers in three positions of tibial rotation: neutral, 30   degrees externally rotated, and 30   degrees internally rotated. An intact ACL will provide a discrete end-point, abruptly stopping the tibia’s forward movement as the ligament reaches its maximum length. No more than 6–8   mm of laxity should be allowed. A positive anterior drawer sign results instead in an unrestrained forward motion (i.e., anterior subluxation of the tibia on the femur), indicating a possible tear of the ACL. As always, compare the affected to the unaffected side.

236 How do you perform the lateral pivot shift test?

By combining a valgus stress (pushing the outside of the knee medially) with a twisting force onto a knee that is being flexed. Ask the patient to lay supine, with the affected knee extended and the tibia internally rotated. Place one hand on the lateral aspect of the knee, and push medially (thus creating a valgus strain), while at the same time supporting and pulling laterally the foot with your other hand. As you slowly flex the knee, keep the foot internally rotated. In a positive test, the tibia “jumps” anteriorly at 10–30   degrees flexion, with an obvious “thud” or “clunk.” This indicates the inability of the ACL to prevent anterior subluxation of the tibia onto the femur.

237 How do you assess the posterior cruciate ligaments?

Through (1) the posterior drawer test and (2) the tibial sag test.

238 How do you perform the posterior drawer test?

Very much like the anterior drawer test (i.e., with knee flexed at 90   degrees, foot resting flat on the table, and you sitting lightly on it), except that this time instead of pulling the leg forward, you should push it backward. An intact PCL will give a discrete end-point, whereas a torn PCL will allow unrestrained backward movement of the tibia in relation to the femur.

239 How do you perform the tibial sag test?

Have the patient flex both knees and hips at 90   degrees; then hold the legs in position by grasping the ankles. Inspect the tibial plateaus for asymmetry. The test is suggestive of PCL tear if one plateau sinks below the patella (i.e., “sagging” in comparison to the other).

240 How do you assess the collateral ligaments?

Hold the knee in your hand, freely relaxed and in approximately 15   degrees of flexion (to avoid locking in full extension). Apply first a varus stress (pressure on the medial aspect of the joint to test the lateral collateral ligament, LCL), and then a valgus stress (pressure on the lateral aspect of the knee, to test the medial collateral ligament, MCL). More specifically, for the MCL, push inward with your left hand along the lateral aspect of the knee, while at the same time applying an opposite force with your right hand. If the MCL is completely torn, the joint will “open up” along the medial aspect. For the LCL, do the opposite: place your right hand along the medial aspect of the knee, place your left hand on the ankle or calf, and push outward with your right hand while applying an opposite force with your left. If the LCL is completely torn, the joint will “open up” along the lateral aspect. An alternative way to test the collateral ligaments consists in cradling the lower leg, and then pressing with your fingers first to the lateral side of the knee (to test the medial collateral ligament) and then to the medial side (to test the lateral collateral ligament). Do this first with the knee flexed at 15   degrees and then at 30   degrees. Any pain or abnormal opening of the joint space indicates instability. When used for the MCL, this maneuver eliminates the medial meniscus from contributing to knee stability and thus tests primarily the MCL.

241 How accurate are these maneuvers?

There is no adequate information for the diagnostic accuracy of maneuvers testing the integrity of collateral ligaments. Conversely, the composite exam for tears of cruciate ligaments is highly predictive—at least as performed by orthopedic physicians. More specifically:

242 How common are meniscal injuries?

They are the most common knee injury, with more than 1.7   million repairs/resections per year. Many eventually cause joint instability, accelerated DJD, and need for knee replacement.

243 What is their mechanism?

Although at times degenerative, meniscal injuries are more frequently due to trauma. Hence, they affect primarily young individuals as a result of either aggressive sports (soccer, football, basketball, and occasionally baseball) or labor activities that predispose to rotational injuries. In sports, most meniscal tears are not due to contact, but to deceleration, like landing after a jump, squatting, and twisting. In fact, the most common mechanism is a varus or valgus force onto a flexed knee, with valgus tearing the medial meniscus, and varus tearing the lateral one. Traumatic meniscal injuries also are associated with collateral ligament tears (ACL more than PCL). Degenerative meniscal tears occur instead with minimal or no trauma—hence, they are more common in older patients.

