Current Diagnosis and Treatment in Orthopedics, 4th Edition

Chapter 4. Sports Medicine


Sports medicine developed in the 1970s as an orthopedic specialty focusing on competitive athletes. Today, sports medicine includes the overall care of athletes from many skill levels. Increasingly, care of recreational athletes has risen to that common for professional athletes. The initial focus of sports medicine on knee injuries now also includes other musculoskeletal injuries, including the shoulder, elbow, and ankle. In addition to the musculoskeletal system, emphasis is placed on the cardiovascular and pulmonary systems, and on training techniques, nutrition, and women's athletics. This wide range of care requires a multidisciplinary team of medical personnel, including athletic trainers, physical therapists, cardiologists, pulmonologists, orthopedic surgeons, and general practitioners.



The bones of the knee are the distal femur, the proximal tibia, and the patella. These bones depend on supporting ligaments, the joint capsule, and the menisci to provide stability for the joint.


The menisci, or semilunar cartilages, are C-shaped fibrocartilaginous disks in the knee that provide shock absorption, allow for increased congruency between joint surfaces, enhance joint stability, and aid in distribution of synovial fluid.

The medial and lateral menisci provide a concave surface with which the convex femoral condyles can articulate. If the menisci are not present, the convex femoral condyles articulate with the relatively flat tibial plateaus, and the joint surfaces are not congruent. This situation decreases the surface area of contact and increases the pressure on the articular cartilage of the tibia and femur, which may lead to rapid deterioration of the joint surface. The medial meniscus is firmly attached to the joint capsule along its entire peripheral edge. The lateral meniscus is attached to the and posterior capsule, but there is a region posterolaterally where it is not firmly attached (Figure 4–1). Therefore, the medial meniscus has less mobility than the lateral meniscus and is more susceptible to tearing when trapped between the femoral condyle and tibial plateau. The lateral meniscus is larger than the medial meniscus, and carries a greater share of the lateral compartment pressure than the medial meniscus carries for the medial compartment.

Figure 4–1.


The medial and lateral menisci with their associated intermeniscal ligaments. Note: The lateral meniscus is not attached in the region of the popliteus tendon.

(Reproduced, with permission, from Scott WN: Ligament and Extensor Mechanism Injuries of the Knee: Diagnosis and Treatment.Mosby-Year Book, 1991.)


Within the knee, the anterior cruciate ligament (ACL) travels from the medial border of the lateral femoral condyle to its insertion site anterolateral to the medial tibial spine. This ligament prevents anterior translation and rotation of the tibia on the femur (Figure 4–2). The posterior cruciate ligament (PCL) prevents posterior subluxation of the tibia on the femur. It runs from the lateral aspect of the medial femoral condyle to the posterior aspect of the tibia, just below the joint line (Figure 4–3). On the medial side, the medial collateral ligament has superficial and deep portions (Figure 4–4), which stabilize the knee to valgus stresses. The lateral collateral or fibular collateral ligament runs from the lateral femoral condyle to the head of the fibula. It is the main stabilizer against varus stress (Figure 4–5). The lateral collateral ligament is part of the posterolateral "complex" or "corner" of the knee that also resists external rotation. An important component is the popliteofibular ligament, present in 90% of knees, that runs from the tendon of the popliteus muscle to the styloid on the posterior fibular head.

Figure 4–2.


Drawing of the anterior cruciate ligament with the knee in extension, showing the course of the ligament as it passes from the medial aspect of the lateral femoral condyle to the lateral portion of the medial tibial spine.

(Reproduced, with permission, from Girgis FG et al: The cruciate ligaments of the knee joint: Anatomical, functional, and experimental analysis. Clin Orthop 1975;106:216.)


Figure 4–3.


Drawing of the posterior cruciate ligament, showing the course of the ligament as it passes from the lateral aspect of the medial femoral condyle to the posterior surface of the tibia.

(Adapted, with permission, from Girgis FG et al: The cruciate ligaments of the knee joint: Anatomical, functional, and experimental analysis. Clin Orthop 1975;106:216.)


Figure 4–4.


Medial capsuloligamentous complex.

(Reproduced, with permission, from Feagin JA Jr: The Crucial Ligaments. Churchill Livingstone, 1988.)


Figure 4–5.


The lateral supporting structures of the knee.

(Reproduced, with permission, from Rockwood CA Jr et al: Fractures in Adults, 2/e. New York Lippincott, 1984.)

History & Physical Examination


The history of knee injury may be obtained by asking the patient the questions listed in Table 4–1. The physical examination begins with observation of the patient's gait. The uninjured knee is then examined as a basis of comparison with the injured knee. Any swelling or effusion should be noted. A small effusion causes obliteration of the recesses on the medial and lateral aspects of the patellar tendon; with a larger effusion, diffuse swelling is present in the region of the suprapatellar pouch. Then, a fluid wave can be palpated on the sides of the patella. Active and then passive range of motion is tested carefully. The knee is palpated to define areas of localized tenderness. The joint lines are located at the level of the inferior pole of the patella when the knee is flexed to 90 degrees.

Table 4–1. History of a Knee Injury.

Did an injury occur?

Yes: possible ligament tear or meniscus tear.

No: overuse problem or degenerative condition.

Was it a noncontact injury?

Yes: often the ACL is the only ligament torn.

Was it a contact injury?

Yes: possible multiple ligament injuries, including ACL and MCL, ACL and LCL, ACL, PCL, and a collateral ligament.

Did the patient hear or feel a pop?

Yes: a pop often occurs with ACL tears.

How long did it take to swell up?

Within hours: often an ACL tear.

Overnight: often a meniscus tear.

Does the knee lock?

Yes: often a meniscus tear flipping into and out of the joint.

Does it buckle (trick knee)?

Yes: not specific; may arise from quadriceps weakness, trapped meniscus, ligament instability, or patella dislocating.

Is climbing or descending stairs difficult?

Often patellofemoral problems.

Are cutting maneuvers difficult?

ACL tear.

Is squatting (deep knee bends) difficult?

Meniscus tear.

Is jumping difficult?

Patellar tendinitis.

Where does it hurt?

Medial joint line: medial meniscus tear or medial compartment arthritis.

MCL: MCL sprain.

Lateral joint line: lateral meniscus tear, injury, iliotibial band tendinitis, popliteus tendinitis.


ACL = anterior cruciate ligament; MCL = medial collateral ligament; LCL = lateral collateral ligament; PCL = posterior cruciate ligament.


To determine varus and valgus stability (Table 4–2), the patient's foot is held between the examiner's elbow and hip, with both hands free to palpate the joint (Figure 4–6). Stability should be determined at both full extension and 30 degrees of knee flexion. Grading of laxity is based on the amount of opening of the joint (grade 1, 0–5 mm; grade 2, 5–10 mm; and grade 3, 10–15 mm). Laxity in full extension to varus or valgus angulation is an ominous sign that indicates disruption of key ligamentous structures. If significant valgus laxity is present in full extension, the posteromedial capsule and medial collateral ligament are torn. With varus laxity in full extension, the posterolateral capsular complex is torn, in addition to the lateral collateral ligament. With either varus or valgus laxity at full extension, anterior and posterior cruciate ligament tears are likely. At 30 degrees of flexion, the posterior capsule and cruciate ligaments are relaxed, and the medial and lateral collateral ligaments can best be isolated. Pain with varus or valgus stress is more suggestive of ligament damage than a meniscus tear.

Table 4–2. Anatomic Correlation of Clinical Ligament Instability Examination of the Knee.

Direction of Force


Ligament Instability

Varus or valgus

Full extension

Posterior cruciate, posterior capsule


Flexion at 30 degrees

Lateral collateral ligament/complex


Flexion at 30 degrees

Medial collateral ligament


Flexion at 30 degrees neutral position (AP)

Anterior cruciate ligament


Flexion at 90 degrees neutral internal or external rotation

Anterior cruciate ligament


90 degrees (sag test)

Posterior cruciate ligament


AP = anteroposterior.

Figure 4–6.


The collateral ligaments being tested in extension and 30 degrees of flexion with the foot held between the examiner's elbow and hip.

(Reproduced, with permission, from Feagin JA Jr: The Crucial Ligaments. Churchill Livingstone, 1988.)

The Lachman Test

The Lachman test is the most sensitive test for ACL tears. It is done with the knee flexed at 20 degrees, stabilizing the distal femur with one hand and pulling forward on the proximal tibia with the other hand. (Figure 4–7). With an intact ligament, minimal translation of the tibia occurs and a firm end point is felt. With a torn ACL, more translation is noted, and the end point is soft or mushy. The hamstring muscles must be relaxed during this maneuver to prevent false-negative findings. Comparison of the injured and uninjured knees is essential.

Figure 4–7.


Lachman test.

(Reproduced, with permission, from Feagin JA Jr: The Crucial Ligaments. Churchill Livingstone, 1988.)

Anterior Drawer Test

The anterior drawer test is done with the knee at 90 degrees of flexion and is not as sensitive as the Lachman test but serves as an adjunct in the evaluation of ACL instability (Figure 4–8). With the patient supine and the knee flexed to 90 degrees (hip flexed to approximately 45 degrees), the foot is restrained by sitting on it, and the examiner's hands are placed around the proximal tibia. Then while the hamstrings are felt to relax and the tibia is pulled forward, the displacement and the endpoint are evaluated.

Figure 4–8.


A positive anterior drawer test signifying a tear of the anterior cruciate ligament.

(Reproduced, with permission, from Insall JN: Surgery of the Knee. Churchill Livingstone, 1984.)

The Losee Test

The pivot shift phenomenon demonstrates the instability associated with an ACL tear. Once demonstrated, it is often difficult to repeat because the patient may find this maneuver uncomfortable and will guard against having it done again. As described by Losee, a valgus and internal rotation force is applied to the tibia (Figure 4–9). Starting at 45 degrees of flexion, the lateral tibial plateau is reduced. Extending the knee causes the lateral plateau to subluxate anteriorly with a thud at approximately 20 degrees of flexion. It reduces quietly at full extension. Many other ways of doing this test are described, but the phenomenon and significance of the different tests are similar.

Figure 4–9.


The Losee pivot shift test.

(Reproduced, with permission, from Scott WN: Ligament and Extensor Mechanism Injuries of the Knee: Diagnosis and Treatment.Mosby-Year Book, 1991.)

