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ports and Performing Arts Medicine

ports and Performing Arts Medicine:. Upper Extremity Injuriesedric K. Akau, MD, Mark A. Harrast, MD, Seneca A. Storm, MD,

onathan T. Finnoff, DO, Stuart Willick, MD

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bjective: This self-directed learning module highlights upper limb sports and perform-ng arts injuries. It is part of the study guide on sports and performing arts medicine in theelf-Directed Physiatric Education Program for practitioners and trainees in physicaledicine and rehabilitation. Using a case vignette format, this article specifically focuses on

houlder, elbow and finger pain in athletes and wrist pain in musicians. The goal of thisrticle is to enhance the learner’s understanding on how to approach common upper limbain conditions and injuries in these populations.

.1 Educational Activity: Formulate a differential diagnosis of impingement in anathlete.

ubacromial impingement syndrome (SIS) is the most common shoulder diagnosis. Itsallmark symptom is anterolateral shoulder pain with overhead activity. Patients with SISlso describe a painful arc of motion that occurs between 70° and 120° of shoulderbduction. SIS may cause rotator cuff injury (tendonitis, tendinopathy, and tears). Symp-oms of rotator cuff injury include the previously described impingement symptoms, andain while side-lying on an adducted shoulder. Shoulder adduction results in decreased bloodow to the supraspinatus muscle 2 cm proximal to its greater tuberosity insertion site, which alsoorresponds to the most common site of rotator cuff tendinopathy. Because the long head of theiceps tendon accompanies the rotator cuff tendons as they exit the supraspinatus outlet,ymptoms of biceps tendinopathy can be associated with subacromial impingement.

The differential diagnosis of shoulder pain in the athlete includes impingement, rotatoruff disease, biceps tendinopathy, and labral pathology [1]. In older individuals, adhesiveapsulitis, osteoarthritis, and calcific tendinopathy should be considered. Cervical sourcesan also refer pain to the shoulder.

There are 2 primary categories of impingement: external and internal (Figure 1) [2,3].xternal (or subacromial) impingement can be subcategorized into primary and secondary

mpingement. Primary external (or outlet) impingement is the classic impingement de-cribed by Neer in the 1970s [2]. It typically affects those over the age of 40 y and is due ton external source (eg, thickened coracoacromial ligament, Type 2 or 3 acromions, acro-ioclavicular joint osteophytes) that reduces the supraspinatus outlet diameter. Secondary

xternal impingement is seen in the younger athlete with instability. Other factors contrib-ting to secondary external impingement include posterior capsular tightness, anterosupe-ior glenohumeral ligamentous laxity, and a protracted and downwardly rotated scapularom scapular muscle imbalances. Due to the complex nature of secondary externalmpingement, it will be discussed in greater detail below. In young throwing athletes,nternal impingement is characterized by posterior shoulder pain during the late cockinghase of throwing and is caused by surface compression of the posterior rotator cuff bursaetween the posterosuperior glenoid rim and the humeral head [4]. Subtle anteriorlenohumeral instability predisposes to internal impingement.

In the normal shoulder, the rotator cuff musculature keeps the humeral head centered inhe glenoid fossa during shoulder movements. When the rotator cuff is dysfunctional forny reason (eg, glenohumeral ligamentous laxity, scapular dyskinesis, overuse) the humeral

ead will not stay centered in the glenoid fossa and secondary external SIS of the rotator cuff

DC

M&R © 2009 by the American Academy of Physical Me934-1482/09/$36.00

rinted in U.S.A. D

.K.A. Division of Physical Medicine and Re-abilitation, University of Hawaii; Departmentf Sports Medicine and Rehabilitation, Straublinic and Hospital, 888 South King Street,onolulu, HI 96813. Address correspondence

o: C.K.A.; e-mail: cakau@straub.netisclosure: nothing to disclose

.A.H. Department of Rehabilitation Medi-ine, Department of Orthopedics and Sportsedicine, University of Washington, Seattle,Aisclosure: nothing to disclose

.A.S. Department of Physical Medicine andehabilitation, Michigan State University Col-

ege of Osteopathic Medicine, Lansing Spine &xtremity Rehabilitation/Lansing Orthopedic,C, Lansing, MIisclosure: nothing to disclose

.T.F. Department of Physical Medicine andehabilitation, College of Medicine, Mayolinic, Rochester, MNisclosure: nothing to disclose

.W. Division of Physical Medicine and Re-abilitation, University of Utah, Salt Lake City,Tisclosure: nothing to disclose

isclosure Key can be found on the Table ofontents and at www.pmrjournal.org

dicine and RehabilitationSuppl. 1, S51-S59, March 2009

OI: 10.1016/j.pmrj.2009.01.019S51

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S52 Akau et al UPPER EXTREMITY INJURIES

igure 1. Impingement syndrome subtypes. ASD � arthroscopic subacromial decompression; NSAIDS � nonsteroidal anti-

nflammatory drugs. Reprinted with permission [3] (p. 229-273).

