Alexandre Rasouli MD
Ranjan Gupta MD
Elbow Pain
Anatomy
The elbow has articulations between three bones: the humerus, ulna, and radius. The humeroulnar articulation is a hinge joint between the trochlea of the medial humeral condyle and semilunar notch of the proximal ulna. The coronoid and olecranon processes of the ulna deepen the semilunar notch and increase contact at the humeroulnar joint. The humeroradial articulation is between the radial head and the capitellum of the lateral humeral condyle. The radius and ulna also articulate with each other to create the proximal radioulnar joint, between the radial head and the sigmoid notch of the ulna. These joints, together with their ligamentous and musculotendinous attachments, allow flexion and extension of the elbow, and pronation and supination of the forearm.
Musculotendinous Attachments
To achieve coordinated motion at each joint, muscle forces are usually balanced to provide precise, controlled motion. The brachialis muscle inserts on the coronoid process anteriorly whereas the triceps inserts broadly on the olecranon process posteriorly. The dorsal extensor mass originates from the lateral humeral epicondyle and includes the extensor carpi radialis longus, extensor carpi radialis brevis, extensor communis, and extensor carpi ulnaris. On the other side of the distal humerus, the pronator–flexor mass originates from the medial epicondyle and medial supracondylar ridge. It includes the pronator teres, flexor carpi radialis, palmaris longus, flexor digitorum superficialis, and flexor carpi ulnaris.
Ligamentous Attachments
Portions of each joint capsule, thickened to provide joint stability, are defined as ligaments. Complex ligamentous structures occur around every component of the elbow joint. A complex of four ligaments stabilizes the lateral elbow. They are all thickenings of the joint capsule and include, from deep to superficial, the lateral collateral ligament (LCL), the annular ligament, the accessory LCL, and the lateral ulnar collateral ligament (LUCL). The LCL attaches to the lateral epicondyle and expands distally to combine with the deep fibers of the annular ligament. The LCL confers varus stability to the elbow and tethers the annular ligament. The annular ligament attaches to the anterior and posterior aspects of the sigmoid notch, forming a ring around the radial head and neck, and provides stability during pronation–supination. The accessory LCL attaches distally to the tubercle of the ulnar supinator crest and merges with and tethers the annular ligament proximally. The LUCL attaches proximally to the lateral humeral epicondyle and distally to the supinator crest, deep to the fascia of the supinator muscle. It stabilizes the lateral elbow against rotary stresses and provides a posterior buttress for the radial head.
The medial side of the elbow is also stabilized by a complex of ligaments formed by capsular thickening. These structures include the anterior band, the posterior band, and the transverse ligament of Cooper. Of these, the anterior band is the most important in stabilizing against valgus stress. It attaches to the medial epicondyle of the humerus and the sublime tubercle of the coronoid process. It provides static and dynamic stability during the throwing arc of motion, from 20° to 120° of flexion. The posterior band stabilizes the medial elbow against internal rotary stress. Its attachments are the lateral humeral epicondyle and the olecranon process. Together with the humeroulnar articulation, the LCL and medial collateral ligament complexes are the three primary stabilizers of the elbow. Injury to any of these primary stabilizers places increased demand on the secondary elbow stabilizers, which include the radial head, the anterior and posterior elbow joint capsule, the extensor–supinator origin, the flexor–pronator origin, the anconeus, the triceps, and the brachialis.
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Neural Structures
The elbow is the causeway for the three major nerves of the distal upper extremity: the radial (and posterior interosseous) nerve, which courses anterolaterally, the median nerve, which courses along the anterior midline, and the ulnar nerve, which lies posteromedially. The radial nerve, formed by the posterior cord of the brachial plexus (roots C6, C7, C8, and T1), innervates the triceps, supinator, and wrist and digital extensors. The ulnar nerve, arising from the medial cord of the brachial plexus (roots C8 and T1), innervates the flexor carpi ulnaris, ulna-two flexor digitorum profundi, ulnar-two lumbricals, dorsal and volar interossei, adductor pollicis, and the hypothenar muscles (oppenes digiti minimi, abductor digiti minimi, and flexor digiti minimi). The median nerve is formed by the lateral and medial cords of the brachial plexus (roots C6, C7, C8, and T1) and innervates the palmaris longus, pronator teres, flexor carpi radialis, flexor digitorum profundus of the index and middle fingers, flexor digitorum sublimis, flexor pollicis longus, pronator quadratus, first and second lumbricals, and the thenar muscles (opponens pollicis, abductor pollicis, and flexor pollicis).
Compression of these nerves along their dedicated anatomic paths is a common and often treatable cause of elbow pain. Potential sites of compression for the radial nerve include the fibrous arch of the lateral head of the triceps, the arcade of Frohse, the origin of the extensor carpi radialis brevis, and neighboring structures (see the section on Radial Tunnel Syndrome). The ulnar nerve can undergo compression at the supracondylar humeral process, the arcade of Struthers, the origin of the flexor carpi ulnaris, and in Guyon's canal at the wrist (see the section on Cubital Tunnel Syndrome). Medial nerve compression can occur at the supracondylar process, ligament of Struthers, flexor digitorum arch, lacertus fibrosis, pronator teres, and the carpal tunnel.
Jobe MT, Martinez SF: Peripheral nerve injuries. In: Campbell's Operative Orthopaedics, 10th ed. Canale ST (editor). Mosby, 2003.
Mehta JA, Bain GI: Posterolateral rotatory instability of the elbow. J Am Acad Orthop Surg 2004;12:405.
Lateral Elbow Pain
Essentials of Diagnosis
Prevention
Recreational and occupational activities that involve repetitive motions predispose to lateral epicondylitis. Prevention involves attention to technique, equipment, and environmental factors. In the case of racket sports, there are several key activities that may help to prevent the development of lateral epicondylitis including (1) avoidance of poor stroke techniques (such as leading with a flexed elbow, striking the ball off center, using a single hand backstroke), (2) the use of proper grip size, (3) the appropriate racket weight, (4) looser string tension, (5) the limitation of play time to less than 2 hours, and (6) play on softer surfaces. With most work-related conditions, attention to the work station to ensure appropriate ergonomics is important in helping to prevent the development of this condition.