244 What is the best way to evaluate a meniscal injury?

Definitely imaging, since all lesions can be visualized by MRI (which is even better than arthroscopy). Yet, meniscal injuries also can be assessed by a series of bedside maneuvers. In fact, in a series of 100 tears confirmed by arthroscopy the clinical diagnosis was correct in 87 cases, correct but incomplete in four, and incorrect in nine.

245 What are the symptoms of meniscal tear? What are their causes?

Symptoms are typically due to a torn piece of cartilage interrupting the normal smooth movement of the knee. This can cause acute pain, swelling, and movement limitation, such as joint “locking” or instability (i.e., “giving out”). It also can cause knee effusion, usually over hours, but more rapidly in case of hemarthrosis. Finally, denudation of the bone may eventually lead to degenerative arthritis. In the same aforementioned series of 100 cases, repeated popping occurred in 43%, swelling in 51%, and pain localized to the joint line in 63%. Joint effusion has a sensitivity for meniscal tear of 35% and a specificity of 100%.

246 What are the physical findings of a meniscal tear?

247 In addition to tenderness over the joint line, what other maneuvers can detect meniscal tears?

(1) Medial-lateral grind test, (2) McMurray test, and (3) Apley’s grind and distraction test. Positive results on any of these tests do not necessarily establish the presence of meniscal lesions, but, along with other findings, may help differentiate a tear from other knee injuries.

248 How do you perform the medial-lateral grind test?

With patients supine, cradle in one hand the calf of the affected leg and place the index finger and thumb of the opposite hand over the joint line. Then apply valgus and varus stresses to the tibia during flexion and extension. The test is positive if you detect a medial-lateral grind over the joint line.

249 What is the McMurray test? How do you perform it?

McMurray is a test of meniscal tears of the middle or posterior horn. For tears of the medial meniscus, apply a valgus force and externally rotate the foot while extending the knee. For tears of the lateral meniscus, apply instead a varus force and internally rotate the foot while extending the knee. More specifically: with patients supine and the right knee and hip fully flexed, place your left thumb on the lateral joint margin, while keeping middle, index, and ring fingers aligned along the medial margins. Then use the right hand to passively extend the leg, flex it, and extend it again, but this time with an external rotation of the leg. To do so, first turn the ankle so that the foot points outward (everted). Then point the knee outward (valgus stress). In this everted position, first extend and then flex the knee. The test is positive for medial meniscal injury when (1) it elicits pain with extension of the knee and external rotation of the leg; (2) it elicits a palpable, audible click or pop over the meniscus; or (3) it elicits locking of the knee. After this is done, flex and extend the knee again, but this time after internal rotation. To do so, turn the foot inward (inversion), and then direct the knee so that it points inward as well (varus stress). Once again, the test is indicative of lateral meniscal injury when (1) it elicits pain with extension of the knee and internal rotation of the leg, (2) it elicits a palpable click over the meniscus, or (3) it elicits locking of the knee. Pops, snaps, and clicks are produced as the torn meniscal fragment rides over the femoral condyle during extension. An audible or palpable pop in extreme flexion indicates a posterior horn tear; a click at 90   degrees of flexion indicates a lesion in the midsection of the meniscus.

250 What is the Apley’s grind and distraction test? How do you perform it?

Apley’s is a test of meniscal tears in the posterior horn of either the medial or lateral meniscus that also can differentiate meniscal from ligamentous injuries. It consists of rotation and compression of the knee. With the patient prone, grab the heel with one hand and flex the knee to 90   degrees. Start with the “grind” part of the test: compress the knee (by applying downward pressure on the foot), while at the same time rotating the foot internally and externally. Pain during this part of the test indicates a meniscal tear. Then distract the knee by rotating the foot internally and externally, but this time pull up on the foot. Since traction on the leg removes pressure on the meniscus, pain during this part of the test indicates instead ligamentous involvement.