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S53PM&R Vol. 1, Iss. 3, Supplement 1, 2009

gainst the coracoacromial arch occurs. Posterior capsularightness contributes to secondary external SIS by reducinglenohumeral joint internal rotation and forcing anterosupe-ior humeral head translation during shoulder flexion. Repet-tive loading of the posteroinferior glenohumeral joint cap-ule during the late follow-through phase of throwing mayead to capsular thickening and a reduction in shouldernternal rotation.

Another cause and/or contributing factor to secondaryxternal SIS is scapular dyskinesis [5]. Normally, scapularnd humeral motions are coordinated for efficient shoulderunction. The most common dysfunctional scapular patterns a protracted and downwardly rotated scapula, which man-fests on clinical exam as a prominence of the inferomedialcapular border. Patterns of scapular dyskinesis result fromuscle imbalances and abnormal muscle activation patterns.

rimary muscle imbalances implicated in scapular dyskinesisith impingement include a weak or inhibited serratus ante-

ior and lower trapezius and a tight or early activated pecto-alis minor and upper trapezius. Thus, rehabilitation mea-ures are initially focused on these muscular imbalances inrder to improve scapulohumeral rhythm and lessen im-ingement.

Treatment of shoulder impingement depends on the ac-uracy of 2 diagnoses: the anatomic diagnosis of the tissuenjury and a biomechanical diagnosis of the predisposingiomechanical deficits [6]. Controlling pain and inflamma-ion with relative rest, medications, and/or injections is im-erative. Kinetic chain deficits should be corrected. This isollowed by re-establishing normal shoulder range of motion,

uscle activation patterns, and scapulohumeral rhythm. Par-icular attention to the serratus anterior and lower trapezius isrequently required to establish proper scapular positioning.he next step is to retrain the individual’s proprioception andeuromuscular control. Integrating the entire kinetic chain

nto sports specific exercises is the final step prior to return toport. Isolated rotator cuff exercises should not be empha-ized.

.2 Clinical Activity: Evaluate and manage an 18-year-old right handed volleyball player experiencingclicking and pain in her right shoulder.

he differential diagnosis of shoulder pain in a competitiveolleyball player includes injury to the rotator cuff, articularartilage, capsuloligamentous structures and glenoid labrum.he glenoid labrum can be injured by direct trauma or

ndirectly via abnormal pull on the biceps anchor at theuperior glenoid. Symptoms include impaired performance,eep pain that may be difficult to localize, and clicking andatching with rotatory motions of the shoulder joint.

Labral injury is a difficult diagnosis to make clinically.hysical examination maneuvers have variable specificitynd sensitivity for labral tears [7]. Imaging of the glenoidabrum has received much attention in recent years. Theabrum is not visualized with plain films, and is inadequately

isualized with computed tomography or ultrasound. Cur- b

ent debate over labral imaging centers on whether magneticesonance arthrography (MRA) offers significant advantagesver standard magnetic resonance imaging (MRI). In MRA,ontrast medium is injected into the glenohumeral joint prioro the scan, in order to increase tissue contrast. Some authorsave reported poor sensitivity and specificity of standard MRIo detect labral pathology, while others have reported sensi-ivities and specificities between 85% and 100% [8]. Pro-pective studies of patients with surgically proven labralathology provided evidence for the diagnostic advantages ofRA over conventional MRI and computed tomography

CT) arthrography. Schulte et al [9] showed a significantmprovement in both the detection rate and characterizationf labral lesions with MRA. With the growing use of MRA,here is now a greater understanding of normal labral varia-ion and its relationship to instability. Additionally, the moreetailed depiction of labrocapsular ligament injuries haspawned a new lexicon of injury pattern acronyms, such asLAP injuries (Superior Labrum tear with Anterior and Pos-erior extension), HAGLE injuries (Humeral Avulsion of thenferior Glenohumeral Ligament), and ALPSA injuries (Ante-ior Labroligamentous Periosteal Sleeve Avulsion).