Posterior Drawer Test

The posterior drawer test evaluates the integrity of the PCL. It is performed with posterior pressure on the proximal tibia with the knee flexed at 90 degrees (Figure 4–10). Normally, the tibial plateau is anterior to the femoral condyles, and a step-off to the tibia is palpated when the thumb is slid down the femoral condyles. With a PCL injury, sagging of the tibial plateau may be appreciated, and no step-off is palpated (Figure 4–11). An associated contusion on the anterior tibia suggests a PCL injury.

Figure 4–10.


The posterior drawer test is done in the same fashion as the anterior drawer test, except that the examiner exerts a posterior force.

(Reproduced, with permission, from Scott WN: Ligament and Extensor Mechanism Injuries of the Knee: Diagnosis and Treatment.Mosby-Year Book, 1991.)


Figure 4–11.


The posterior sag seen in posterior cruciate disruption.

(Reproduced, with permission, from Scott WN: Ligament and Extensor Mechanism Injuries of the Knee: Diagnosis and Treatment.Mosby-Year Book, 1991.)

The McMurray Test

With the McMurray test, forced flexion and rotation of the knee elicits a clunk along the joint line if there is a meniscus injury (see Figure 4–12). Found in less than 10 percent of patients with a meniscus injury, joint line pain with the McMurray test is much more common.

Figure 4–12.


The McMurray test to produce click.

(Reproduced, with permission, from American Academy of Orthopaedic Surgeons: Athletic Training and Sports Medicine, 2nd ed., 1991.)

Arthroscopic Examination


Indications for arthroscopic examination in the knee include the following:


1. acute hemarthrosis;

2. meniscus injuries;

3. loose bodies;

4. selected tibial plateau fractures;

5. patellar chondromalacia and/or malalignment;

6. chronic synovitis;

7. knee instability;

8. recurrent effusions; and

9. chondral and osteochondral fractures.

Today, a specific diagnosis of the type of knee injury can now usually be made with a history, physical examination, and appropriate imaging studies. With an examination under anesthesia and arthroscopic evaluation, a specific diagnosis can be confirmed, expanded, or revised, and treatment can be rendered as needed.


Examination under anesthesia is very helpful in diagnosing ligament injuries and instability. It should be performed before the beginning of the procedure, before preparing and draping the extremity. For diagnostic arthroscopy, the knee joint is distended with irrigating fluid (usually saline or lactated Ringer's solution), which washes away blood and debris from the joint. A lateral portal, for the arthroscope, is placed approximately a thumb's breadth above the joint line and just lateral to the patellar tendon. The medial portal is placed at approximately the same level, but just medial to the patellar tendon for introducing arthroscopic tools such as a probe. One approach to the general inspection of the joint is to start in the suprapatellar pouch. Loose bodies and plicas are sought. The patellofemoral joint is then inspected and observed for tracking problems and cartilage damage. The lateral gutter and the popliteus tendon are examined by flexion and valgus stress to the leg, prior to entering the medial compartment. The medial meniscus is probed using a nerve hook through the medial portal. The intercondylar notch, including the , is inspected. The lateral compartment is then examined in a similar manner. Documentation of findings and procedures performed is important and may be done by videotape, photographs, and diagrammatic sketches. With assessment of the pathologic changes, treatment can be initiated, such as debridement and repair of meniscus tears, removal of loose bodies, or ACL reconstruction.

Imaging & Other Studies


MRI is a powerful technique for evaluation of the knee joint. Although the diagnosis is usually evident from the history and physical examination, MRI can be used to confirm the suspected injury. Other times, when a physical examination is not possible because of pain or the diagnosis remains elusive, MRI can aid in proper diagnosis. The specificity, sensitivity, and accuracy of MRI are greater than 90% for the medial and lateral menisci and the ACL and PCL. Therefore, MRI is often appropriate for ruling out the need for diagnostic arthroscopic examination. It is less helpful for the diagnosis of problems in knees with previous surgery.


Roentgenographic examination of the knee is indicated in the evaluation of traumatic injury. In cases of minimal trauma, radiographs may not be needed if the injury proves to be self-limited. Arthrographic examination can be helpful in patients who are unable to undergo MRI because of claustrophobia, metal in the body that may be dislodged, or other contraindications.


Laboratory tests may be helpful in ruling out nonmechanical disorders such as inflammatory arthritis as described in Chapter 7.

Chang CY et al: Imaging evaluation of meniscal injury of the knee joint: A comparative MR imaging and arthroscopic study. Clin Imaging 2004;28:372. [PMID: 15471672] 

Luhmann SJ et al: Magnetic resonance imaging of the knee in children and adolescents. Its role in clinical decision-making. J Bone Joint Surg Am 2005;87-A:497. [PMID: 15741613] 

Sanders TG, Miller MD: A systematic approach to magnetic resonance imaging interpretation of sports medicine injuries of the knee. Am J Sports Med 2005;33(1):131. [PMID: 15611010] 

Scholten RJ et al. The accuracy of physical examination diagnostic tests for assessing meniscus lesions of the knee: A meta-analysis. J Fam Pract 2001,50:938. [PMID: 11711009] 


Meniscal injuries are the most common reason for arthroscopy of the knee. The medial meniscus is more frequently torn than the lateral meniscus because the medial meniscus is securely attached around the entire periphery of the joint capsule, whereas the lateral meniscus has a mobile area where it is not attached. Meniscus injury is rare in childhood, occurs in the late teens, and peaks in the third and fourth decades. After 50 years of age, meniscus tears are more often the result of arthritis than trauma.

Clinical Findings

Acute traumatic tears of the menisci are often caused by axial loading combined with rotation. Patients typically report pain and swelling. Patients with smaller tears may have a sensation of clicking or catching in the knee. Patients with larger tears in the meniscus may complain of locking of the knee as the meniscus displaces into the joint and/or femoral notch. Loss of knee motion with a block to extension may result from a large bucket-handle tear. In acute tears involving an associated ACL injury, the swelling may be more significant and acute. ACL injuries often involve a lateral meniscus tear as the lateral compartment of the knee subluxates forward, trapping the lateral meniscus between the femur and tibia.

Conversely, chronic or degenerative tears of the menisci often present in older patients (more than 40 years old) with the history of an insidious onset of pain and swelling with or without an acute increase superimposed. Often no identifiable history of trauma is obtained, or the inciting event may be quite minor, such as a bending or squatting motion.

The most important physical examination findings in the knee with a meniscus tear are joint line tenderness and an effusion. Other specialized tests include the McMurray, flexion McMurray, and Apley grind tests. The McMurray test is performed with the patient lying supine with the hip and knee flexed to approximately 90 degrees. While one hand holds the foot and twists it from external to internal rotation, the other hand holds the knee and applies compression (see Figure 4–12). A positive test is one that elicits a pop or click that can be felt by the examiner when the torn meniscus is trapped between the femoral condyle and tibial plateau. A variation of this test is the flexion McMurray, in which the knee is held as for the McMurray test. To test the medial meniscus, the foot is externally rotated and the knee maximally flexed. A positive test occurs when the patient experiences pain over the posteromedial joint line as the knee is gradually extended. The Apley grind test requires placing the patient prone with the knee flexed to 90 degrees. The examiner applies downward pressure to the sole of the foot while twisting the lower leg in external and internal rotation. A positive tests results in pain at either joint line.

In addition to the procedure just described, physical examination of the entire leg is essential. Assessing hip range of motion and irritability is useful, especially in children, because referred pain from the hip to the knee area is common. Examining for quadriceps atrophy and the presence of a knee effusion should also be done. Measurement of range of motion may reveal a loss of the normal knee extension. Assessing for tenderness of the femoral condyles, joint lines, tibial plateaus, and patellofemoral joint may give clues as to a possible osteochondral lesion, meniscus lesion, fracture, or chondrosis, respectively. Ligamentous testing, including varus and valgus stress testing at full extension and 30 degrees of flexion; Lachman; anterior drawer; and posterior drawer testing should be done to assess stability.

Tear Classification

Meniscal tears can be classified either by etiology or by their arthroscopic and MRI appearance. Etiologic classification divides tears into either acute tears (excessive force applied to an otherwise normal meniscus) or degenerative tears (normal force applied to a degenerative structure).

Classification should describe the tear location and its associated vascularity, morphology, and stability. Tear location is described by its location in the anteroposterior plane (anterior, middle, or posterior) and its circumferential location with respect to its vascularity. The common vascular zones include the most peripheral red/red zone near the meniscocapsular junction, the intermediate red/white zone, and the most central white/white zone. As tears occur more centrally, the vascularity decreases, as do the associated healing rates.

Tear morphology describes the orientation of the tear within the meniscus and includes vertical or horizontal longitudinal, radial (transverse), oblique, and complex (including degenerative) tears (Figure 4–13). Most acute tears in patients less than 40 years old involve vertical longitudinal or oblique tears, whereas complex and degenerative tears occur more commonly in patients more than 50 years old. Vertical longitudinal, or bucket-handle tears, can be complete or incomplete and usually start in the posterior horn and continue anteriorly a variable distance. Long tears can cause significant mobility of the torn meniscal fragment, allowing it to displace into the femoral notch and cause a locked knee (Figure 4–14). This more commonly occurs in the medial meniscus, possibly owing to its decreased mobility, which leads to increased sheer stresses. Oblique tears commonly occur at the junction of the middle and posterior thirds. They are often smaller tears, but the free edge of the tear can catch in the joint and cause symptoms of catching. Complex or degenerative tears occur in multiple planes, are often located in or near the posterior horns, and are more common in patients more than 50 years old with degenerative menisci. Horizontal longitudinal tears are often associated with meniscal cysts. They usually start at the inner margin of the meniscus and extend toward the meniscocapsular junction. They are thought to result from shear stresses and, when associated with meniscal cysts, they occur in the medial meniscus and cause localized swelling at the joint line.

Figure 4–13.


Patterns of meniscal tears: bucket-handle, flap, horizontal cleavage, radial, degenerative, and double radial tear of a discoid meniscus.

(Reproduced, with permission, from Scott WN: Arthroscopy of the Knee. WB Saunders, 1990.)


Figure 4–14.


A: Diagram of a typical bucket-handle tear of the medial meniscus. B: Arthroscopic view of a bucket-handle fragment displaced into the intercondylar notch.