Clinical Findings
Most patients will complain of chronic pain in the elbow of the dominant arm, with insidious onset and localization to the lateral epicondyle. Palpation will elicit tenderness over the common extensor origin and more specifically over the origin of the ECRB. Wrist and middle finger extension against resistance with the elbow extended will replicate the primary complaint. Range of motion typically is not affected nor is sensation. Any distal motor weakness should be attributable only to pain. If there is muscle atrophy or true muscle weakness, alternative diagnoses should be explored. To address radiculopathic, arthritic, or neurologic sources that may also produce lateral elbow pain, a thorough examination of the entire upper extremity and neck should be performed. Plain radiographs of the elbow are obtained to rule out other etiologies, but will usually appear normal in the case of lateral epicondylitis. Some cases may exhibit inconsequential calcification of tissue around the lateral epicondyle. If classical signs are not present, cervical radiographs and/or electrodiagnostic tests may be performed to explore other causes of elbow pain as mentioned above.
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Gross pathological specimens of debrided tissue have revealed partial or complete tears in the origin of an extensor tendon, most often that of the extensor carpi radialis brevis. The pathologic changes are consistent with a chronic degenerative inflammatory process: edema, fibrillation, granulation, and loss of parallel collagen fiber orientation.
Treatment
Nonoperative intervention is the mainstay of treatment. Most conservative modalities aim to relieve pain, reverse inflammation, and strengthen the extensor mass. The offending activity should be either suspended or modified significantly, but cessation of all activity is to be avoided. Oral antiinflammatory agents are instituted. Poor technique and equipment are identified and should be rectified. Counterforce bracing, which increases force distribution across the extensor mass, can be adopted with a lateral arm strap. A rehabilitation program to stretch and strengthen the forearm extensor muscles is started, initially with isometric and then with progressively concentric and eccentric resistive exercises. It is often quite helpful for the patient to abduct the shoulder to 90° and have the offending arm held in extension. With the nonaffected arm, flex the wrist of the offending arm. Three sets of 10 stretches of this gradual stretching exercise should be performed four times a day. If these exercises fail to ameliorate the problem, modalities such as ultrasonography and electrical stimulation may have some utility. If pain persists, a corticosteroid injection may be administered deep to the ECRB origin, into the subaponeurotic recess. Superficial injections or injections into the substance of the tendon should be avoided.
Although most compliant patients will respond completely to a nonoperative program, persistent cases will require surgery. Surgical indications include failure of a conservative trial that lasts at least 1 year with the elimination of other possible etiologies. All surgical techniques must address the inflamed tendon. Historically, four techniques have been used: release of the common extensor origin (Hohmann tension relieving technique), lengthening of the extensor carpi radialis, intraarticular synovial and annular ligament excision, and debridement of pathological tendinous tissue with reattachment to the lateral epicondyle. The fourth technique allows resolution of symptoms and avoids some of the strength deficits reported after the classical Hohmann technique. With this technique, the extensor origin is subperiosteally detached, its inflammatory portions are sharply debrided, and it is then reattached to decorticated lateral epicondyle by sutures through transosseous tunnels. After brief postoperative immobilization, progressive range of motion is begun; light resistance exer-cises and strengthening exercises are started at 4 and 6 weeks postoperatively, respectively.
Complications
Complications of surgical intervention include strength deficits, recalcitrant pain, and functional limitation in activities such as heavy lifting.
Prognosis
Outcome in both nonsurgical and surgical cases is excellent, with up to 90% of patients reporting near to complete resolution of symptoms and return to previous level of activity.
Return to Play
A patient capable of rapid repetitive motion exercises without pain may return to normal activity with progressive increase in duration and load. Return to play usually occurs by 16 weeks.
Miller MD: Sports medicine. In: Review of Orthopaedics, 3rd ed. Miller MD (editor). W.B. Saunders, 2000.
Essentials of Diagnosis
Prevention
Radial tunnel syndrome affects individuals whose activities involve repetitive elbow extension, forearm pronation, and wrist flexion for prolonged durations. Prevention is aimed at ergonomic optimization in those settings.
Clinical Findings
Patients will complain only of pain, with tenderness to palpation most severe 2–3 cm distal to the radial head
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along the radial tunnel. The radial tunnel transmits the posterior interosseous nerve and runs from the distal aspect of the radiohumeral joint to the distal extent of the supinator muscle. The anatomic structures along the course of the tunnel can cause compression of the nerve: the fibrous margin of the ECRB, fibrous bands at the radiohumeral joint, branches of the radial recurrent artery, the arcade of Frohse, and the distal end of the supinator muscle.
The area of maximal lateral elbow tenderness is slightly distal to that observed in lateral epicondylitis. Diagnosis relies on two provocative tests. The resisted forearm supination test will reproduce the nature and location of the pain. The long finger extension test will also produce forearm pain and is elicited by resisted extension of the long finger with pressure over the P1 pulley while the forearm is supinated and the wrist extended. Although radial tunnel syndrome involves the same nerve and the same sites of compression as posterior interosseous nerve compression syndrome, there will be no reports or findings consistent with motor or sensory deficits. Consequently and in contrast to posterior interosseous nerve compression syndrome, electromyographic and nerve conduction velocity studies will be negative. In this respect, radial tunnel syndrome is unique in that its clinical manifestations have little to do with the distribution of the nerve involved.
Treatment
Nonoperative management is begun and includes rest, antiinflammatory medication, activity modification, stretching, and temporary splinting in neutral elbow position. If pain persists after 12 weeks of conservative therapy, a corticosteroid injection around the nerve at the site of maximal tenderness may be administered.