Chronic labral tears often result in the development ofaralabral synovial cysts. These cysts can attain considerableize and dissect away from their point of origin in the labrumroximally along the scapular spine. Superior paralabralysts associated with SLAP tears can extend into the supra-capular notch and compress the suprascapular nerve thatnnervates the supraspinatus and infraspinatus muscles. Su-rascapular neuropathy commonly presents as impaired per-ormance, shoulder weakness and denervation of these 2uscles. If the cyst arises from a posterior labral tear, it mayissect its way into the spinoglenoid notch, resulting inompression of the suprascapular nerve branch to the in-raspinatus only, with sparing of the supraspinatus.

There are several diagnostic and treatment options for this8-year-old athlete. Diagnostically, after a thorough history isbtained, a comprehensive neuromusculoskeletal examina-ion should be performed. The examination should includeervical spine and neurologic examinations to rule out otherauses of shoulder pain such as C4 or C5 radiculopathy.nspection should include looking for poor posture, asym-etric shoulder positioning and shoulder girdle atrophy.lenohumeral and scapulothoracic motion should be testedctively and passively. Rotator cuff strength should be tested.ests for impingement and acromioclavicular joint pathologyhould be included. Biceps, labral and capsule provocationests should be completed, including the apprehension andelocation tests, Speed’s test, Yergason’s test, O’Brien test andhe crank test.

Symptomatic treatment including acetaminophen, non-teroidal anti-inflammatory drugs and ice may be used toecrease pain and inflammation. Aggravating activitieshould be avoided when the injury is acutely flared up.adiographs should be obtained to look for occult bone and

oint injuries. If a suprascapular neuropathy is suspected,

ased on the clinical examination, electrodiagnostic testing

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S54 Akau et al UPPER EXTREMITY INJURIES

ay be warranted. If there is not great time pressure to returnhe athlete to play quickly, then a period of relative rest andhysical therapy may be instituted. Physical therapy shouldddress the rotator cuff, scapular stabilizers and any otheriomechanical deficits along the kinetic chain. In a compet-

tive athlete, however, there is often a need to quickly estab-ish a definitive anatomic diagnosis. Therefore, one shouldbtain an MRA of the shoulder to better assess the soft tissues,ncluding the labrum. If a labral tear is present, the sports

edicine team, including the athlete, trainer, therapist, phy-ician and coach need to confer on how much time, if any,hould be given to conservative care prior to proceeding withrthroscopic repair of the labral injury [10,11]. In high levelthletes competing in overhead sports, arthroscopic repairffers the greatest chance of return to elite competition.

.3 Clinical Activity: Evaluate and manage a 21-year-old baseball pitcher with elbow pain in his throw-ing arm.

he position of the elbow during overhead throwing subjectst to high repetitive loads [12]. Intense valgus and extensionorces result in medial tensile, lateral compressive, and pos-eromedial sheer stresses, respectively [13]. This section dis-usses elbow injuries in the adult athlete whose injuries resultrom these forces.

The evaluation begins with a detailed throwing history.requently, the acute presentation of elbow pain is precededy a history of chronic overuse. One must identify recenthanges in training regimen, playing position, or participa-ion level; or injuries to the elbow, shoulder, trunk, hip or leg12,14]. The pain location, its characteristics (including neu-ovascular symptoms), and the exacerbating phase of throw-ng should be identified and inquiries made about decreasedhrowing velocity and accuracy, and early fatigue [15]. Infor-ation regarding prior evaluation and treatment is veryelpful.

Physical examination of the athlete starts with a kinetichain evaluation of the leg, hip, and trunk. Two risk factorsor elbow injury are asymmetric loss of shoulder internalotation greater than 25° and weak scapular stabilizers [12].fter observing for postural asymmetry, atrophy, and inflam-atory signs, one should conduct a thorough side to side

ssessment of tenderness, range of motion (ROM), jointaxity, and neurovascular status [13,14]. Common throwingrm adaptations include an increased carrying angle (morealgus), loss of elbow extension, hypertrophy of the flexor-ronator muscle (FPM) group, and increased laxity of thelnar collateral ligament (UCL) [15].

Medial elbow tensile stress may lead to FPM tendinopa-hy, strain or tear; UCL insufficiency, or ulnar neuritis [13].he FPM injuries usually have an insidious onset and arectivity related. Physical examination reveals localized ten-erness over the involved structure with complaints of painpon isometric-resisted forearm pronation and/or wrist flex-

on [15]. It is important not to overlook an associated UCL c

ear. The FPM injuries typically respond to conservativereatment.