(Reproduced, with permission, from McGinty JB: Operative Arthroscopy. Raven Press, 1991.)

Treatment & Prognosis

Small stable asymptomatic meniscus tears do not need to be treated surgically. Those causing persistent symptoms should be assessed with the arthroscope. Before the importance of the meniscus was understood and arthroscopy became available, the meniscus was often removed, even when normal. We now attempt to remove only the torn portion of the meniscus or repair the meniscus, if possible.

During arthroscopy, the meniscus should be visualized and palpated with a hooked probe. The inner two thirds of the meniscus is avascular and often requires resection when torn. A biting instrument is used to complete the resection of the torn portion of the meniscus, and the meniscus fragment is removed with a grasping instrument. Power shavers are used to smooth and contour the remaining meniscus to prevent further tearing from a jagged edge. Return to full function may be expected in 6–8 weeks.

Tears in the peripheral third of the meniscus, if small (less than 15 mm), may heal spontaneously because there is a blood supply in this portion of the adult meniscus. Larger tears need to be repaired. Patients who undergo meniscectomy at less than 40 years old are at risk of early osteoarthritis. These changes were first described by Fairbanks and include flattening of the femoral condyle, joint space narrowing, and osteophyte formation. Therefore, if a meniscus can be saved, it should be.


Partial meniscectomy has 90% good or excellent results in patients with normal knee stability and no degenerative changes. A major advantage over meniscus repair is a short recovery period, but results after partial meniscectomy are not as satisfactory when degenerative changes or knee ligament injuries are present. Also, results diminish over time; degenerative changes occur with follow-up beyond 10 years. Medial meniscus tears generally do better than lateral tears after partial resection, and an intact meniscal rim and normal articular cartilage surfaces are associated with a better prognosis.


Most surgeons attempt a meniscus repair rather than a partial meniscectomy in individuals less than 40 years old. Other commonly accepted criteria for meniscus repair include a complete vertical longitudinal tear greater than 15 mm in length, a tear within the peripheral 10–30% of the meniscus (ie, within 3–4 mm of the meniscocapsular junction), a peripheral tear that can be displaced toward the center of the plateau with a probe, the absence of secondary meniscus degeneration, and a tear in a patient undergoing concurrent ligament or articular cartilage repair.

Multiple factors affect the success of meniscus repair. Although no absolute age limit exists, patients younger than 40 years are thought to have a better chance for healing. Knees with associated ligamentous instability, particularly ACL instability, have inferior rates of meniscus healing because of abnormal meniscus stresses from tibiofemoral instability. The location of the tear and the time lapsed from injury to treatment are also important. Acute tears located in the peripheral red/red or red/white zone have better healing capability than chronic tears located in the red/white or white/white zones. Tears 5 mm or more from the periphery are considered avascular (white zone); those between 3 and 5 mm are variable in vascularity (red/white), and tears in the peripheral 3 mm are considered vascular (red). In areas with marginal vascularization, abrasion of the meniscocapsular junction or use of a fibrin clot may be used. It is thought that a vascular pannus forms from the abraded tissue, which aids in meniscus healing. Finally, the stability of the meniscus repair is a factor, with vertical mattress sutures generally considered the gold standard in meniscus repair.

Meniscus repair is successful in up to 90% of meniscus tears when done in conjunction with ACL reconstructions, as compared to approximately 50% in patients with stable ACLs who had meniscus repairs.

Types of repairs include the traditional open repair and arthroscopic repairs that can be dome with inside-out, outside-in, or all-inside techniques. Inside-out and outside-in repairs require a mini-incision and securing of the meniscus to the capsule with sutures. The all-inside technique has many device options, including both absorbable and nonabsorbable arrows, tacks, darts, and fasteners. Regardless of the type of repair chosen, adequate preparation of the tear site is required. The tear edges should be debrided or abraded with a shaver or rasp to stimulate bleeding. Restoration of biomechanical function is encouraged by anatomic apposition of the tear's edges to ensure good healing potential.


Open repair of meniscus tears has successful long-term results. The technique involves making a small incision through the subcutaneous tissue, capsule, and synovium to visualize the tear directly. Open repair is most useful in peripheral or meniscocapsular tears, often occurring in conjunction with open repair of a collateral ligament injury or a tibial plateau fracture. Follow-up studies of 10 years or longer show survival rates of repaired menisci of 80–90%, in part influenced by the peripheral nature of the tear and the associated hemarthrosis present in ligament tears or fracture repair cases.


Inside-Out Meniscal Repair

Arthroscopic inside-out meniscus repairs are performed using long needles introduced through cannula systems with attached absorbable or nonabsorbable sutures passed perpendicularly across the tear from inside the knee to a protected area outside the joint capsule. These sutures are able to obtain consistent perpendicular placement across the meniscus tear, which gives this method an advantage over other repair techniques. Improved suture placement is gained at the expense of possible neurovascular injury from passing the needle from inside the knee to outside the joint. This technique requires a posteromedial or posterolateral incision to protect the neurovascular structures and safely retrieve the exiting needles. Secondary to its ability to gain vertical mattress suture fixation, this technique remains the gold standard for many surgeons. Numerous retrospective and prospective studies using second-look arthroscopy or arthrography to evaluate healing of the meniscus repairs consistently show rates of 70–90% in isolated repairs and greater than 90% when done in conjunction with an ACL reconstruction. This technique is ideal for posterior and midposterior horn tears. There is difficulty in passing needles in mid- to anterior horn meniscus tears.

Outside-in Meniscal Repair

The arthroscopic outside-in repair was developed in part to decrease the neurovascular risk associated with the inside-out technique. The outside-in technique involves passing a needle from outside the joint, across the tear, and into the joint. Two options then exist for repair of the meniscus tear. One option is to retrieve the suture through an anterior portal, tie a knot outside the knee joint, and then bring the knot back in through the anterior portal placing the knot against the reduced meniscus body fragment. A second option is to use parallel needles and retrieve the suture through the second needle. This can be done using a suture relay. A knot is then tied outside the joint over the capsule. This method is useful for tears in the anterior horn or body of the menisci, but it does not work for tears in or near the posterior horn. Results of the outside-in technique using MRI, arthrography, or second-look arthroscopy to assess healing show complete or partial healing in between 74% and 87% of meniscus repairs that were successful. As expected, more posterior horn tears and tears in unstable knees did worse.

All-Inside Meniscal Repair

The popularity of the all-inside repairs has increased as numerous devices and techniques have been introduced in the last few years. Their popularity is due in part to the fact that they do not require accessory incisions thereby saving operative time, and they avoid more technical arthroscopic techniques required in other types of repairs. However, because of the speed of their introduction, their documented clinical effectiveness compared to more traditional techniques has lagged behind their use.

The initial devices introduced in the early 1990s included biodegradable meniscus arrows, meniscus darts, and simple suture devices such as the T-Fix (Acufex, Mansfield, MA). There was a good initial experience with these devices, particularly the meniscus arrows, which were the first to be introduced. Early studies showed success rates of 80% or higher at 1–2 year follow-ups. However, complications with these first-generation devices began to be reported and included retained fragments, foreign body reactions, inflammation, chronic effusions, and articular cartilage injuries. Additionally, mechanical testing of these first-generation devices showed pull-to-failure strengths closer to those of horizontal, not vertical, sutures.

Updated first-generation and second-generation devices were developed in response to these biomechanical strength concerns and to address the early complication rates. Implant design modifications included a change to smaller or rounded heads on the meniscus arrow and darts, polymer composition changes to decrease their resorption times, and the introduction of suture-based implants that did not require arthroscopic knot tying. Examples included contoured and headless arrow designs and suture based implants such as the FasT-Fix (Smith & Nephew, Endoscopy Div., Andover, MA) and RapidLoc (Mitek, Westwood, MA) devices.

It is difficult to compare studies for these updated first-generation devices or second-generation devices, but in general, studies can be classified into two groups: follow-up clinical studies on human implanted devices, and biomechanical cadaveric or animal studies. Secondary to their earlier introduction into clinical use, long-term follow-up studies are most prevalent for updated first-generation meniscus arrow devices. First reported in 1993, multiple studies show 60–90% clinical success rates using either second-look arthroscopy or clinical exam evaluations. Some were even comparable to traditional open suture techniques. Complications, including inflammatory reactions and articular cartilage damage, remain a concern for sutureless devices that may migrate from their original implanted meniscus tear position.

Biomechanical studies on second-generation devices are also published. A follow-up to the initial T-Fix device, the second-generation FasT-Fix suture device, shows superior results. Its biomechanical performance in load-to-failure, stiffness, and cyclic displacement tests has been equivalent to the gold standard of vertical mattress sutures. Other devices including other suture devices and the various meniscus arrows or screws have equivalent biomechanical performance to that of horizontal mattress sutures. It is generally believed that the superiority of vertical mattress over horizontal mattress sutures is derived from the ability of vertical mattress sutures to capture the strong circumferential fibers of the meniscus. Additionally, suture devices in general have a lower risk of loose body reactions because their fixation device is extracapsular. However, there is a learning curve associated with placement of suture devices that may cause their fixation strength to be suboptimal until the technique is mastered.

Caution should be exercised in interpreting biomechanical studies of meniscus repair devices. Virtually all larger studies involve porcine, bovine, or canine models secondary to increased cost and availability issues in obtaining human cadaveric menisci. Studies involving human menisci should also be evaluated for the source of their menisci because as older samples taken from arthritic total joint patients may not accurately reflect in vivo conditions. It is also not known if in vitro load to failure or cyclic loading testing is applicable to the in vivo stress environment.

In general, however, multidevice studies show that (1) vertical mattress sutures are superior to horizontal, (2) arrows and other nonsuture devices have 40–70% of the pull-to-failure strength and cyclic load displacement of vertical mattress sutures, and (3) sutures devices like the FasT-Fix have biomechanical profiles similar to vertical mattress sutures. What remains to be known, however, is the minimal strength that meniscus repair devices need to provide for meniscus healing to occur in vivo.

Repairable meniscus tears often occur with an ACL tear. Stabilizing the knee with ACL reconstruction protects the repaired meniscus from abnormal knee motion, which has a higher rate of success than if the knee is left unstable.


An alternative to leaving the patient with a meniscus-deficient knee, and almost certain early osteoarthrosis, is meniscus transplantation. This technique yields satisfactory results in approximately two thirds of patients after a short-term follow-up. In the future, biologic scaffolds may enable menisci to be regenerated after meniscectomy.