251 Who were these folks?

252 How accurate are these tests?

Not as accurate as the maneuvers for evaluation of ligamentous injuries. Using arthroscopy as a reference standard, bedside evaluation has sensitivity of 77% and specificity of 91%, with a positive LR of 2.7 and a negative LR of 0.4. Still, one third of meniscal tears may be missed by clinical screening. Moreover, exam cannot demonstrate location, shape, or length of the tear—something that MRI does instead very well. As for individual findings, joint-line tenderness has a mean sensitivity of 79% and a specificity of 15%, with an LR of 0.9 for a positive test and 1.1 for a negative test. Hence, it is not a super finding, even though its accuracy may be greater for tears of the lateral meniscus as compared to those of the medial one. Of the various maneuvers, the medial-lateral grind test is the most accurate, with sensitivity of 69% and specificity of 86%; McMurray is most helpful when positive, with a sensitivity and specificity of 53% and 59%, respectively, and a positive LR of 1.3 and a negative LR of 0.8. Apley has instead a sensitivity so low (about 16%) that many authors even discourage its use. In a series of 100 meniscal tears, at least one of these maneuvers was positive in 79% of the cases. Yet, accuracy may decrease significantly in patients with multiple knee lesions (down to 30%). For example, in cases of acute ACL tear, the sensitivity for associated medial meniscus tear is 45% and for lateral meniscus tear is 58%. Finally, concomitant presence of a joint effusion lowers the sensitivity for meniscal tear to 35% (specificity, though, is a solid 100%). Overall, exam is more specific than sensitive.

253 When should x-rays be ordered?

When the Ottawa Knee Rules are met: (1) age 55 or older, (2) tenderness at the head of the fibula, (3) isolated tenderness of the patella, (4) inability to flex the knee to 90   degrees, and (5) inability to take four weight-bearing steps (regardless of limping), both at the time of injury and in the exam room. “Ottawa” does not apply to children. In fact, anyone younger than 12 should have x-rays.

254 How is quadriceps atrophy detected?

By palpating the quadriceps above the knee and comparing its muscle bulk to the uninvolved side. To quantify atrophy, measure the quadriceps circumference at a point that is 5 and 20  cm above the upper pole of the patella. For more subtle atrophies, ask the patient to contract the quadriceps. This will accentuate its anatomy and allow better appreciation of unilateral muscle loss.

255 What is a Baker’s (popliteal) cyst? Where can it be palpated?

Baker’s is a synovial cyst (i.e., a collection of fluid that has escaped the joint and collected into a new sac in the popliteal space). First described in 1877 by the English surgeon William Morrant Baker, who reported eight cases, this periarticular cyst represents the most common popliteal mass. It is around 3   cm³ in size and is often encountered in patients with either inflammatory or degenerative arthritides. To feel it, ask the patient to partially flex the knee, and then palpate the popliteal fossa behind the medial femoral condyle, between the medial head of the gastrocnemius and the semi-membranous bursa. The cyst will present as a fluctuant popliteal swelling. In 10% of patients, it will evolve into a pseudothrombophlebitis syndrome.

256 What is the pseudothrombophlebitis syndrome?

A syndrome characterized by dissection of a Baker’s cyst down the leg and into the calf. This results into swelling and tenderness, often mimicking thrombophlebitis—hence, the term, pseudothrombophlebitis. Note that the cyst can also rupture. In this case, it presents as an enlarging mass in the calf, with fluid draining down the fascial plane, causing exquisite leg pain, calf swelling, and erythema, plus a crescent-shaped ecchymosis at the medial or lateral malleolus (crescent sign). Of interest, the presence of a Baker’s cyst per se may predispose to true thrombophlebitis—by compressing the surrounding vein.

257 What is the function of the ankle?

The ankle serves as a hinge, which has to support 1.5   times the body weight while walking and up to 8   times while running. Hence, despite being rather sturdy, it is a common site of injury, especially in athletes. A thorough knowledge of the anatomy is key for an accurate diagnosis.

258 What is the anatomy of the ankle?

The ankle comprises three bones: distal tibia, distal fibula, and talus. The distal tibia articulates with the talus on its concave plafond, forming the medial malleolus in its inner aspect. The distal fibula articulates with both the talus and distal tibia, forming the lateral malleolus in its outer portion. The malleoli serve as buttresses of the talus, while the talus is the real hinge, allowing the foot to dorsiflex and plantarflex. It comprises a head, neck, and body, with several tubercles arising from the latter. One, the lateral tubercle, arises from the os trigonum. This is a separate ossification center that occasionally may remain unfused, thus causing a painful impingement syndrome. Finally, the talus joins the calcaneus on its lower aspect.