Because the anterior band of the UCL is the primaryestraint to valgus stress, it is therefore prone to injury [14].ost patients present with an acute injury, although some

eport a history of FPM injury or ulnar neuritis [13]. Thesethletes often do not experience pain when throwing below5% of maximum [14]. The pain will occur during thecceleration phase in 85% of patients, and during the decel-ration phase in less than 25% of patients [13]. Physicalxamination reveals UCL tenderness, pain with or withoutaxity upon valgus stress, and minimal or no pain uponsometric forearm muscle contraction [13,15]. The UCL isest palpated with the elbow in 70° to 90° flexion, since thisosition moves the FPM anterior to the UCL [13,15]. Severalalgus stress tests have been described (Figure 2) [13].

It is clinically difficult to distinguish between partial andomplete tears of the UCL. An MRA can assist in this differ-ntiation [15]. Musculoskeletal ultrasonography showsromise as a noninvasive dynamic imaging technique. Surgi-al indications for the competitive athlete’s throwing armnclude a complete tear or a symptomatic partial tear despitetrial of rehabilitation. For the athlete who chooses not to

eturn to competitive throwing, injures the nonthrowing armr has a partial tear, rehabilitation is often successful. Reha-ilitation starts with decreasing the pain and inflammationhile encouraging active rest with progressive ROM exer-

ises followed by dynamic stabilization, strengthening exer-ises and finally a step-wise return to throwing [16]. Kibler12] also recommends correcting kinetic chain deficiencies,uch as hip internal rotation inflexibility, hip abductioneakness, and restricted glenohumeral internal rotation.Although less common than UCL injuries, ulnar neurop-

thy at the elbow may arise from valgus stress, compressionrom adhesions, or from osteophytes, muscle hypertrophy orerve subluxation [14]. Athletes often present with paresthe-ias in the 4th and 5th digits and forearm and elbow achexacerbated by throwing [14]. There is usually tendernessver the nerve at the compression site and often a positiveinel’s sign [14]. Conservative treatment similar to that ofCL injuries along with protection of the nerve at the elbow

s often successful [14].Posterior elbow pain often results from valgus extension

verload (VEO) syndrome, which causes olecranon osteo-hytes, trochlear chondromalacia, olecranon stress fracturer triceps tendonitis [14]. Athletes with olecranon osteo-hytes typically complain of pain at the posteromedial elbowuring the early acceleration and follow-through phases ofhrowing [15,16]. Stress fractures present with pain over theosterolateral aspect of the olecranon during the decelerationnd follow-through phase of throwing and upon olecranonalpation [14]. Nonsurgical treatment emphasizes eccentrictrengthening exercises of the elbow flexors and correction ofaulty throwing mechanics [16]. Surgery is generally indi-

ated for athletes who fail nonsurgical treatment [14].

S55PM&R Vol. 1, Iss. 3, Supplement 1, 2009

Figure 2. Ulnar collateral ligament stress test (a) and milking maneuver (b).

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.4 Educational Activity: Develop a differential diag-nosis of wrist pain in a 23-year-old saxophonist.

ost instruments are not designed with ergonomics in mindhich often leads to awkward positioning or posture. Inoodwind instrumentalists, wrist and digits account for 31%

nd 47% of upper extremity pain complaints, respectively17]. The following section will discuss instrumentalist wristnjuries.

Patterns of injury correlate to particular instruments andeflect the demands of holding and playing the instrument.mall reed instruments do not use external supports (eg,hest harness in baritone saxophone). Therefore, the instru-ent’s full weight is borne through the musician’s posture

nd by the instrumentalist’s hand, particularly the thumb.ight thumb pain is common in clarinet and oboe players17]. Forty percent of woodwind players complain of thumbain [17]. Two common etiologies of thumb pain includeeQuervain tenosynovitis and first metacarpophalangealMCP) joint UCL laxity. Wrist hyperflexion, as seen in gui-arists, or hyperextension, as seen in harpists may result inerve entrapment or ligamentous injury. Table 1 lists theifferential diagnoses of wrist pain [18].