Ahn JH, Wang JH, Yoo JC: Arthroscopic all-inside suture repair of medial meniscus lesion in anterior cruciate ligament—deficient knees: results of second-look arthroscopies in 39 cases. Arthroscopy 2004;20:936. [PMID: 15525926] 

Englund M et al: Patient-relevant outcomes fourteen years after meniscectomy: Influence of the type of meniscus tear and size of resection. Rheumatology (Oxford) 2001,40:631. [PMID: 11426019] 

McNicholas MJ et al: Total meniscectomy in adolescence: A thirty-year follow-up. J Bone Joint Surg 2000,82B:217. [PMID: 10755429]

Metcalf MH, Barrett GR: Prospective evaluation of 1485 meniscal tear patterns in patients with stable knees. Am J Sports Med 2004;32:675. [PMID: 15090384] 

Rijk PC. Meniscal allograft transplantation—part I: Background, results, graft selection and preservation, and surgical considerations. Arthroscopy 2004;20:728. [PMID: 15483548] 

Shelbourne KD, Dersam MD: Comparison of partial meniscectomy versus meniscus repair for bucket-handle lateral meniscus tears in anterior cruciate ligament reconstructed knees. Arthroscopy 2004;20:581. [PMID: 15241307] 

Steenbrugge F, Verstraete K, Verdonk R. Magnetic resonance imaging of the surgically repaired meniscus: A 13-year follow-up study of 13 knees. Acta Orthop Scand 2004;75:323. [PMID: 15260425] 


Articular cartilage injuries of the knee are infrequent, and the examiner must have a high index of suspicion to detect them. Arthroscopy is very helpful with these injuries, especially pure articular cartilage injuries, where radiographs will be normal.

Osteochondral Lesions

Osteochondral Fracture

There is much confusion about the nomenclature and etiology of juvenile and adult osteochondral lesions (OCLs) of the knee. Initially, an inflammatory etiology for the condition was suggested. Further inquiry attributed the condition to an ossification abnormality. Still others thought that avascular necrosis might be responsible for the lesions. However, work in basic science, histopathology, and vascular studies did not support any of these etiologies as the cause of OCLs. The term osteochondral injuries was used to describe injuries ranging from acute osteochondral fractures to pure chondral injuries. Currently, OCLs are defined as potentially reversible idiopathic lesions of subchondral bone resulting in possible delamination or fragmentation with or without destruction of the overlying articular cartilage. OCLs are subdivided into juvenile and adult forms depending on the presence of an open distal femoral physes. In children, a combination of etiologies is now thought to be responsible for OCL lesions. For example, a stress fracture may develop in the subchondral bone of the distal femoral condyle. Such an injury may provoke further vascular compromise, which results in injury to the subchondral bone that was initially covered with normal articular cartilage. Loss of support from the subchondral bone may result in damage to the overlying articular cartilage. The vast majority of adult OCLs lesions are thought to have arisen from a persistent juvenile OCL lesion, although new lesions in adults are possible as well.

Both adult and juvenile lesions that do not heal have the potential for further sequelae including degenerative osteoarthritis. Juvenile lesions, defined as knees with an open physes, generally have a better prognosis than adult lesions. The classic location of an OCL is the posterolateral aspect of the medial femoral condyle, which accounts for 70–80% of all OCLs. Lateral condyle lesions are seen in 15–20% of patients, and patellar involvement ranges from 5% to 10%. The increased use of MRI and arthroscopy over the past decade may have resulted in greater recognition of OCL lesions.

Clinical Findings

A common presentation of a patient with an OCL is aching and activity-related anterior knee pain that is poorly localized. Pain may worsen with stair climbing or running. Patients with early or stable lesions usually do not complain of mechanical symptoms or knee instability. Mechanical symptoms are more common in patients with unstable or loose OCLs. Parents may note a limp in their child, and patients may complain of knee swelling with possible crepitus.

An antalgic gait may be observed as the patient. An effusion may be variably present, but generally crepitus or pain with range of motion is absent in patients with stable lesions. Tenderness with palpation of the femoral condyle may be observed with various degrees of knee flexion. Loss of range of motion or quadriceps atrophy may be noted in more long-standing cases.

Patients with unstable lesions may have crepitus and pain with range of motion, and an effusion is typically present in these patients. Involvement is bilateral in up to 25% of cases, so both knees should be evaluated regardless of symptoms. Initial evaluation should include anteroposterior, lateral, and tunnel views of both knees. The goal of plain radiographs is to exclude any bony pathology, evaluate the physes, and localize the lesion. Lesion location and an estimation of size can be determined as described by Cahill. MRI is frequently obtained once the diagnosis is confirmed on plain radiographs. MRI can give an estimation of the size of the lesion, the condition of the overlying cartilage and underlying subchondral bone, the extent of bony edema, the presence of a high signal zone beneath the fragment, and the presence of any loose bodies. There are four MRI criteria on T2-weighted images: a line of high signal intensity at least 5 mm in length between the OCL and underlying bone, an area of increased homogeneous signal at least 5 mm in diameter beneath the lesion, a focal defect of 5 mm or more in the articular surface, and a high signal line traversing the subchondral plate into the lesion. A high signal line is the most common sign in patients found to have unstable lesions that are most likely to fail nonoperative treatment. Patient maturity and lesion size are also important predictors of failure of nonoperative treatment.

Equivocal prognostic value was found in the use of intravenous gadolinium in OCLs. Technetium bone scans were initially proposed to monitor the presence of healing. However, with MRI, that eliminates ionizing radiation and increased time required in bone scanning, it is not widely used.

Treatment & Prognosis

There is general agreement that initial nonoperative management should be pursued in the case of a child with open physes who presents with a stable OCL. The goal of nonoperative treatment is to obtain a healed lesion before physis closure so as to prevent early-onset osteoarthritis. Even if patients are within 6–12 months of physeal closure, a trial of nonoperative treatment is warranted.

As failure of the subchondral bone precedes failure of the overlying articular cartilage, most orthopedists recommend some sort of activity modification. Debate exists whether activity modification should include the use of cast or brace immobilization. The tenet of nonoperative treatment is to reduce the activity level where pain-free activities of daily living are possible. However, there is no optimal immobilization protocol available in the literature.

A general consensus is that patients should at least be non– or partial weight bearing with crutches for 3–6 weeks or until they are pain free. Repeat radiographs are obtained at approximately 6-week intervals. Physical therapy with full weight bearing may be initiated once patients are pain free. Physical therapy should focus on low-impact quadriceps and hamstring strengthening. If patients remain asymptomatic during this phase up to at least 3 months postdiagnosis, activity may be slowly advanced to higher impact activities such as running or jumping. Any recurrence of symptoms or pain or any progression of the OCL on plain radiographs should prompt repeat non–weight bearing and possible immobilization for a longer period. Obvious patient frustration and lack of compliance, especially in adolescents, is common, and a full discussion on the risks and benefits of nonoperative or operative treatment is required.

Operative treatment should be considered in the following instances: (1) detachment or instability of the fragment while the patient is under treatment, (2) persistence of symptoms despite nonoperative treatment in a compliant patient, (3) persistently elevated or worsening radiographic appearance (plain radiographs or MRI), (4) approaching or complete epiphyseal closure. Goals of operative treatment should include achievement of a stable osteochondral fragment that maintains joint congruity and allows early range of motion.

For stable lesions with an intact articular surface, arthroscopic drilling of the lesions is preferred. This creates channels for potential revascularization through the subchondral bone plate. Options include transarticular drilling versus transepiphyseal drilling. Multiple studies show radiographic healing and relief of symptoms in 80–90% of patients with open physes. This decreases to 50–75% in patients with closed physes.

Patients with flap lesions or partially unstable lesions should be managed depending on the status of the subchondral bone. Fibrous tissue between the lesion and subchondral bone should be debrided. If significant subchondral bone loss occurs, packing of autogenous bone graft in the crater prior to fragment reduction and fixation is advised. If significant subchondral bone remains attached to the fragment such that an anatomic fit into its donor site is possible, fixation should be attempted. Various fixation methods are described, including Herbert or cannulated screws and bioabsorbable screws or pins. Complication, however, is associated with these treatments.

Simple excision of the larger fragments shows poor results with more rapid progression of radiographic osteoarthritic changes. For lesions greater than 2 cm2, drilling or microfracture methods that depend on replacement of the defect with fibrocartilage also show inferior results. These results tend to deteriorate with time with worsening radiographic changes. For these larger lesions, transplantation of autologous osteochondral plugs or autologous chondrocyte implantation was tried. Disadvantages of autologous osteochondral plugs or mosaicplasty include donor site morbidity and incongruent articular fit. Advantages include biologic fixation of autogenous material. Longer term results are now being published in patients less than 40 years old showing successful clinical results in up to 90% of patients. However, additional larger and longer term follow-up studies are needed.

Cepero S, Ullot R, Sastre S: Osteochondritis of the femoral condyles in children and adolescents: Our experience over the last 28 years. J Pediatr Orthop B 2005;14:24. [PMID: 15577303] 


Knee injuries occur during both contact and noncontact athletic activities. Advances in the diagnosis and treatment of ligament injuries now allow athletes at all levels of ability to return to sports at their preinjury level of activity. The ligaments and menisci of the knee work in concert with one another, and frequently more than one structure is damaged when an acute injury occurs.

Ligament injuries are graded as follows: grade 1, stretching of the ligament with no detectable instability; grade 2, further stretching of the ligament with detectable instability, but with the fibers in continuity; and grade 3, complete disruption of the ligament.


Knee stability requires proper functioning of four ligaments. These ligaments include the ACL, the PCL, the medial collateral ligament (MCL), and the lateral collateral ligament (LCL). There are also several accessory or secondary stabilizers of the knee. Secondary stabilizers of the knee include the menisci, iliotibial band, and biceps femoris. These secondary stabilizers become more important when a primary stabilizer is injured.

The MCL is the primary static stabilizer against valgus stress at the knee. The MCL originates from the central sulcus of the medial epicondyle. The sulcus of the C-shaped medial epicondyle is located anterior and distal to the adductor tubercle. The MCL is made up of three main static medial stabilizers of the knee. This includes the superficial MCL, the posterior oblique ligament, and the deep capsular ligament.