259 How do you approach a patient with ankle injury?

By determining the mechanism of injury, since this can narrow the differential diagnosis. To do so, separate inversion from eversion, plantar flexion, dorsiflexion, or a combination thereof. Also, determine whether the affected joint was previously injured, and what treatment might have been given. Finally, always compare the affected to the unaffected leg (and remove all socks and shoes).

260 What should one look for in the ankle exam?

For deformities and swelling, since these may help localizing the affected structure. ROM should then be tested, and compared to the unaffected side.

261 How do you test ROM?

By using a goniometer, while the patient sits on the exam table with legs freely hanging down. Test both active and passive dorsiflexion (20   degrees) and plantar flexion (50   degrees).

262 What ankle structures should be palpated?

263 How do you identify an injury of the lateral ligaments?

By palpation. Since lateral ligaments are thin enough to be very difficult to palpate in isolation, pain on palpation (or even simple swelling) usually indicates injury. Of the three ligaments, the one most prone to injury is the anterior talofibular. The calcaneofibular ligament is instead torn only after the anterior talofibular ligament, usually resulting in ankle instability. Finally, the posterior talofibular ligament is only torn with massive trauma, as in cases of ankle dislocation.

264 How do you assess the anterior talofibular ligament?

Through the anterior drawer test. To carry this out, have the patient sit on the edge of the bed with the legs freely dangling down. Place one hand on the lower tibia, and wrap the other around the heel. Then pull the heel forward, while pushing the tibia backward. The test is positive when the talus moves anteriorly, suggesting a tear of the anterior talofibular ligament. Compare sides.

265 What is the “talar tilt” test?

A test of combined anterior talofibular and calcaneofibular tear, an injury severe enough to cause major lateral ankle instability. To carry this out, have the patient sit on the edge of the bed with the legs freely dangling down. Grasp the heel with one hand, and evert the foot while stabilizing the tibia. The test is positive when the talus rocks within the joint.

266 What is the cause of pain posterior to the fibula?

Pain behind the fibula and lateral malleolus usually indicates peroneal tendon pathology. This may be confirmed by palpating the posterior fibular groove, while actively resisting dorsiflexion and eversion of the foot.

267 What is the “squeeze test”?

A maneuver that identifies injury of the syndesmosis connecting the tibia and fibula. To perform this test, place your hand midway along the lower leg, and gently squeeze tibia and fibula together. Pain along the anterior joint line of the ankle indicates syndesmosis pathology.

268 When should x-rays be ordered?

When the Ottawa Ankle Rules are met: (1) inability to take four weight-bearing steps immediately after injury or at the time of the exam and (2) pain with palpation of the lateral or medial malleoli and 6  cm proximally along the tibia and fibula.

269 What are pes cavus and pes planus?

The two most common foot deformities (Fig. 21-15). A pes cavus has an abnormally high longitudinal arch, whereas a planus has lost the arch completely (i.e., flat foot). This loss may be flexible or fixed, insofar as a flexible flat foot has some discernible arch at rest, but loses it with weight-bearing, whereas a fixed flat foot lacks the arch even at rest.

Figure 21-15 A, Pes planus (flat foot). B, Pes cavus (high-arched foot).

(From Mellion MB, Walsh WM, Shelton GL: The Team Physician’s Handbook, 2nd ed. Philadelphia, Hanley & Belfus, 1997.)

270 What ankle deformity is associated with pes planus?

An inversion of the ankle, also called valgus or pronation. This can be easily appreciated by observing the patient in a standing position. There will be a variable degree of inward rotation of the medial malleolus, and the patient will admit to walking on the inside of the foot.

271 What are the typical changes of the rheumatoid foot?

Several. RA can in fact cause extensive deformities: (1) pes planus with pronation deformity of the ankle, (2) loss of the anterior arch with widening of the foot, (3) hallux valgus, (4) cock-up deformities of the toes (hammer toes), (5) dropped metatarsal heads, and (6) rheumatoid nodules.