Surgical release of the compressed nerve has equivocal results and is reserved for confirmed refractory cases after at least 12 months of conservative management. Both a transverse and Thompson approach to the radial tunnel have been described. All potential sites of compression along the radial tunnel should be released. Brief postoperative immobilization is followed by increased range of motion and extensor stretching exercises.
Return to Play
Return to previous activity is permitted when provocative tests are no longer positive. For operative cases, gradual return to play may take between 6 and 12 weeks, but maximal recovery postoperatively may not occur for up to 18 months.
Lubahn JD, Cermak MB: Uncommon nerve compression syndromes of the upper extremity. J Am Acad Orthop Surg 1998;6:378.
Medial Elbow Pain
Essentials of Diagnosis
Prevention
Prevention relies on optimal pitch or stroke technique, adequate conditioning, and proper preactivity stretching and warm-up.
Clinical Findings
Medial epicondylitis is a less common cause of elbow pain in athletes than lateral epicondylitis. The primary complaint is gradual onset medial elbow pain usually without limitation in range of motion, strength, or sensation. Tenderness is maximal distal and lateral to medial epicondyle, over the origins of the two muscles that arise from the supracondylar ridge: pronator teres and flexor carpi ulnaris. Resisted forearm pronation or wrist flexion will reproduce the primary complaint. The physical examination must include an assessment of medial elbow stability, as collateral ligament sprains can mimic symptoms of epicondylitis. Ulnar nerve compression at the cubital tunnel can also replicate and may coexist with the clinical spectrum of medial epicondylitis. Radiographs may show medial collateral ligament calcification in some athletes, but are otherwise unremarkable. Magnetic resonance imaging (MRI) is useful in cases in which the diagnosis is less certain or is obfuscated by coexisting syndromes, and can be used in situations in which conservative management has failed. MRI will reveal increased signal intensity within the involved tendinous structures, consistent with an inflammatory degenerative process.
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Treatment
As with lateral epicondylitis, treatment is initially nonoperative and employs the usual modalities of rest, ice, antiinflammatory medications, temporary counterforce bracing, and perhaps adjuncts such as electrical stimulation. Limited corticosteroid injections around the area of the involved tendons may provide relief if pain persists. Modification and enhancement of the throwing technique are then initiated, along with flexor and pronator group stretching. Isometric exercises are gradually added to the rehabilitation program and when strength has improved, additional more intensive resistance exercises are started. In cases in which supervised conservative management has been attempted for at least 6 months and has failed, surgical intervention is indicated. Current techniques not only address the inflamed myotendinous structures, but also aim to preserve flexor–pronator strength. In one technique, debridement and reapproximation of the flexor–pronator mass are performed. An oblique incision is made over the medial epicondyle. The flexor–pronator origin is incised (without violation of the medial collateral complex) and elevated, and inflamed tissue is sharply debrided. The origin is then securely reapproximated to the medial epicondyle to preserve the strength afforded by the muscle group. After brief postoperative immobilization, gentle range of motion is begun in the elbow and wrist. At 6 weeks, resisted wrist flexion and forearm pronation exercises are started, with a strengthening program to follow.
Complications
Complications occur infrequently but include weakening of the flexor–pronator mass despite the best efforts to preserve its origin and reattach the flexor–pronator mass to the distal humerus.
Prognosis
Both conservative and surgical approaches lead to excellent results in about 90% of patients.
Return to Play
Gradual return to activity is permitted in nonoperative cases if resistive exercises and occupational simulation can be performed without pain. In operative cases, return to play is usually permitted by the fourth postoperative month.
Chen FS et al: Medial elbow problems in the overhead-throwing athlete. J Am Acad Orthop Surg 2001;9:99.
Essentials of Diagnosis
Prevention
Prevention relies on sound throwing techniques that minimize the valgus load on the elbow. Correction of known causes of nerve irritation including valgus instability of the elbow may also prevent the syndrome.
Clinical Findings
The cubital tunnel proper is formed by the medial epicondyle anteriorly, the elbow joint laterally, and the two heads of the flexor carpi ulnaris medially. There are structures proximal to, within, and distal to the tunnel that can cause compression, entrapment, traction, subluxation, or irritation of the ulnar nerve. Proximally, these structures include the arcade of Struthers (not to be confused with the ligament of Struthers, which is associated with median neuropathy) and the medial head of the triceps; within the groove they include the medial epicondyle, the epicondylar groove, the anconeus epitrochlearis, the two heads of the flexi carpi ulnaris, and their interconnecting ligament of Osborne; distally, offending structures include the deep flexor–pronator fascia. Regardless of cause or site, the final common pathway of cubital tunnel syndrome is the onset of nerve ischemia and fibrosis.
The syndrome will initially produce varying degrees of medial elbow pain with occasional radiation to the medial forearm. Paresthesias may occur in the ulnar two fingers. Athletes will often present before onset of weakness. Care must be taken to evaluate for ulnar collateral ligament injury, which may occur concomitantly with cubital tunnel syndrome. Mechanical complaints such as snapping may occur with nerve subluxation. The diagnosis is primarily
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clinical and relies on two provocative tests. Most patients will exhibit a positive Tinel's sign over the course of the pathology. The elbow flexion test is performed by placing the elbow in full flexion and the wrist in maximal extension. A test is positive if pain or paresthesias are elicited after 1 minute. Sensory changes can be detected with Semmes–Weinstein monofilament testing, and in more advanced cases, with two-point discrimination tests. Motor deficits often occur late and are thus infrequently observed in athletes. Changes include asymmetric hypothenar atrophy, decreased pinch and grip strength, abducted small finger or Wartenberg's sign, Froment's sign, and clawing of the ulnar two fingers. Motor deficits may not be present, even in late cases, if the intrinsic muscles of the hand receive innervation from the median nerve–the result of an anatomic variant known as the Martin–Gruber anastomosis.
A thorough examination of the neck and proximal upper extremity is performed to eliminate neuropathic etiologies with similar manifestations such as cervical radiculopathy, brachial plexopathy (of the medial cord), and thoracic outlet syndrome.