The history should include attention to nonmusical activ-

able 1. Differential Diagnoses of Wrist Pain

TendinopathiesdeQuervain tenosynovitisIntersection syndromeExtensor pollicis longus tenosynovitisExtensor indicis proprius (EIP) syndromeExtensor digiti minimi (EDM) tendonitisStenosing tenosynovitis and subluxation of the ECUFlexor carpi ulnaris tendonitisDigital flexor tendinitisFlexor carpi radialis tendinitis

Anomalous tendon interconnectionsLinberg syndromeSuperficialis interconnections

Ligamentous injuriesTriangular fibrocartilage complexDistal radioulnar joint subluxationCarpal instability (may feel clunk on ulnar deviation)Scapholunate dislocation

Neurologic causesDistal posterior interosseus neuropathyCarpal tunnel syndromeUlnar neuropathy at Guyon canalThoracic outlet syndromeAnterior interosseus neuropathy

Idiopathic avascular necrosisKienboch diseasePreiser disease

Rheumatologic causesOsteoarthritisRheumatoid arthritisCrystal arthropathy

dapted with permission from Forman et al [18].

ties and hobbies that may result in pain while playing music, [

ew routines on second instruments, change in practiceabits, erratic playing routines, or increased computer use atome or work.

The physical examination should include inspection, pal-ation, ROM, neuromusculoskeletal assessment and specialesting. Assessment for local joint instability and generalizedigamentous laxity should be performed. The musicianhould be observed while playing, for technique, posture,uscle tension, and shoulder, elbow, wrist, hand and digitositions.

Treatment principles for instrumentalist overuse injurynclude: relative rest (eg, pacing and limiting playing/ractice duration), postural evaluation, technique and

nstrument modifications, ensuring adequate instrumentaintenance, and warm-up exercises. Exercises to correct

inetic chain and local strength and flexibility imbalanceshould be instituted. Use of additional supports, Coban™aping or ring splints may assist in joint stabilization oracilitate retraining [19]. Physical modalities and splintingan be used for pain control. Acetaminophen and nonste-oidal anti-inflammatory medications are occasionally re-uired. In recalcitrant cases, local injections may be ben-ficial. Surgery is rarely indicated.

DeQuervain tenosynovitis involves the first dorsal com-artment of the wrist, which contains the abductor pollicis

ongus (APL) and extensor pollicis brevis (EPB) tendonsFigure 3) [20,21]. Examination may reveal tenderness andwelling over the proximal tip of the radial styloid, pain withctive or passive first carpometacarpal (CMC) joint motions,nd a positive Finkelstein test [20]. Resisted thumb extensionay cause pain in deQuervain tenosynovitis, but if theinkelstein’s test is negative, may signal CMC joint arthritis

igure 3. Locations of tenderness for several dorsal wrist ten-inopathies and tendon pain syndromes. Reprinted with per-ission [21].

19]. The previously discussed nonsurgical treatments are

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S57PM&R Vol. 1, Iss. 3, Supplement 1, 2009

ffective in 25%-90% of cases [20]. Refractory cases mayequire surgery.

Intersection syndrome occurs over the dorsal radialorearm, 4-8 cm proximal to the distal radius in the regionhere the first dorsal compartment tendons (APL andPB) cross over the second dorsal compartment tendonsextensor carpi radialis longus and brevis) (Figure 3) [21].t is characterized by pain and crepitus with active wristexion and extension. The conservative treatments out-

ined above may be effective. If wrist immobilization istilized, it should occur in 15° of extension. Surgical care

s reserved for refractory cases [20].Anterior interosseus neuropathy may present as a painless

ollapsing of the index finger’s distal interphalangeal jointDIP) while playing. This rare entity causes weakness inecond and occasionally third DIP joint flexion, first inter-halangeal joint flexion, and forearm pronation, which mayave significant functional impact on performing artists. Sen-ory deficits are absent. The instrumentalist will not be ableo perform an “OK sign” due to the aforementioned weak-esses. Electrodiagnostic studies aid in the diagnosis. Diffi-ult cases may require ultrasound or MRI to identify a com-ressive lesion. Symptoms may adversely affect playingcutely, but frequently recover over time. The principles of

Figure 4. Palmar (a) and dorsal (b) ligaments of the hand.

onsurgical treatment outlined above are usually effective. t

erial neurological examinations monitor progression. Sur-ery is not routinely required [22].