272 What are hammer toes?

They are cock-up toes, the price the civilized man has paid for the privilege of wearing shoes—usually short shoes. Cock-up deformities are caused by ligamentous instability, which in turn leads to subluxation of the metatarsophalangeal (MTP) joints and compensatory flexion at the proximal interphalangeal (PIP) joints. Often, the toe no longer touches the floor when the patient stands. As for semantics, a hammertoe deformity is characterized by an upward-cocked MTP and a downward-bent PIP. A claw toe deformity is one characterized by a cocked-up MTP, but PIP and DIP that are both curled downward—like a claw.

273 What is hallux valgus? What are bunions?

Hallux valgus is a common deformity of the big toe, characterized by lateral deviation (i.e., away from the midline—valgus) and toward the second toe. Osteophytes may be palpable at the joint line. When the deviation is extreme, there may be a palpable bump (bunion) over the medial border of the first MTP joint, caused by a varus (i.e., inward) deviation of the first metatarsal. As a result, the second toe may even override the first toe. This bunion is actually just a fluid-filled bursa, which with time may become inflamed (bursitis). Of interest, hallux valgus and bunion almost never occur in societies that go shoeless. Pointed shoes, such as high heels and cowboy boots, are major culprits in its development. Inelegant but wide shoes, with plenty of room for the toes, reduce the risk of developing the deformity and help reduce the irritation on the bunion if already in place. But they also may get you fewer dates.

274 Describe the findings with dropped metatarsal heads

A dropped metatarsal head is a condition wherein one of the metatarsal bones (usually the second metatarsal) is lower than the rest at the distal end (i.e., subluxated), and can now be palpated along the plantar surface of the foot. Subluxation of the heads is a typical foot deformity of rheumatoid arthritis. In this regard, overpronation may play a role, since abnormal weight distributions in an abnormally pronated foot does tend to throw too much weight to the second metatarsal. With more severe degrees of subluxation, the protrusion of the bone is not only palpable, but visible, too. There also may be thickening of the plantar skin (calluses) over the protruding bone. Patients usually complain of pain and the sensation of walking on a stone.

275 What are corns?

Areas of skin thickening that develop over toes as a result of chronic mechanical irritation, most commonly from ill-fitting shoes or foot deformities that make shoe-fitting difficult. Hard corns develop over interphalangeal joints when a cock-up deformity causes pressure against the shoe. Soft corns are instead areas of interphalangeal skin thickening, caused by the abnormal pressure as the toes move against each other.

276 What is Morton’s neuroma? How is it demonstrated?

Morton’s is not a true neuroma but rather a perineural fibrosis and nerve degeneration of the common digital nerve (Fig. 21-16). This also is the result of repetitive friction, usually from ill-fitting shoes. It develops most frequently between the third and fourth metatarsal heads (i.e., third web space), but is also found in the second web space. Morton first described it in 1876:

Figure 21-16 Morton’s neuroma.

(From Mellion MB, Walsh WM, Shelton GL: The Team Physician’s Handbook, 2nd ed. Philadelphia, Hanley & Belfus, 1997.)

This Dr. Thomas George Morton (1835?1903) was a Philadelphia born and educated surgeon, who became head physician of many local hospitals (including St. Mary’s, Wills Eye, and the Pennsylvania Hospital), until dying of cholera at age 68. Active during the American Civil War, he was for most of his life a hospital administrator, but also a charismatic teacher and an excellent practitioner. In fact, he was one of the first surgeons who were able to remove an appendix after a correct diagnosis, and see the patient survive. His eponymous condition is a rather frequent one, affecting females five times more than males (because of narrower and more pointed shoes?). The most common presentation is sharp and burning pain in the forefoot and toes adjacent to the neuroma. There also may be numbness, often during episodes of pain. In fact, pain is typically intermittent, single or in multiple attacks, with episodes lasting minutes to hours and followed by asymptomatic periods of weeks to months. Patients often describe the sensation of “walking on a marble.” Firm squeezing of the metatarsal head with one hand, while applying direct pressure to the dorsal and plantar interspace with the other hand, may reproduce the pain. Conversely, palpation of the actual neuroma is rarely successful.