Plain radiographs including special views such as a cubital tunnel view may reveal derangements in osseous anatomy that cause compression. Similarly, MRI may identify soft tissue abnormalities with mass effect against the nerve. Electromyographic and nerve conduction velocity studies will be negative in more than 50% of patients with the syndrome. Slowing of conduction velocities to less than 50 m/s when the elbow is flexed is indicative of disease. Reduction in sensory nerve action potential also confirms early neuropathy.
Treatment
Treatment of ulnar neuropathy at the cubital tunnel is initially nonoperative: rest, ice, antiinflammatory medication, and padded splinting at 30–45° elbow flexion. Nighttime extension splinting is often quite helpful in reducing symptoms early in the disease process. Corticosteroid injections are not recommended due to the superficial position of the nerve. Conservative management will often fail in athletes due to high biomechanical demand and the potential of a subluxing ulnar nerve. Surgical indications include failed nonoperative management, ulnar nerve subluxation, and predisposing elbow pathology such as medial instability. Several techniques have been used: simple decompression, medial epicondylectomy, subcutaneous transposition, and submuscular transposition. With each technique, the ulnar nerve should be released at all possible sites of compression, from the ligament of Struthers proximally, through the cubital tunnel, past the two heads of the flexor carpi ulnaris.
Although each technique has potential complications and each has an approximately 85% success rate with primary surgery, the submuscular technique is the technique currently used for athletes. Simple decompression alone may lead to recurrence, as the medial epicondyle remains a potential offending structure. Medial epicondylectomy alone may destabilize the ulnar nerve and may disturb the medial ligamentous complex. As such, a subtotal medial epicondylectomy has been recommended in select patients. A subcutaneous transposition may leave the ulnar nerve vulnerable to direct trauma. The submuscular technique decompresses the nerve, relieves tension by transposition, and confers protection via placement between the flexor mass and pronator mass. It does require extensive dissection and may weaken the flexor–pronator musculature by altering the muscle mass origin. The flexor mass is incised to prepare the transposition bed and is reattached after anterior transposition of the released nerve. After brief postoperative immobilization, passive and then active range of motion is begun (by 4 weeks). Strengthening and throwing exercises are started by the eighth postoperative week.
Complications
Complications are uncommon but include injury to the medial antebrachial cutaneous nerve, injury to the medial collateral ligament complex, and perineural scarring. Coexisting medial elbow pathology may also limit the success of surgical intervention.
Prognosis
Conservative therapy has excellent results except in high-demand athletes. Results of surgical intervention vary inversely with the degree of preoperative nerve involvement. This can be a career-ending insult to a throwing athlete if the pathology had been present for a prolonged time prior to treatment.
Return to Play
Many patients with good to excellent results return to unrestricted play by 6 months postoperatively.
Chen FS et al: Medial elbow problems in the overhead-throwing athlete. J Am Acad Orthop Surg 2001;9:99.
Dinh PT, Gupta R: Subtotal medial epicondylectomy as a surgical option for treatment of cubital tunnel syndrome. Tech Hand Upper Extremity Surg 2005;9(1):52.
Essentials of Diagnosis
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Prevention
Proper throwing technique and exercises that enhance flexibility help minimize the risk of ligament injury during play.
Clinical Findings
A patient with acute medial collateral injury will have sudden moderate to severe pain at the posteromedial elbow and will not be able to resume activity until treated. Patients may report feeling a “pop” at the time of injury and some patients may be unable to resume throwing. Activities of daily living are not affected, however, and most patients will report pain only during the act of throwing. Mechanical symptoms such as locking may also occur if loose bodies are present. In addition to palpation, physical examination relies on valgus stressing of the elbow to reproduce the primary complaint. Valgus stressing is performed with the elbow in 30° of flexion, which specifically stresses the anterior band. Increased medial space opening, lack of a firm endpoint, apprehension, and/or elicitation of pain all suggest medial collateral ligament failure. The crucial posterior aspect of the anterior band can be stressed using the “milking maneuver,” in which valgus force is applied to the maximally flexed elbow (>90°) with the forearm in supination. Joint space opening, apprehension, or replication of medial side pain reveals ligament injury. Chronically affected athletes may exhibit limitation in elbow extension due to flexion contractures caused by the inflammatory process. Patients with chronic injury may exhibit signs and symptoms consistent with ulnar neuropathy from secondary cubital tunnel syndrome secondary to traction forces.
Stress radiographs are used to quantify the degree of joint space opening. The threshold above which medial collateral ligament incompetence is suspected is 3 mm of gapping. Standard plain films are obtained to rule out other pathology and to identify the presence of loose bodies secondary to injury. Calcification of ligament structures is expected in chronic cases. Furthermore, chronic medial instability will overload the lateral aspect of the elbow at the radiocapitellar joint. Plain films should be evaluated to determine if joint space narrowing and asymmetry are present. MRI can verify the diagnosis and may help to characterize the nature of the injury as avulsion or tear.
Treatment
In about 50% of injured athletes, nonoperative intervention is effective. Rest and antiinflammatory medication are used to address the pain. A rehabilitation program consisting of flexor–pronator mass strengthening is then started to enhance dynamic elbow stabilization. Throwing exercises are then started at 3 months, with gradual return to play when the symptoms do not recur. In cases in which the athlete does not respond to nonoperative therapy by 3 months or in acute cases of total ligament rupture or major avulsion, surgical intervention is indicated. Avulsion is treated by repair of the ligament back to its respective attachment. Ligament reconstruction, usually with the palmaris longus tendon, is employed in more chronic cases or with mid-substance tears. In ligament reconstruction, the elbow is approached through a medial incision centered at the epicondyle and the flexor–pronator origin is left intact. The flexor mass is longitudinally split and the ligament and capsule are then incised; transosseous tunnels in the coronoid and epicondyle are created. The harvested graft is then applied and appropriately tensioned in a figure-of-eight configuration. Ulnar nerve transposition is performed only if there is evidence of attendant ulnar nerve irritation or subluxation.