The LCL is the primary static stabilizer against varus stress at the knee. The LCL originates from the lateral epicondyle. This is the most prominent point of the lateral femoral condyle. The LCL insertion is on the styloid process of the fibular head, which projects superiorly from the posterolateral fibular head. The LCL joins with the arcuate ligament, the popliteus muscle, and the lateral head of the gastrocnemius to form a lateral arcuate complex to control statically and dynamically varus angulation and external tibial torsion. The iliotibial band and biceps femoris also contribute to stability on the lateral aspect of the knee.

The ACL is the primary static stabilizer of the knee against anterior translation of the tibia with respect to the femur. The ACL originates from the posteromedial surface of the lateral femoral condyle in the intercondylar notch. The ACL inserts on the tibial plateau just medial to the anterior horn of the lateral meniscus, approximately 15 mm posterior to the anterior edge of the tibial articular surface. The blood supply to the ACL and PCL is the middle geniculate artery. Both the ACL and PCL are covered by a layer of synovium, making these ligaments intra-articular and extrasynovial.

The PCL is the primary static stabilizer of the knee against posterior translation of the tibia with respect to the femur. The PCL originates from the posterior aspect of the lateral surface of the medial femoral condyle in the intercondylar notch. The PCL inserts on the posterior aspect of the tibial plateau in a central depression just posterior to the articular surface. The insertion extends distally along the posterior aspect of the tibia for up to 1 cm in length. The PCL is a complex structure consisting of two major bands: the anterolateral and posteromedial bands. The anterolateral band is tight in flexion and loose in extension. The posteromedial band is loose in flexion and tight in extension. The cross-sectional area of the anterolateral band is twice as large as the posteromedial band. The meniscofemoral ligaments, the ligaments of Wrisberg and Humphrey, are the third component of the PCL. The meniscofemoral ligaments travel from the posterior horn of the lateral meniscus to the posteromedial femoral condyle.

Differential Diagnosis of Knee Instability

The differential diagnosis of acute or chronic knee instability can involve any of the knee ligaments and/or the structures of the posterolateral corner. There are often combinations of ligament injuries in addition to injuries of secondary stabilizing structures such as the menisci. The history and mechanism of injury are valuable information, if available. Similarly, the location of pain can help narrow the diagnosis. Clearly, however, a thorough physical examination helps distinguish which ligaments are injured. Additionally, imaging studies are often obtained to confirm clinical suspicions and to evaluate for occult injuries.

Brown JR, Trojian TH: Anterior and posterior cruciate ligament injuries. Prim Care 2004;31:925. [PMID: 15544828] 

Medial Collateral Ligament Injuries

Clinical Findings

An MCL tear typically presents with medial knee pain after either a noncontact rotational injury or a direct valgus blow to the lateral knee. Instability may or may not be present, depending on the severity of the injury.

Symptoms (History)

How and when the patient was hurt are important parts of the history. Lower grade MCL injuries typically occur in a noncontact external rotational injury, whereas higher grade injuries generally involve lateral contact to the thigh or upper leg. Other important pieces of historical information include the location and presence of pain, instability, timing of swelling, and sensation of a pop or tear. Surprisingly, grade I and II injuries are often more painful than complete MCL rupture. Immediate swelling should make one suspicious of an associated cruciate ligament injury, fracture, and/or patellar dislocation. A prior history of knee injuries or instability should always be sought when evaluating a new knee injury.

Signs (Physical Examination)

MCL injuries are evaluated with a complete knee examination to evaluate for any other coexisting injuries. This is especially true with ACL and PCL evaluation because an injury to either of these ligaments would significantly change the treatment. Given the frequency of coexisting patellar dislocations in MCL injuries, palpation of the patella and the medial parapatellar stabilizing ligaments should be performed in addition to patellar apprehension testing.

Medial joint line tenderness along the course of the MCL is typical at the location of the tear. Laxity to valgus stresses is assessed by the amount of medial joint space opening that occurs at 30 degrees of flexion. It is important to stress the knee at 30 degrees of flexion because with the knee in full extension, the posterior capsule and PCL stabilizes the knee to valgus stress. This stability to valgus stress in full extension could mislead the examiner to believe that the MCL is intact. Zero opening is considered normal, with 1–4 mm indicating a grade I injury; 5–9 mm indicating a grade II injury; and 10–15 mm indicating a complete or grade III injury. Additionally, grade I and II injuries typically have a firm endpoint, whereas a grade III injury tends to have a soft endpoint to valgus stress.

Imaging Studies


A series of knee radiographs should be obtained in any patient with a suspected significant knee injury. Radiographs should be inspected for acute fracture, lateral capsular avulsion (the Segond fracture; see ACL imaging), loose bodies, Pellegrini-Stieda lesion (MCL calcification), and evidence of patellar dislocation. Stress radiographs should be obtained in patients prior to skeletal maturity to rule out an epiphyseal fracture.


MRI is useful for confirming MCL injury and identifying the site of injury as well as the presence of meniscal and other injuries to the knee. Relative indications for an MRI include an uncertain ACL status despite multiple examinations, evaluation of a suspected meniscal tear, or preoperative evaluation for a planned MCL reconstruction or repair.


An examination under anesthesia can be valuable when physical examination is unreliable because of the patient guarding the knee. Diagnostic arthroscopy can also be used to evaluate for coexistent pathology. MRI has largely replaced both of these diagnostic methods, however.

Treatment: Nonsurgical & Surgical

Treatment of an isolated MCL injury is generally nonoperative with protection against valgus stress and early motion. Grade I and grade II injuries can be placed in either a cast or a brace and bear weight as tolerated. Generally, knee motion is started within the first week or two, and full recovery is usually achieved more rapidly with early knee range of motion.

Grade III injuries are a bit more controversial. Several authors show increased instability in grade III tears treated nonsurgically, although most of these did not exclude knees with multiligamentous injuries. Comparison of isolated grade III MCL tears treated with surgical reconstruction versus nonsurgical management showed that the nonsurgical treatment group enjoyed better results in both subjective scoring and earlier return to activity.

The exception to the current trend of nonsurgical treatment of grade III injuries is in the setting of a multiligamentous knee injury. In this setting, particularly with a distal tibial avulsion of the MCL, nonsurgical treatment has not fared nearly as well as in isolated MCL injuries. MCL repair in the acute setting can include a primary repair, with shortening if needed, of the torn ligament. Similarly, avulsion fragments are treated with reduction and fixation in the acute setting. Primary repairs can be reinforced with autograft or allograft tissues if the remaining MCL is insufficient for a stand alone repair. Chronic reconstructions also often include autograft or allograft tissue reconstruction.

Traditionally, casting or operative treatment of MCL injuries significantly limited an early return to range-of-motion exercises. With the addition of functional bracing and early motion to a nonsurgical treatment protocol, motion and strengthening of the knee can occur at an early stage while the ligament is protected from valgus stress. As knee motion improves, isotonic strengthening exercises are introduced. As the strength of the extremity improves, the intensity of functional rehabilitation increases accordingly.


With nonsurgical treatment becoming the standard of care, complications associated with a MCL injury are decreasing. The main complication of nonsurgical therapy is residual valgus laxity or medial knee pain. Radiographs may show residual calcification of the MCL (Pellegrini-Stieda lesion). Potential surgical complications include arthrofibrosis, infection, damage to the saphenous nerve or vein, or recurrent valgus laxity.

Results/Return to Play

In general, good outcomes can be achieved with nonsurgical treatment and rehabilitation of isolated MCL injuries. Return to professional football after nonsurgical treatment of isolated MCL injuries is 98%.

Robinson JR et al: The posteromedial corner revisited. An anatomical description of the passive restraining structures of the medial aspect of the human knee. J Bone Joint Surg Br 2004;86:674. [PMID: 15274262] 

Woo SL, Vogrin TM, Abramowitch SD: Healing and repair of ligament injuries in the knee. J Am Acad Orthop Surg 2000;8:364. [PMID: 11104400] 

Lateral Collateral Ligament Injuries

Symptoms (History)

The most consistent symptom of an acute LCL injury is lateral knee pain. However, the symptoms of lateral and posterolateral instability are quite variable and depend on the severity of injury, patient activity level, overall limb alignment, and other associated knee injuries. For example, a sedentary individual with minimal laxity and overall valgus alignment typically has few if any symptoms. However, if LCL laxity is combined with overall varus alignment, hyperextension, and an increased activity level, symptoms are quite pronounced. These patients may complain of lateral joint line pain and a varus thrust of their leg with everyday activities. This is often described as the knee buckling into hyperextension with normal gait.

Signs (Physical Examination)

Patients with a LCL and/or posterolateral corner injury often also have additional ligamentous injuries to the knee. Therefore, a thorough knee examination should be performed to evaluate for coexistent knee pathology. Additionally, a careful neurovascular examination should be performed because the incidence of neurovascular injury, particularly peroneal nerve injury, is reported in 12–29% of posterolateral knee injuries.

The integrity of the LCL is assessed with a varus stress with the knee in full extension and 30 degrees of flexion. Baseline varus opening is widely variable and should be compared to the contralateral leg. The average baseline for varus opening is 7 degrees. Exam findings with an isolated LCL injury should include varus laxity at 30 degrees of flexion and no instability in full extension. This is because of the stabilizing effect that the intact cruciate ligaments provide in full extension.

Note that a significant posterolateral knee injury can be present without significant varus laxity. The most useful test to evaluate for posterolateral instability is the dial test, which is done by externally rotating each tibia and noting the angle subtended between the thigh and the foot. The dial test is performed at 30 degrees and 90 degrees of flexion with a significant difference being an angle 5 degrees or greater than the contralateral leg.

Imaging Studies


A series of knee radiographs should be obtained in any patient with a suspected significant knee injury. Radiographs should be inspected for acute fractures, lateral capsular avulsion (Segond fracture; see ACL imaging), loose bodies, fibular head avulsions, and evidence of patellar dislocation. With chronic posterolateral instability, degenerative changes of the lateral compartment are often noted. Lateral joint space narrowing with osteophytes and subchondral sclerosis can be seen. Stress radiographs can help better quantify the amount of varus angulation present.


MRI is often a useful adjunct for diagnosing posterolateral corner and LCL injuries in the severely injured knee. As mentioned earlier, this posterolateral injury can often go unnoticed during an initial evaluation, and MRI findings can refocus the examination to the posterolateral structures. Pain and guarding at the time of injury can often obscure posterolateral injury, and MRI can prove to be an extremely valuable adjunct in diagnosis.