277 What is the Achilles tendon? What is Achilles tendinitis?

The Achilles tendon is properly named after the “almost” indestructible Achaean warrior, since this is the largest and strongest tendon in the body, but also a weak spot that could lead to demise, like in the case of its namesake. “Achilles tendinitis” is a spectrum of tendon injuries, ranging from inflammation to rupture. Rupture is usually due to overuse, though deconditioning, overtraining, inadequate footwear, use of poor running surfaces, and predisposing intrinsic factors (such as age, pes cavus, and varus deformities) also may play a role. Tendinitis usually develops insidiously, after repetitive stresses during prolonged jumping or running. Patients complain initially of localized burning pain during or after activity, such as walking—especially when pushing off on the toes. With time, this progresses to more protracted pain, and, eventually, pain at rest. On exam, there may be tenderness along the tendon. Yet, wear-and-tear degeneration of the tendon (i.e., tendinosis) may be entirely asymptomatic.

278 What are the physical findings of Achilles tendinitis?

On palpation, there may be swelling of the tendon sheath (diffuse or at midpoint—i.e., at the Achilles bursa), with nodularity, tenderness, and possibly crepitation. There also may be tenderness where the tendon inserts into the calcaneus (retroachilles bursa). Finally, there may be tendon pain upon passive dorsiflexion of the foot or active plantar flexion (standing on toes).

279 What is Achilles tendon bursitis?

It is an inflammation of the bursae associated with the calcaneal insertion of the Achilles tendon: (1) the retrocalcaneal (which is anterior to the tendon, deeply sandwiched between the distal part of the Achilles and the calcaneus) and (2) the tendocalcaneal (i.e., Achilles’ bursa), which is instead superficial, between the posterior aspect of the tendon and the skin. Both bursae limit the friction of the tendon, and both, if inflamed, may cause posterior heel pain. This may be severe enough to cause limping. The patient also may complain of noticeable redness, warmth, and swelling (often referred to as “pump bump,” from the infamous high-heeled shoes—or “pumps”).

280 What are the causes of this bursitis?

In addition to bad footwear, rheumatologic conditions also can predispose to bursitis. These include gout, rheumatoid arthritis, and seronegative spondyloarthropathies.

281 What about tendon tear?

An Achilles tendon rupture is usually a very dramatic event, often accompanied by an audible snap and by the sensation of being violently kicked in the calf. It is typical of older recreational athletes (i.e., “weekend warriors”), whose tendon has undergone degenerative changes that cause it to snap after a sudden eccentric force is applied to a dorsiflexed foot.

282 What is the presentation of an Achilles tendon tear?

The patient is unable to run, climb stairs, or plantarflex the ankle or foot (i.e., stand on toes). There is pain, tenderness, ecchymosis, and swelling along the entire gastrocnemius-soleus musculotendinous unit. In patients with complete rupture, there is a palpable gap in the Achilles tendon, 2–6   cm above its insertion. To better differentiate complete from incomplete tear, perform a Thompson test: with the patient prone and the knee flexed, squeeze the calf proximally to the affected area. The test is negative if it achieves a passive plantar flexion of the foot, suggesting that the Achilles tendon is at least partially intact. If it achieves no ankle motion whatsoever, then the test is positive, and the tendineal rupture is complete. The hyperdorsiflexion sign also may help: with the patient prone and both knees flexed to 90   degrees, maximally dorsiflex both ankles, and compare the injured to the uninjured side.

283 What is the plantar fascia?

It is the dense band of tissue that fans out from the anteromedial border of the calcaneus (medial calcaneal tuberosity), providing support for the medial longitudinal arch of the foot. Since the fascia has no elastic properties, repetitive stretching will result in microtears and inflammation. One half of patients also may have spurs. Contrary to popular belief, these do not cause pain per se. In fact, it is the chronic inflammation of the torn fascia that causes the pain. The spurs are more a result than a cause of the fasciitis.