Complications
Complications include graft rupture or fatigue, ulnar nerve injury, medial antebrachial cutaneous nerve injury, and, rarely, donor site morbidity when grafts other than the palmaris longus are used. Postoperative immobilization is brief, with active range of motion started early. Strengthening exercises are started by 4–6 weeks postoperatively.
Prognosis
Some athletes treated nonoperatively will be able to return to play by 3 months. Those who eventually require surgery usually have good to excellent results.
Return to Play
Return to play is gradual. Valgus stressing of the elbow is to be avoided until 4 months, at which time gentle throwing exercises are begun. Throwing intensity is slowly increased with a return to the previous level of play not occurring until about 12–18 months postoperatively.
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Cain EL Jr et al: Elbow injuries in throwing athletes: a current concepts review. Am J Sports Med 2003;31:621.
Chen FS et al: Medial elbow problems in the overhead-throwing athlete. J Am Acad Orthop Surg 2001;9:99.
Posterior Elbow Pain
Essentials of Diagnosis
Prevention
Development of a sound throwing technique and proper conditioning of the flexor–pronator mass will minimize excessive stress on the posteromedial elbow during throwing. Early identification of valgus elbow instability may prevent secondary impingement.
Clinical Findings
The acceleration and follow-through phases of throwing place enormous stress on the medial collateral ligament complex of the elbow. Overuse and lack of support from a properly conditioned flexor–pronator mass will lead to valgus extension overload: microtears in the medial collateral ligament complex allow transient valgus elbow subluxation during extension (late-phase throwing), whereby excessive force is transmitted to the posterior aspect of the elbow. The altered biomechanics create abnormal cyclic impaction of the olecranon against the olecranon fossa and trochlea, which produces hypertrophy and osteophyte formation on these structures. The resulting limitation in joint space leads to posterior impingement.
Patients will complain of posterior elbow pain during terminal extension. Catching and locking may be present if the osteophytes have become loose bodies. Physical examination will reveal tenderness to palpation along the posteromedial olecranon. Range of motion is limited at the extremes of extension, and rapid extension with valgus stress on the elbow will reproduce the primary complaint (the valgus extension overload test). An assessment of gross elbow valgus stability should also be performed as posterior impingement is associated with instability and will recur if the instability is not addressed. Plain radiographs, especially the true lateral elbow view, may demonstrate olecranon or olecranon fossa osteophytes, although such osteophytes are often not detected with radiography. Stress views and MRI are used to evaluate for medial collateral ligament failure. The latter can also reveal loose bodies when intraarticular contrast is used.
Treatment
Throwing is initially avoided. A treatment regime of rest, ice, antiinflammatory medication, and flexor–pronator mass strengthening is initiated. If the pain ceases, an interval-throwing plan is started. Athletes whose symptoms persist despite extended rehabilitation or whose pathology is secondary to established valgus laxity are candidates for surgery. Surgery usually involves arthroscopic excision of olecranon osteophytes, removal of loose bodies, and debridement of areas with chondromalacia. Lesions of the medial collateral complex can also be visualized for later open repair. Excision should be limited to the osteophyte itself, as removal of additional normal bone will lead to increased valgus angulation of the elbow. Elbow range of motion is started the day of surgery, and strengthening exercises of the wrist and forearm are started shortly thereafter. Shoulder strengthening and interval-throwing exercises are implemented by 10 weeks.
Complications
The most serious complication is damage to neurovascular structures during arthroscopic portal introduction and debridement. Inadequate surgeon experience or knowledge of anatomic relationships will place the radial, median, ulnar, medial antebrachial cutaneous, and anterior interosseous nerves all at risk.
Prognosis
Outcome as measured by return to previous level of activity is excellent for most operative and nonoperative cases. Some patients may require further surgical procedures if there is recurrence. The precise recurrence rate is not known, but is higher when primary causes such as instability are not corrected.
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Return to Play
In operative cases, unrestricted play is usually allowed by 12 weeks postoperatively.
Essentials of Diagnosis
As with posterior impingement syndrome, posteromedial shear is secondary to valgus extension overload. The excessive valgus torque through the posteromedial elbow causes shear stress between the posteromedial olecranon and the olecranon fossa, which results in pain during the acceleration phase of throwing. Prevention, clinical findings, treatment, and prognosis are similar to those for posterior impingement syndrome (see above). Traction spurs on the medial aspect of the olecranon notch are especially common.
Cain EL Jr, Andrews JR: Arthroscopic management of posterior elbow impingement in throwers. Tech Shoulder Elbow Surg 2001;2:118.
Essentials of Diagnosis
Prevention
Proper conditioning and throwing technique and avoidance of overuse are the fundamentals of prevention.
Clinical Findings
Patients are principally male and are involved in high-intensity throwing or heavy manual labor. The precipitating injury is traction of the tendon at its olecranon insertion site during resisted elbow extension. The primary complaint is posterior elbow pain with extension against resistance. Maximal tenderness is directly over the triceps insertion. Both of these clinical hallmarks distinguish this overuse syndrome from other causes of posterior elbow pain. Plain radiographs should be obtained, and will often reveal olecranon osteophytes at the insertion site. These osteophytes serve to exacerbate injury and perpetuate symptoms.
Treatment
Treatment is almost always nonoperative and consists of rest, ice packs, antiinflammatory agents, and temporary bracing. Stretching and strengthening exercises are started when acute pain subsides. Corticosteroid injections will weaken the triceps tendon and are contraindicated. If pain persists despite 3–6 months of conservative management and other causes have been ruled out, excision of the spur and repair of the triceps tendon (so as to avoid the complication of tendon rupture) may be performed. A rehabilitative regime similar to that of nonoperative treatment is then instituted.
Return to Play
Return to unrestricted activity is permitted when the patient no longer has symptoms associated with provocative maneuvers and has regained full extension strength and range of motion.
Gabel GT: Acute and chronic tendinopathies at the elbow. Curr Opin Orthoped 2000;11:56.