Reverse Pivot Shift Test

This test involves starting with the knee flexed to 90 degrees. While the knee is extended, the leg is loaded axially with a valgus stress applied to the knee and the foot held in external rotation. A palpable shift is noted as the tibia reduces from its posteriorly subluxed position as the knee is extended.

External Rotation Recurvatum Test

This test is performed with the patient supine and the hip and knee fully extended. The leg is lifted off the bed by the toes. Hyperextension, varus instability, and external rotation of the tibial tubercle occurs with adequate quadriceps relaxation in a patient with posterolateral instability.

Posterolateral Drawer Test

A standard posterior drawer test (see PCL physical examination) is performed with the tibia in internal rotation, neutral, and externally rotated positions. With posterolateral injury, the magnitude of the posterior drawer displacement is greatest with external tibial rotation.

Examination under Anesthesia

An examination while the patient is relaxed under general anesthetic is extremely useful, particularly in the acute setting. If the patient with a multiligamentous knee injury is taken to the operating room, this is an excellent opportunity to examine the knee without guarding to improve the accuracy of the examination.



Isolated LCL ligament injuries, as noted earlier, are rare injuries. However, in the case of an isolated LCL ligament injury with grade II or less magnitude, a period of immobilization from 2 to 4 weeks followed by a quadriceps strengthening program usually yields good results. Grade III injuries often have better results with surgical treatment. The combination of delayed diagnosis along with an uncertain natural history of posterolateral instability make the treatment of these injuries a challenge.


LCL and posterolateral ligaments, as already discussed, rarely occur in isolation. Therefore, other injuries must also be considered in the treatment plan of the multiligament knee injury. Ideally, the posterolateral and LCL injury is diagnosed in the acute setting. This allows the preferred surgical treatment of a primary repair of the injured structures with augmentation as needed. Primary repair is generally only feasible in the first few weeks following the knee injury.

The knee with chronic posterolateral instability often requires ligamentous reconstruction or advancement to reconstitute a static restraint to varus stresses. The key biomechanical concept of any lateral ligamentous reconstruction is that the isometric point of the LCL lies between the fibular head and the lateral epicondyle. Therefore, regardless of the graft material used to reconstruct the lateral ligamentous complex, a portion of the graft must pass between the lateral femoral epicondyle and the fibular head.

To improve the success rate of reconstruction of chronic lateral ligamentous instability, a proximal tibial valgus osteotomy may be performed to decrease the stress on the lateral structures of the knee.


The rehabilitation of the knee after posterolateral reconstructions or repairs is largely guided by associated injuries to the ACL or PCL. It is generally necessary, however, to limit weight bearing for at least 6 weeks and protect the lateral structures with a brace for at least 3 months.


The peroneal nerve runs just posterior to the fibular head. It is important to isolate the peroneal nerve prior to any lateral knee exposure to minimize the complication of a peroneal nerve injury.


If injuries to the posterolateral corner of the knee are diagnosed and repaired acutely, the results are good for restoration of varus stability and return to play. Chronic posterolateral corner injury reconstructions also perform well when an isometric lateral reconstruction is achieved.

Jakob RP, Warner JP: Lateral and posterolateral instability of the knee. In Orthopaedic Sports Medicine: Principles and Practice. Eds. DeLee J, Drez D, Stanitski CL. Philadelphia: WB Saunders, 1994. [NLMID: 9411843]

Ross G et al: Evaluation and treatment of acute posterolateral corner/anterior cruciate ligament injuries of the knee. J Bone Joint Surg Am 2004;86 (Suppl 2):2. [PMID: 15691102] 

Shahane SA, Ibbotson C, Strachan R et al: The popliteofibular ligament. An anatomical study of the posterolateral corner of the knee. J Bone Joint Surg Br 1999;81:636. [PMID: 10463736] 

Anterior Cruciate Ligament Injuries

Symptoms (History)

The mechanism of injury should be elicited in any knee injury evaluation. This can guide the examination to additional structures that may also be injured. ACL injury can occur in a variety of ways; a few mechanisms predominate, however. The most common noncontact ACL injury mechanism involves a deceleration and rotational injury during running, cutting, or jumping activities. The most common contact injury involves either hyperextension and/or valgus forces to the knee by a direct blow.

ACL injury is often associated with a pop heard by the patient at the time of injury. This piece of history is not ACL specific, however. Upon return to competition, the patient often notices instability of the knee or describes the knee "giving out" with twisting activities. Substantial knee swelling secondary to a hemarthrosis typically occurs within the first 4 to 12 hours following the injury.

Signs (Physical Examination)

With the history obtained and a proper physical examination, an ACL tear should be able to be diagnosed without any additional tests. A complete examination of the knee should be performed to evaluate for any other associated injuries. The uninjured knee is examined first to familiarize the patient with the knee examination.

The Lachman test is the most useful test for anterior laxity of the knee. It is performed with the knee in 20–30 degrees of flexion as an anterior force is applied to the tibia while the other hand stabilizes the distal femur. The degree of anterior translation, as well as the presence and character of an endpoint, is assessed. The laxity is graded based on comparison to the uninjured contralateral knee. Grade 1 laxity is 1–5 mm of increased translation. Grade 2 laxity is 6–10 mm of increased translation. Grade 3 laxity is more than 10 mm of translation as compared to the injured contralateral knee.

The anterior drawer test is another test to evaluate anterior tibial translation. This is performed with the knee in 90 degrees of flexion as an anterior force is applied to the tibia. This test is less sensitive than the Lachman test.

In the acute setting of an ACL tear, there is often a window where an accurate examination can occur before extensive knee swelling and guarding inhibit examination. Aspiration of a hemarthrosis can help decrease pain and improve the quality of the examination in the acute setting as well.

The pivot shift test is performed to test the rotational instability associated with an ACL tear. The test is based on the lateral tibial plateau subluxing anteriorly with extension and reduction of the lateral compartment with flexion. The most effective method of achieving this result is by flexing the knee with an axial load from full extension with valgus stress at the knee and internal rotation of the tibia. The reduction of the subluxation should occur at approximately 30 degrees of flexion. MCL injury and some meniscal tears may produce a false-negative test.

The pivot shift test is considered the most functional test to evaluate knee stability after ACL injury. An examination under anesthesia is also often useful in obtaining a more accurate pivot shift test. This can be useful in a patient with an unclear history of instability and an equivocal examination in the office.

Imaging Studies

Plain radiographs of the knee should be obtained to rule out fractures about the knee. The Segond fracture, as discussed earlier, is an avulsion of the anterolateral capsule of the tibia. Before skeletal maturity, an avulsion of the tibial insertion of the ACL can also be seen radiographically. Following radiographs, an MRI is the most useful examination for an evaluation of associated injuries. Although generally not needed for diagnosis of an ACL tear, MRI can diagnose an ACL tear with 95% or better accuracy. Bone bruises of the lateral femoral condyle and lateral tibial plateau are noted in up to 80% of ACL injuries.

Special Studies

Instrumented laxity evaluations can augment the physical examination and provide an objective baseline for future comparison. The most commonly used arthrometer, the KT-1000 (MEDmetric, San Diego, CA), uses a series of standard forces to measure anterior translation of the tibia with the knee in 20–30 degrees of flexion, similar to the Lachman test.



Rehabilitation following an isolated ACL injury should include an effort to regain knee motion and strengthen the muscles about the knee. Returning to activities that produce episodes of instability is discouraged. Once motion and strength are restored, a gradual return to activities can be attempted to determine the functional level that can be attained without instability.

Nonoperative management with rehabilitation after an ACL injury generally yields poor results in patients who return to competitive activities. Significant episodes of instability resulting in pain, swelling, and disability occur in approximately 80% of individuals that participate in sporting activities such as tennis, football and soccer. These episodes of instability are thought to place the menisci and articular cartilage of the knee at risk for further injury (Figure 4–15).

Figure 4–15.


Flow chart that summarizes the current management of acute anterior cruciate ligament injuries.

(Reproduced, with permission, from Marzo JM, Warren RF: Results of nonoperative treatment of anterior cruciate ligament injury: Changing perspectives. Adv Orthop Surg 1991;15:59.)


The decision to reconstruct an ACL tear surgically is individualized and based on the patient's desire to return to competition, age, accompanying degenerative changes, and objective and subjective knee instability. For example, an active patient less than 40 years old with continued desire to compete in cutting and jumping sports with both objective and subjective knee instability may be best treated with surgical reconstruction. But an older patient with some degenerative arthritis of the knee and minimal desire for continued competitive athletics and no subjective instability would be much more suited to nonsurgical care.

Early in the history of ACL surgery, primary repairs of the ligament were found to do poorly. This gave way to ligament reconstruction using a variety of graft materials. Everything from synthetics to autograft and allograft tissues were used for reconstruction of the ACL. Over time, autograft bone-patellar tendon-bone, semitendinosus/gracilis hamstring autograft, and allograft bone-patellar tendon-bone constructs have proven to be the most commonly used grafts and are successful for ACL reconstructions.

The goal of ACL reconstruction is to reproduce the strength, location, and function of the intact ACL. Therefore, once a graft of adequate strength is selected, the location of the graft is of utmost importance. The graft is generally passed through a bone tunnel in the tibia and a bone tunnel through the femur. The intraarticular placement of the tibial tunnel is generally in the center of the native ACL stump just in front of the PCL origin and just medial to the center of the notch in the coronal plane (Figures 4–16 and 4–17).

Figure 4–16.


Drawing of the medial surface of the right lateral femoral condyle showing the average measurements and body relations of the femoral attachment of the anterior cruciate ligament.

(Reproduced, with permission, from Arnoczky SP: Anatomy of the anterior cruciate ligament. Clin Orthop 1983;172:19.)


Figure 4–17.


The upper surface of the tibial plateau to show average measurements and relations of the tibial attachments of the anterior cruciate ligament.

(Reproduced, with permission, from Girgis FC et al: The cruciate ligaments of the knee joint: Anatomical, functional, and experimental analysis. Clin Orthop 1975;106:216.)