.5 Clinical Activity: Evaluate and manage a thumbinjury sustained in a fall by a 38-year-old skier.

rist and hand injuries account for 3%-9% of all upperxtremity athletic injuries [23]. In the hand, the first MCPnd CMC joints and the proximal interphalangeal (PIP) jointsf the fingers are the joints most commonly injured [23].igament injuries can be classified into three grades. Grade 1

s characterized by tenderness, no laxity; grade 2, tenderness,ild laxity, firm endpoint upon stress testing; grade 3, ten-erness, significant laxity, no endpoint upon stress testing.he PIP joint’s stability comes from its structure, which is a-sided box configuration consisting of the volar plate on thealmar aspect of the joint, and the proper and accessory collat-ral ligaments on either side of the joint (Figure 4) [23]. Thehick distal aspect of the volar plate firmly attaches to the base ofhe middle phalanx, and 2 thickened proximal slips attach to theroximal phalanx to form checkrein ligaments [23].

The commonest injury to the PIP joint is a radial collateraligament (RCL) sprain [23]. This type of injury is sustainedhen an axial load combined with dorsiflexion occurs across

ted with permission from Mayo Clinic, Rochester MN, 2008.

he PIP joint [23]. Most RCL sprains are grade 1, and can be

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reated with buddy taping (taping the injured finger to andjacent finger) and ROM exercises [23]. Grade 2 injuries arereated with PIP splint immobilization in extension for 2-3eeks followed by 2-3 weeks of buddy taping [23]. Grade 3CL injuries are treated surgically if dynamic instability isresent [23]. Grade 3 injuries are rare.

The PIP joint is the most frequently dislocated joint in theand, and may occur in volar, dorsal, or lateral directionshen an axial load is applied to the hyperextended joint [23].ccasionally an avulsion fracture of the middle phalangealase occurs at the volar plate attachment [23]. Most disloca-ions can be treated with closed reduction followed by ther-py specific to the injury, as follows: (1) dorsal dislocations:plint the PIP joint in 40° flexion during week 1, then 30°exion during week 2, and 20° flexion during week 3,ollowed by 2-3 weeks of buddy taping; (2) volar disloca-ions: splint the PIP joint in extension for 3 weeks followed by-3 weeks of buddy taping [23]; (3) unstable PIP jointislocations: treat surgically [23].

The MCP joint of the thumb is susceptible to dorsalislocations following hyperextension with or without a con-omitant torsional stress [23,24]. Usually, the volar plateisrupts proximally, which permits closed reduction [23]. Ifhe volar plate disrupts distally, soft tissues become inter-osed between the dislocated segments, necessitating openeduction [23]. When closed reduction is successful, immo-ilization of the 1st MCP joint in 40° of flexion for 10 to 21ays can be employed [24]. The athlete can usually return toompetition with a protective splint within 7 to 10 days afterhe reduction [24]. Following open reduction, a thumb spicaplint is required to facilitate safe healing of the incision sites24]. Protected return to play can be considered at 2 to 3eeks after the surgery [24].Injuries to the first MCP joint UCL are frequently referred

o as “gamekeeper’s” or “skier’s” thumb [24]. UCL injuries areue to radially directed forces to the athlete’s thumb [23].requently, with a grade 3 injury, the adductor aponeurosisecomes interposed between the ends of the ruptured UCL,hus preventing healing [24]. The palpable UCL ligamentemnant is referred to as a Stener lesion [24].

Grade 1 and 2 UCL sprains are diagnosed according to theigament injury grading criteria described above. Grade 3prains demonstrate a greater than 30° side to side MCP jointaxity difference and lack of an endpoint during stress eval-ation in full extension and 30° of flexion [23,24]. A wristlock for anesthesia, or re-examination 7 to 10 days postin-

ury can facilitate an accurate assessment [24]. Radiographicvaluation assists in ruling out fractures, and MRI can fre-uently assist in grading the injury and identifying a Stener

esion (Figure 5) [24].Treatment of grade 1 or 2 injuries consists of 2 weeks of

mmobilization in a forearm- based thumb spica orthosis,ollowed by 2 to 3 more weeks in a hand-based thumb spicarthosis [24]. This can be followed by taping the area for theemainder of the competitive season. Grade 3 injuries are

reated surgically [23,24]. *

The first MCP joint RCL is injured by ulnar-directed forces.rade 1 and 2 sprains are treated with 1 to 3 weeks of splint

mmobilization, followed by splinting during sports for 3 addi-ional weeks. Grade 3 sprains are treated surgically [24].

CKNOWLEDGMENT

he authors thank Mark S. Collins, MD, for providing theadiologic images for this Study Guide chapter.

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Figure 5. MRI image of a Stener lesion (arrow).

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*

*

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