Elbow Instability
Valgus Instability
The essential features, diagnosis, treatment, and prognosis of valgus elbow instability are described in the section on Medial Elbow Pain and the section on Ulnar Collateral Ligament Sprain & Valgus Instability.
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Posterolateral Rotary Instability
Essentials of Diagnosis
Prevention
In the athletic setting, posterolateral rotary instability (PLRI) is usually a sequela of elbow trauma, and prevention is less important than early detection, which comes from a meticulous history and physical examination. PLRI can also be an iatrogenic injury and may result from surgical approaches that violate the LCL (Kocher approach) or release the LCL from its distal attachment (Boyd approach). The incidence of PLRI decreases when the LCL is repaired or reattached during these procedures.
Clinical Findings
PLRI may have many causes including previous elbow dislocation, elbow sprains, destabilizing fractures of the radial head, fractures of the coronoid, global ligament laxity, and cubitus varus elbow alignment. The final common pathway is laxity or complete disruption of the LUCL, which renders the elbow unstable against the combined vector of axial compression, external rotation (or ulnar supination), and valgus force. As a result, the ulna can undergo an abnormal external rotary moment about the humerus, which causes the radial head to sublux behind the capitellum.
PLRI not only eliminates athletic performance, it also significantly affects regular daily activities of living. Patients may report recurrent subluxations/dislocations of the elbow, painful clicking, and mechanical symptoms. Apprehension is reported when the forearm is in extension and supination. Clinical examination will reveal no areas of tenderness and standard tests for varus or valgus laxity are unremarkable. Diagnosis depends on a positive posterolateral rotary instability test, described by O'Driscoll et al. The patient is supine while the arm is placed over the head. The examiner holds the forearm in full supination and extension, and applies a gradual flexion, varus, and axial moment to the elbow. At mid-flexion, the elbow will undergo external rotary subluxation, with subluxation of the radial head that can be palpated posteriorly. Continued flexion will cause the triceps to reduce the radial head, which produces a noticeable clunk. The series of events, or apprehension during the provocative maneuvers, constitutes a positive test. This test may be positive only when the patient is evaluated under anesthesia. The supination chair push-up test and posterolateral rotary drawer test are also useful clinical indicators.
Plain radiographs may reveal abnormal humeroulnar joint widening and stress views or fluoroscopy during the PLRI test may show rotary subluxation.
Treatment
Nonsurgical management is rarely appropriate, particularly for the high-level athlete. Surgical correction relies either on (1) proximal advancement of the lateral collateral ligament complex if the tissue is structurally intact, or (2) reconstruction of the lateral complex using a palmaris longus graft with transosseous suture fixation in chronic cases or when sufficient ligamentous tissue is not present. Other autogenous graft sources may also be used. The approach in either case, as described by Mehta and Bain, is a lateral Z arthrotomy centered over the annular ligament to prevent further injury to lateral structures. Postoperative management consists of brief splinting of the elbow at 90° of flexion and the forearm in mid-pronation. A gradual increase in extension is allowed in a locking hinged elbow brace.
Complications
Complications include elbow flexion contracture, but this is often less than 20°.
Prognosis
Successful repair or reconstruction of the lateral complex allows return to play by 6 months in most cases.
Mehta JA, Bain GI: Posterolateral rotatory instability of the elbow. J Am Acad Orthop Surg 2004;12:405.
O'Driscoll SW et al: Posterolateral rotatory instability of the elbow. J Bone Joint Surg Am 1991;73:440.
Wrist Pain
Anatomy
The wrist includes the distal radioulnar joint, radiocarpal joint, triangular fibrocartilaginous complex, and eight carpal bones. The carpal bones include the capitate,
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trapezoid, trapezium, scaphoid, lunate, triquetrum, hamate, and pisiform.
The ulnar head articulates with the distal radius at its lesser sigmoid notch to form the distal radioulnar joint. The joint is principally stabilized by the dorsal and volar radioulnar joints. The radius also articulates with the scaphoid and lunate at its respective facets to form the radiocarpal joint. These articulations are in turn stabilized by a series of extrinsic (wrist-spanning) ligaments: the radial collateral, radioscaphoid, radiolunate, radiotriquetral, radioscaphocapitate, radiolunotriquetral, and radioscapholunate. The radiocarpal joint alone transmits up to 75% of the axial load across the wrist.
Analogous to the articulation between the radius and carpus, the ulna is also intimately associated with the proximal carpal row via the triangular fibrocartilagenous complex (TFCC). The TFCC is a network of ligamentous and cartilagenous structures that spans the wrist between the ulna, radius, and carpus; it allows the ulna to bear 25% of the axial wrist load. The TFCC is composed of the ulnar collateral ligament, the dorsal and volar radioulnar ligaments, the sheath of the extensor carpi ulnaris, the articular disc, the meniscal homologue, and the ulnolunate and ulnotriquetral ligaments.
The carpal bones are organized into proximal (scaphoid, lunate, triquetrum, pisiform) and distal (trapezium, trapezoid, capitate, hamate) rows. Proper wrist kinematics and stability rely heavily on the numerous intrinsic (interosseous) ligaments that interconnect every and all carpal bones. Dorsally, these include the intercarpal, trapeziotrapezoid, dorsal capitotrapezoid, and dorsal capitohamate ligaments. Volarly, they include the volar capitohamate, volar capitotrapezoid, deltoid (between the trapezium and capitate and triquetrum and capitate), lunotriquetral, and scapholunate ligaments.
Gupta R et al: Kinematic analysis of the distal radioulnar joint after a simulated progressive ulnar-sided wrist injury. J Hand Surg 2002;27A:854.
Wright PE II: Wrist disorders. In: Campbell's Operative Orthopaedics, 10th ed. Canale ST (editor). Mosby, 2003.
Scaphoid Fracture
Essentials of Diagnosis
Prevention
Although scaphoid fractures cannot be avoided, early clinical detection and prompt treatment will prevent complications of fracture nonunion and wrist instability.