Once the graft is in place, the proper tension and fixation of the graft must occur to achieve a successful ACL reconstruction. Establishing proper tension in the graft is important. A lax ACL graft may not restore stability to the knee, and an overtightened graft may cause failure of the graft or limit knee range of motion. Fixation of the graft is achieved through a variety of measures. The most common method involves placing an interference screw up the bone tunnel that captures the graft in the tunnel. The graft can also be fixed via sutures tied over various devices located on the outer cortex of the tunnels.


Although ACL reconstruction often results in a successful outcome, several complications can occur. One of the most common is a loss of knee motion, which is minimized by obtaining and maintaining full knee extension immediately following surgery. Knee flexion exercises are begun as soon as possible postoperatively with a goal of 90 degrees by 1 week after surgery. Additionally, patellar mobilization is performed in an attempt to minimize patellofemoral scarring. Another common complication of ACL reconstruction is anterior knee pain. The exact etiology of this pain is unclear; however, it is thought that patellar tendon autograft harvest may increase the incidence of patellofemoral pain. Less common complications (less than 1%) include patellar fracture, patellar tendon rupture, and quadriceps tendon rupture, depending on the graft harvest site.

Results/Return to Play

The goal of any rehabilitation protocol for an ACL reconstruction is to return the patient to the full desired level of activity in a short amount of time as possible while avoiding any complications or setbacks. Through improved surgical techniques and accelerated rehabilitation protocols, most studies show a 90% or better return to play and patient satisfaction. Patients generally are able to return between 4 and 6 months postoperatively, with some professional athletes returning successfully to competition in 3 months. Specific criteria for a return to sports vary from institution to institution with a combination of functional testing, subjective reporting, and clinical examination contributing to the decision. In general, the criteria for return to sports includes full range of motion, KT1000 testing within 2–3 mm of the uninjured knee, 85% or more of quadriceps strength and full hamstring strength, and functional testing within 85% of the contralateral leg.

Herrington L et al: Anterior cruciate ligament reconstruction, hamstring versus bone-patella tendon-bone grafts: A systematic literature review of outcome from surgery. Knee 2005;12:41. [PMID: 15664877] 

Hewett TE, Myer GD, Ford KR: Reducing knee and anterior cruciate ligament injuries among female athletes: A systematic review of neuromuscular training interventions. J Knee Surg 2005;18:82. [PMID: 15742602] 

Laxdal G et al: A prospective randomized comparison of bone-patellar tendon-bone and hamstring grafts for anterior cruciate ligament reconstruction. Arthroscopy 2005;21:34. [PMID: 15650664] 

Marx RG et al: Beliefs and attitudes of members of the American Academy of Orthopaedic Surgeons regarding the treatment of anterior cruciate ligament injury. Arthroscopy 2003;19:762. [PMID: 12966385] 

Seitz H et al: Anterior instability of the knee despite an intensive rehabilitation program. Clin Orthop 1996;328:159. [PMID: 8653950] 

Posterior Cruciate Ligament Injuries

Symptoms (History)

When evaluating a patient for a PCL injury, it is important to obtain the mechanism of injury, the severity of the injury, and any potential associated injuries. In contrast to an ACL tear, it is rare for patients with PCL injuries to report hearing a pop or report any feelings of subjective instability. More commonly, patients complain of knee pain, swelling, and stiffness.

The presentation of a patient with a subacute or chronically injured PCL can range from asymptomatic to significant instability and pain. Patients with significant varus alignment or injury to the lateral structures of the knee often complain of feelings of instability and giving way. There are a few characteristic mechanisms of PCL injury that differ significantly from the mechanism of ACL injuries. One of the most common mechanisms of PCL injury is the so-called dashboard, injury during which the anterior tibia sustains a posteriorly directed force from the dashboard with the knee in 90 degrees of flexion. Sports injuries to the PCL result from an outside force or blow, in contrast to the typical deceleration twisting mechanism of an ACL injury. The most common methods of a sports PCL injury include a direct blow to the anterior tibia or via a fall onto the flexed knee with the foot in plantar flexion. The most common mechanism for isolated PCL injury in the athlete is a partial tear associated with hyperflexion of the knee. Additionally, significant knee multiligamentous injuries with PCL tears can be seen after a varus or valgus stress is applied to the hyperextended knee.

Signs (Physical Examination)

As with other ligamentous injuries, a thorough knee examination is necessary. Specific cues to injury to the PCL on initial inspection include abrasions or ecchymosis around the proximal anterior tibia and ecchymosis in the popliteal fossa. Assessment for meniscal damage and associated ligamentous injury should be performed. Evaluation of ACL laxity in the presence of an acute PCL injury is challenging because of the lack of a stable reference point to perform a Lachman or anterior drawer test.

Examination of the PCL in the acutely injured knee can be challenging. Despite increased awareness of the injury, many PCL injuries go undiagnosed in the acute setting. The most accurate clinical test of PCL integrity is the posterior drawer test. The knee is flexed to 90 degrees with the patient supine, and a posteriorly directed force is applied to the anterior tibia. The amount of posterior translation and the presence and character of the endpoint is noted. The extent of translation is assessed by noting the change in the distance of the step-off between the anteromedial tibial plateau and the medial femoral condyle. The tibial plateau is approximately 1 cm anterior to the medial femoral condyle on average. However, the contralateral knee must be examined to establish a baseline.

Another test for examination of the PCL is the posterior sag or Godfrey test. This test involves flexing the knee and hip and noting the posterior pull of gravity creating posterior "sag" of the tibia on the femur. An adjunct to this test involves watching for a reduction of this subluxation with active quadriceps contraction.

The reverse pivot shift is the analogue to the pivot shift in the evaluation of an ACL injury. This is performed by placing a valgus stress on the knee with the foot externally rotated. The knee is then extended from 90 degrees of flexion and a palpable reduction of the posterolateral tibial plateau is noted between 20 and 30 degrees of flexion.

It is extremely important to evaluate the posterolateral structures of the knee in the setting of a suspected PCL injury. Injury to the posterolateral structures is reported to occur in up to 60% of PCL injuries.

Imaging Studies


Given the magnitude of the forces required to injure the PCL, plain radiographs of the knee are essential to evaluate for bony injuries, dislocation, or evidence of other associated injuries. Subtle posterior subluxation on the lateral radiograph may also indicate PCL injury. Stress posterior drawer radiographs and contralateral comparisons may also increase the sensitivity for detecting PCL injuries with plain radiographs. In the chronic setting of PCL injury, radiographs are useful to assess for patellofemoral and medial compartment degenerative changes that can occur over time.


Although plain films are necessary and useful in the evaluations of these injuries, MRI is the diagnostic study of choice for the knee with a presumed PCL injury. MRI is from 96% to 100% sensitive at diagnosing PCL tears. Equally or more importantly, MRI is extremely valuable in its ability to detect associated injuries. This is particularly important in diagnosing posterolateral corner injuries because these can often be missed on the initial clinical examination. In multiligamentous knee injuries, MRI can also be useful in assessing the ACL because clinical examination of the ACL is challenging in the setting of a complete PCL tear.


In the setting of a chronic isolated PCL tear, pain in the medial and patellofemoral compartments are generally evaluated with radiographs. If these are normal, some surgeons proceed with a bone scan to evaluate for increased uptake in these areas. Areas under increased stress demonstrate increased uptake on the bone scan before signs of advanced arthritis occur on radiographs. This subset of patients may benefit from a PCL reconstruction to decrease the stress and delay osteoarthritis.


There is significant controversy in the treatment of isolated PCL injuries. Multiple factors must be evaluated in the decision to treat a complete PCL rupture. The patient's age, activity level, expectations, and associated injuries must be taken into account. The literature on operative versus nonsurgical treatment of these injuries can be difficult to interpret, and there is no long-term follow-up studies of randomized patient groups.


Rehabilitation of the PCL injured knee often largely depends on the associated injuries sustained by the knee. This is particularly true with the commonly associated posterolateral corner injury. Therefore, we focus on the rehabilitation of the isolated PCL injured knee. Regaining motion and strength are the two key objectives of a rehabilitation program. Obtaining full quadriceps strength is essential for achieving the optimal result with nonsurgical treatment. The initial treatment is aimed at keeping the tibia reduced under the femur and minimizing tension on the injured PCL. With partial injuries (grade I and II), the prognosis is quite good, and early motion with weight bearing is the usual course of therapy. In a complete PCL tear, most keep the knee immobilized in extension to protect the posterolateral structures. Early strengthening exercises focus on quadriceps strength with quadriceps sets, straight leg raises, and partial weight bearing in extension.

Overall, most patients benefit from nonsurgical treatment of a PCL tear. Despite objective findings of instability that are often noted on examination, most patients subjectively are satisfied with the function of the knee. Bracing is generally ineffective in controlling PCL laxity clinically.

The main subjective complaint with chronic PCL insufficiency, however, is pain rather than instability. A PCL deficient knee with posterior tibial subluxation places significantly increased stresses on the patellofemoral and medial compartments of the knee. In one series in which patients with PCL injuries were followed with serial radiographs, 60% of patients displayed some degenerative changes of the medial compartment.


Surgical management of PCL injuries are broken down into avulsion fractures, isolated acute PCL injuries, multiligament injuries, and chronic PCL insufficiency. Avulsion fractures of the PCL are rare fractures. If nondisplaced, these injuries are treated nonsurgically. If significantly displaced, these fractures are generally treated with open reduction and internal fixation.

The majority of surgeons generally still treat isolated PCL injuries with nonsurgical care. However, nonoperative care of these injuries is not without consequences. Although subjective results in these patients are good in the short term, many continue to have objective instability and display degenerative arthritic changes over time. A follow up of PCL deficient knees at an average of 15 years after injury found 89% of patients with persistent pain and half with chronic effusions. All patients in this group showed degenerative changes when followed for 25 years. Therefore, given the risks of continued instability and the potential of an increased chance of arthritic changes, surgical reconstruction of the PCL is a reasonable choice.

Initially, surgical care of complete PCL tears consisted of a primary repair of midsubstance tears. The objective stability of these repairs was generally disappointing. Current reconstruction methods generally involve routing either autograft or allograft tendons through bone tunnels to reconstruct the PCL in an anatomic fashion. Although there are several different methods of reconstructing the PCL, the two main categories of PCL reconstruction consist of single- and double-bundle repairs. Classically, reconstructions of the PCL anatomically replicated the anterolateral bundle of the native PCL with a single-bundle reconstruction. As problems were noted with recurrence of posterior laxity in the postoperative period, a double-bundle technique was derived to reconstruct both the anterolateral and posteromedial bundles of the native PCL. The advantages of the double-bundle technique are thus far theoretical, and there is no long-term clinical follow-up demonstrating the superiority of a double-bundle reconstruction at this time.