284 What is plantar fasciitis? What is its presentation?

Plantar fasciitis is the most common cause of pain on the bottom of the heel. In fact, pain is on the plantar aspect of the calcaneus, dull and similar to that of a toothache. It typically starts upon standing or walking or running. It is usually most prominent with the first morning steps, possibly decreasing as activity progresses, but only to return after a period of rest is followed by resumption of activity. Pain resolves with rest (since this allows contraction of the plantar fascia [i.e., plantar flexion]), but restarts as soon as the first dorsiflexion step of the day restretches the irritated fascia. Although typically at the heel, pain also may radiate throughout the bottom of the foot and toward the toes. On exam, there is calcaneal tenderness at the midpoint of the plantar surface, but no tenderness with medial-to-lateral heel compression (which would otherwise suggest a stress fracture or osteomyelitis). There also may be heel tenderness with dorsiflexion of the foot or great toe, resolving with plantar flexion of the foot (since this relaxes the fascia). Edema is usually mild. There also may be a radiographic spur at the attachment of the plantar fascia, although this is not the pain’s cause (see question 283).

285 What are the causes of plantar fasciitis?

Repetitive stretching of a tight plantar fascial band, leading to microtears at its calcaneal origin, and chronic inflammation. Hence, it is common in runners and dancers who use repetitive maximal plantar flexion of the ankle and dorsiflexion of the metatarsophalangeal joints. It is especially frequent when activity level is increased, or weight suddenly gained. It is also quite common in situations of prolonged weight-bearing, such as obese patients or policemen (“policeman’s heel”).

286 What is tarsal tunnel syndrome (TTS)?

It is to the ankle what carpal tunnel syndrome is to the wrist: an entrapment of the tibial nerve or its associated branches as they pass underneath the flexor retinaculum at the medial malleolus (Fig. 21-17). This leads to numbness, tingling, and pain along the posterior tibial nerve (medial plantar surface of the foot, from first toe to heel). It also may cause motor dysfunction, weakness, and atrophy.

Figure 21-17 Tarsal tunnel syndrome.

(From Mellion MB, Walsh WM, Shelton GL: The Team Physician’s Handbook, 2nd ed. Philadelphia, Hanley & Belfus, 1997.)

287 What are the symptoms of tarsal tunnel syndrome?

The most common is a vague pain in the sole of the foot. Most patients describe this as burning or tingling. Pain and paresthesias radiate from the medial ankle distally and, occasionally, proximally. Symptoms are typically worsened by activity, especially standing and prolonged walking. They are instead reduced by rest. Findings include (1) sensory disturbance (ranging from sharp pain to loss of sensation), (2) motor disturbance (with resultant atrophy of intrinsic musculature), and (3) gait abnormality (overpronation, and a limp due to pain with weight-bearing).There also may be pain to palpation along the course of the nerve. If the condition deteriorates, the foot may become numb and weak. Tarsal tunnel syndrome can be demonstrated by tapping beneath the malleolus, which will reproduce (or worsen) the symptoms. In this regard, the tarsal tunnel tap is analogous to Tinel’s sign in carpal tunnel syndrome.

288 What are the causes of tarsal tunnel syndrome?

They may be extrinsic and intrinsic. In fact, anything that creates pressure in the tarsal tunnel can cause TTS. Extrinsic causes include crush injury, stretch injury, fracture, dislocations of the ankle, and even varicose veins (that may or may not be visible). Intrinsic causes include instead space-occupying masses such as localized tumors or cysts, bony spurs, inflammation of the tendon sheath, nerve ganglions, a venous plexus within the tarsal canal, or simply swelling from a broken or sprained ankle. Note that TTS is more common in athletes, active individuals, or those who stand a lot, since all these people put more stress on the tarsal tunnel area. A pes planus (flat foot), also may cause an increase in pressure in the tunnel region, and thus result in nerve compression. The same can occur with excessive pronation or pes cavus. Finally, patients with lower back problems (L4, L5, and S1) may have TTS too. In fact, they may have a “Double Crush” issue: one due to the nerve pinch (or entrapment) in the lower back, and the second one in the tunnel area.

Acknowledgment

The author gratefully acknowledges the contributions of Bruce I. Hoffman, MD, to this chapter in the first edition of Physical Diagnosis Secrets.