Clinical Findings
Athletes will complain of radial wrist pain (classically dorsal, but also volar), with swelling, and wrist stiffness after a fall on the outstretched hand. Tenderness is elicited over the anatomic snuffbox between the tendons of the extensor pollicis longus and brevis, or over the tubercle at the scaphotrapezial joint. A thorough radiographic assessment is essential, but will fail to detect fractures 36% of the time. The series should consist of posteroanterior (PA), lateral, and clenched fist ulnar deviation views. Lateral views should be reviewed for intrascaphoid angulation and the presence of carpal instability patterns [such as dorsal intercalary instability (DISI)], which indicate an unstable fracture. Although bone scans have historically been used to evaluate for occult scaphoid fractures, MRI is now more routinely used for immediate radiographic diagnosis. MRI also plays a role in assessing the viability of fracture fragments in the case of nonunions, particularly if the fracture involves the watershed region at or proximal to the scaphoid waist. Computed tomography (CT) scans are useful for assessing fracture union during treatment or in cases in which nonunion is suspected.
Treatment
Only stable scaphoid fractures—nondisplaced, nonangulated fractures without associated carpal instability—may be treated nonoperatively. A short arm thumb spica cast is applied for 12–16 weeks. Healing time approaches 12 weeks, but union rates approach 90% with appropriate treatment. Recent research has demonstrated that even stable fractures may be treated operatively with percutaneous screw fixation with minimal additional morbidity. In cases of elite athletes, the fracture can be percutaneously fixed and placed in a playing cast. Patients may return to competition in about 2 weeks but continue to wear the cast until healing is clinically and radiographically evident.
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Unstable fractures, which have ≥1.0 mm displacement, are comminuted, are fractured at the proximal pole, have an intrascaphoid angulation >45°, or exhibit carpal instability patterns should undergo reduction and internal fixation. Without operative intervention, the risk of nonunion/malunion and disability is high. Union is often assessed by CT scan. Nonunions must undergo open treatment and internal fixation, with or without vascularized bone grafting, depending on the viability of the proximal fragments. Proximal pole fracture and nonunions are approached dorsally, whereas waist fractures are usually addressed volarly.
Prognosis
Both nonoperative and operative outcomes are very good. Highly comminuted fractures, nonunions that undergo correction, and cases with carpal instability have more variable results.
Return to Play
Return to play after fixation of unstable fractures depends on postoperative fracture stability. Unprotected play is allowed when the patient is no longer symptomatic, has regained full range of motion, and has exhibited complete healing on radiographs or CT scan.
Bond CT et al: Percutaneous screw fixation or cast immobilization for nondisplaced scaphoid fractures. J Bone Joint Surg Am 2001;83-A(4):483.
Morgan WJ, Slowman LS: Acute hand and wrist injuries in athletes: evaluation and management. J Am Acad Orthop Surg 2001;9:389.
Trumble TE et al: Management of scaphoid nonunions. J Am Orthop Surg 2003;11:380.
WRIST SPRAINS
Injury to the scapholunate ligament occurs in contact/ collision or after a fall on a hand with wrist extension and ulnar deviation (intercarpal supination). Patients will exhibit swelling and pain along the dorsum of the wrist. Tenderness is maximal at the scapholunate interval dorsally. The Watson's sign is elicited by placing dorsal pressure over the distal scaphoid while shifting the wrist from ulnar to radial deviation; the maneuver will result in pain and an audible click. With established, complete ligament tears, plain PA radiographs will show that the scapholunate interval or gap is 2 mm or greater, and the lateral view will demonstrate the characteristic DISI pattern. The clenched-fist view can also further demonstrate the injury. MRI can diagnose complete ligament tears with ease, but partial tears are harder to appreciate and clinical acumen is required. Treatment involves arthroscopic confirmation of the diagnosis and then open repair or reconstruction. In cases in which the tear is incomplete, percutaneous pinning for 4–6 weeks may be employed. In acute cases, open repair of the ligament is performed with or without augmentation using the dorsal intercarpal ligament. Chronic cases may not be amenable to repair after 9 months and remain an unsolved problem. Salvage procedures include bone–ligament–bone graft reconstruction or partial carpal fusion. Untreated patients will invariably develop carpal collapse and wrist arthritis. Carpectomy or arthrodesis may need to be performed in these cases. Results are variable and depend on the severity and chronicity of the injury.
Tears in the lunotriquetral ligament result from a fall on an outstretched hand, with the wrist in extension and radial deviation (intercarpal pronation). The patient will report ulnar-sided wrist pain, weakness, and other mechanical complaints. Tenderness is maximal over the lunotriquetral interval. Pain is reproduced with the lunotriquetral shear test, in which the pisiform and triquetrum are pressed in a dorsal direction while the lunate is pressed in a volar direction. Diagnosis in most cases is clinical. Radiographs are often normal but may show the characteristic volar intercalary instability (VISI), which will occur if the dorsal radiotriquetral ligament is also torn. MRI exhibits poor resolution of this ligament. Treatment by immobilization is successful in most patients, with return to play in a matter of weeks if the ligament is not completely torn. Surgery is reserved for only the most resistant cases, as return to play is lengthy, from 2 to 6 months. Procedures include bone–ligament–bone reconstruction, arthroscopic debridement, carpal fusion, and ulnar shortening osteotomy.
Instability between a proximal and distal row (carpal instability nondissociative) occurs when the ligamentous attachment between the capitate and the proximal carpal row is injured. Athletes will report ulnar wrist pain. The catch-up clunk is a diagnostic maneuver in which the proximal row does not move into dorsiflexion until late into a sweep from radial to ulnar deviation. The sudden shift is manifested as a clunk. Abrogation of the clunk with dorsally directed pressure over the pisiform secures the diagnosis. Radiographs may show a volar intercalary instability pattern. Treatment is usually nonoperative, and employs ulnar carpus support splinting
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and antiinflammatory medication. Surgical procedures are reserved for severe cases, and include thermal shrinkage, ligament reconstruction, or midcarpal arthrodesis. Results are unimpressive.
Injuries to the distal radioulnar joint (DRUJ) and its closely associated structure, the TFCC, are common in a wide range of sports. Tears may be either traumatic or degenerative. Hypersupination, traction, and axial loading with rotational stress are possible mechanisms. Tenderness over the TFCC is best assessed by palpating between the ulnar styloid and pisiform. Damage to the DRUJ is often revealed by painful and excessive volar–dorsal shuck between the radius and ulna at the wrist, a provocative maneuver known as the piano key sign. The TFCC grind is another provocative maneuver performed with the wrist in ulnar deviation and dorsiflexion, while the carpus is rotated on the wrist by the examiner as an axial load is applied on the hand. Physical examination as described above is often the most reliable diagnostic modality. Plain radiographs may reveal ulnar styloid fractures, widened radioulnar joint space, and distal ulnar subluxation. Comparison CT images of the DRUJ with the forearm in supination and pronation may reveal abnormal excursion and hence instability. High-quality MR images may show TFCC tears, but are often equivocal based on the quality of the imaging system. Wrist arthroscopy is used to confirm the diagnosis and is considered the gold standard. For individuals with central lesions, early arthroscopic debridement of the TFCC is advocated, followed by splinting and early range of motion. Return to play with restrictions occurs by 6 weeks. With peripheral sided tears, arthroscopic repair is performed followed by immobilization for 6 weeks. A DRUJ that remains unstable after arthroscopic repair may be augmented by pinning the DRUJ with the forearm in maximum supination. Return to play is allowed at 4 months. Results for both groups are excellent. With chronic or degenerative injuries, a shift in wrist biomechanics occurs, with increased load through the radiocarpal joint. Abnormal ulnar variance may be present and ulnar shortening procedures along with carpal arthroscopy may be indicated.
Gupta R et al: Wrist anthroscopy: indications and technique. J Am Acad Orthop Surg 2001;9(3):200.
Gupta R et al: Kinematic analysis of the distal radioulnar joint after a simulated progressive ulnar-sided wrist injury. J Hand Surg 2002;27A:854.
Rettig AC: Athletic injuries of the wrist and hand, part 1: traumatic injuries of the wrist. Am J Sports Med 2003;31:1038.
Hand Pain
Ulnar Collateral Ligament Injury of the Thumb
Essentials of Diagnosis
Clinical Findings
In addition to obtaining a history and performing a physical examination, careful palpation of the MCP base should be performed to identify the Stener lesion. This lesion occurs when there is complete detachment of the ulnar collateral ligament from the phalangeal base and displacement over the adductor pollicis. This interposition will prevent proper healing unless surgically corrected. Radiographic stress views will reveal MCP joint instability and the degree of ligament injury. A complete rupture is indicated by opening of 30° or more on multiple views.
Treatment
Nondisplaced avulsion fractures are treated with a thumb spica cast for 4 weeks, and the thumb is then protected in a custom-molded splint after return to play is allowed. In patients with complete ruptures and Stener lesions, surgical correction is required acutely. This is done by a tension band technique, interfragmentary screw, or the use of mini-Mitek suture anchors. Immobilization lasts for 4 weeks, after which a custom-molded splint is applied.
Prognosis
Outcomes for both nonoperative and successful operative cases are excellent, provided the patient is compliant with protection splinting and taping.
Return to Play
Return to play is permitted with a protection splint and rigid taping of the thumb MCP.
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Finger Injuries
Mallet Finger & Jersey Finger
Mallet finger is a flexion deformity of the distal interphalangeal (DIP) joint that is the result of a disruption in the extensor mechanism. The unopposed force of the flexor digitorum profundus moves the terminal phalanx into flexion. Injury is usually the result of forcible flexion of the joint during active extension, usually when catching a ball, hence the injury is commonly called “baseball” or “drop finger.” Two forms of mallet finger exist, one involving only the tendon and the other involving an avulsed fracture fragment. Three-view radiographs are recommended as bony mallets are difficult to diagnose by physical examination alone. Severe injuries may involve volar subluxation of the distal phalanx. Treatment includes extension splinting for 8 weeks with 80% achieving good to excellent results. If the injury is associated with a fracture or subluxation, reduction of the distal fragment should be performed. Mallet finger can be treated for up to 4 months after the initial injury. After that time, provided the joint is supple and without arthritis, reconstruction of the tendon may be a treatment option. In other cases, DIP fusion is recommended. Swan neck deformities may develop over time if there is laxity of the volar plate. Follow-up examinations should be performed every 2 weeks, and the finger retested. An additional 2–4 weeks of splinting may be required.
A Jersey finger is the result of the avulsion of the flexor digitorum profundus when a flexed DIP joint is forced into extension. Injuries can occur when a player grabs another jersey during a game, or when lifting a latch on a car door. The ring finger is most commonly affected. Patients are unable to flex the DIP joint and have swelling and prominence of the digit. Three-view radiographs are recommended to identify bony avulsions. Early diagnosis is important as the treatment for Jersey fingers is almost always operative. Delays can result in fibrosis and scarring of the tendon sheath. Pure tendinous injuries allow the flexor digitorum profundus to retract to the palm, whereas injuries with bone fragments tend to limit retraction to the level of the middle phalanx.
The Jersey finger is classified into four types: Type I, the tendon retracts to the palm with rupture of the vincula; Type II, the tendon retracts to the proximal interphalangeal joint and is held by the vinculum; Type III, a large bony fragment catches on a pulley at the middle phalanx; and Type IV, a bony avulsion with the tendon avulsed to the fragment.
Treatment varies by type. Type I injuries should be repaired in 7–10 days from the onset of injury as the tendon is dysvascular. Repair of Type II injuries can be done within 6 weeks. In Type III injuries, open reduction with internal fixation (ORIF) is performed. Type III injuries involve repair of the articular fragment with secondary repair of the distal phalanx. Type IV injuries involve dynamic rehabilitation of the tendon with passive flexion, dorsal block splint, and active extension exercises.