The severe instability noted with PCL injuries associated with multiligamentous knee injuries make the argument for ligament reconstruction more compelling in this patient population. Many of the studies involving PCL reconstruction in these complex knee injuries have involved primary repair attempts. Although subjective results were generally good, residual excessive, objective laxity was very common following repairs. More recently ligament reconstructions with allograft and autograft have become the dominant method of PCL reconstruction in this challenging patient population.


The most common complication following PCL reconstruction is the return of objective posterior laxity on physical examination. This does not present as subjective laxity, however, and patient satisfaction remains high despite objective laxity. Acute PCL reconstructions in the setting of a multiligamentous knee repair/reconstruction can result in arthrofibrosis with extensive postoperative scarring.

Results/Return to Play

Even with nonsurgical management of a PCL injury, the prognosis for a functional recovery and return to competition is very good. A strong quadriceps muscle and extensor mechanism can significantly compensate for PCL laxity. Athletes should spend a minimum of 3 months in rehabilitation before attempting a return to competition. However, there is a subset of patients that experiences significant instability with a grade III PCL injury that does not allow a return to competition. This is a subset of patients that may benefit from PCL reconstruction.

However, the prognosis for a PCL tear associated with a multiligamentous knee injury is guarded with respect to return to play. Although prompt recognition of a multiligamentous injury and appropriately timed treatment, reconstruction, and rehabilitation is essential for optimal recovery, these injuries are such that a significant percentage of patients are not able to return to full competition.

Allen CR, Kaplan LD, Fluhme DJ et al: Posterior cruciate ligament injuries. Curr Opin Rheumatol 2002;14:142. [PMID: 11845019] 

Fanelli GC, Edson CJ: Combined posterior cruciate ligament-posterolateral reconstructions with Achilles tendon allograft and biceps femoris tendon tenodesis: 2- to 10-year follow-up. Arthroscopy 2004;20:339. [PMID: 15067271] 

Patella Dislocation

Dislocation of the patella is a potential cause of acute hemarthrosis and must be considered when evaluating a patient with an acute knee injury. The injury occurs when valgus force and external rotation of the tibia is applied to a flexed leg. It is most common in females in the second decade of life.

Clinical Findings

The patella almost always dislocates laterally. The patient may notice the patella sitting laterally or might say that the rest of the knee has shifted medially. It is unusual to see actual dislocation of the patella except at the time of injury. Reduction occurs when the knee is extended.

Examination demonstrates tenderness over the medial retinaculum and adductor tubercle, which is the origin of the medial patellofemoral ligament. The patient also has pain and apprehension when the patella is pushed laterally with the knee slightly bent. Radiographs, including an axial patellar view, should be obtained to determine whether there are osteochondral fractures. Often, a small fleck of bone is avulsed by the capsule on the medial aspect of the patella. This is not intraarticular and does not require removal. A displaced osteochondral fracture require excisions or internal fixation. Examination of the uninjured knee is recommended to determine whether there are predisposing factors for dislocation, such as patella alta, genu recurvatum, increased Q angle, and patellar hypermobility. Patella alta, or high-riding patella, is identified by measuring the length of the patellar tendon and dividing by the length of the patella. The upper limit of normal is 1.2. The Q angle is formed by a line through the patellar tendon intersecting a line from the anterior superior iliac spine in the center of the patella. A normal Q angle is approximately 10 degrees, with a range of approximately plus or minus 5 degrees. Patients with generalized hypermobility have increased extension of the knee, or genu recurvatum, which in effect gives them patella alta. They also often have hypermobility of all the capsular ligamentous structures, including the static stabilizers of the kneecap, giving them significant patellar hypermobility.

Treatment & Prognosis

A wide variety of treatment options are recommended for patellar dislocations, including immediate mobilization and strengthening exercises, immobilization in a cylinder cast for 6 weeks followed by rehabilitation, arthroscopy with or without retinacular repair, surgical repair of the torn retinaculum, or immediate patellar realignment.

Treatment is based on which predisposing factors are present. Little is lost by functional treatment, similar to the treatment of isolated medial collateral ligament sprains, which is often successful. If dislocation recurs, realignment may be performed. A long-term study showed that patients treated surgically for patellar malalignment problems had a higher incidence of osteoarthritis than those treated nonoperatively.

Atkin DM et al: Characteristics of patients with primary acute lateral patella dislocation and their recovery within the first 6 months of injury. Am J Sports Med 2000;28:472. [PMID: 10921637] 

Bensahal H et al: The unstable patella in children. J Pediatr Orthop 2000,9:265. [PMID: 11143470] 

Buchner M et al: Acute traumatic primary patellar dislocation: Long-term results comparing conservative and surgical treatment. Clin J Sport Med 2005;15:62. [PMID: 15782048] 


Ruptures of the quadriceps and patellar tendons usually result from a tremendous eccentric contraction of the quadriceps muscle, which may occur when an athlete stumbles and tries not to fall.

Rupture of the Quadriceps Tendon

Quadriceps tendon ruptures occur most frequently in patients older than 40 years. Biopsies of fresh rupture sites showed local degenerative changes already present, consistent with the theory that normal tendons do not rupture. Rarely, the injury occurs bilaterally, and it is often associated with gout, diabetes, or steroid use. When it does occur bilaterally with only a small amount of trauma, the diagnosis may be difficult to make because of the small amount of swelling or symptoms of injury.

The cardinal symptom is inability to extend the knee. When extension is attempted, a gap develops in the suprapatellar region. The patella rides at a slightly lower level, and the anterior border of the femoral condyles may be palpated.

Acute complete quadriceps tendon ruptures should be paired surgically. If left untreated, proximal migration and scarring of the quadriceps muscle occurs. Direct-end repair produces excellent results. Neutralizing the forces across the repair is difficult, and immobilization in extension is recommended. Repair of ruptures more than 2 weeks old may be difficult and may require quadriceps lengthening, muscle or tendon transfers, or a combination of these procedures.

Ilan DI et al: Quadriceps tendon rupture. J Am Acad Orthop Surg 2003;11:192. [PMID: 112828449] 

Konrath GA et al: Outcomes following repair of quadriceps tendon ruptures. J Orthop Trauma 1998,12:273. [PMID: 9619463] 

Rupture of the Patellar Tendon

Rupture of the patella tendon occurs more frequently in patients younger than 40 years. The patient cannot actively extend the knee, the patella is high riding, and a defect is palpable beneath the patella. Surgical repair is the treatment of choice. The tendon, along with the medial and lateral retinaculum, should be sewn end to end. A stress-relieving wire may be placed around the patella and through the tibial tubercle. The wire should be removed in 6–8 weeks. Chronic patellar tendon ruptures are very hard to treat. The quadriceps must be freed up from the femur and the patella pulled down to the proper location. The gracilis and semitendinosus tendons can be used to substitute for the patellar tendon.

The extensor mechanism may also be disrupted at the inferior pole of the patella where the patellar tendon originates. This usually occurs in a child between 8 and 12 years of age. The distal pole of the patella plus a large sleeve of articular cartilage is pulled off (Figure 4–18). This may be easily misdiagnosed if the fragment of bone is small. Reestablishment of an intact extensor mechanism is necessary. With displaced fractures, open reduction and internal fixation with tension band wiring are recommended.

Figure 4–18.


Sleeve fracture of the patella. A: A small segment of the distal pole of the patella is avulsed with a relatively large portion of the articular surface. B: Lateral radiograph of the knee with a displaced sleeve fracture of the patella. Note that the small osseous portion of the displaced fragment is visible, but the cartilaginous portion is not seen.

(Reproduced, with permission, from Rockwood CA Jr, ed: Fractures in Children, 3rd ed. Lippincott, 1991.)


Pain in the knee region is a very common complaint of athletes. If there is no history of an acute injury, overuse is commonly the cause. The patient is often able to point to the area of pain. The history of activity must be obtained as well as overall evaluation of the extremities.

Anterior Knee Pain

Clinical Findings


Anterior knee pain is a common complaint and frequently bilateral. It is most common in females during the second decade of life. The patellofemoral joint is often the source of pain. Entities such as chondromalacia patella, patellofemoral arthralgia, and lateral patellofemoral compression syndrome are diagnostic considerations.

Patellar pain is often felt when going up or down hills or stairs, and there may be complaints of instability during walking, running, or other sports activities. These activities may create a joint reaction force of several times the body weight on the patella with each step. Swelling is seldom a complaint. If the pain is in one knee only, the patient may alter the way of climbing and descending stairs so that the affected leg is kept straight and each step leads with the same foot. This strategy significantly decreases the joint reaction force on the patellofemoral joint.

Many of these problems arise because the patellofemoral joint is semiconstrained, especially in the range of 0–20 degrees of flexion, and the constraint increases as flexion increases. The degree of constraint also depends on a number of other factors, including the angle of the sulcus of the femur, the presence or absence of patella alta, and the generalized ligamentous laxity of the patient. In addition, femoral anteversion and increased Q angle (Figure 4–19) may lead to increased instability of the patellofemoral joint. This lack of constraint may predispose the patella to frank dislocation, although subluxation is a much more common finding. The degree of congruity is anatomically variable and may lead to high-contact stresses caused by anatomic configuration and static and dynamic constraints on the patella. Increased pressure may cause pain and patellofemoral osteoarthritis.

Figure 4–19.


Q angle and valgus angulation.

(Reproduced, with permission, from American Academy of Orthopaedic Surgeons: Athletic Training and Sports Medicine, 2nd ed. AAOS, 1991.)

On physical examination of the patient with patellofemoral subluxation, minimal findings in relation to complaints may be present. Occasionally, crepitance, a crackling or clicking sound or feeling, is found with flexion and extension. Quadriceps strength, tone, and bulk are usually reduced. Pain may be elicited at a particular angle of flexion by putting the knee through its range of motion with resistance. Subluxation may often be diagnosed with the apprehension sign, a rapid contraction of the quadriceps when the patella is passively moved laterally.


Roentgenographic examination frequently shows a valgus angulation of the knee on anteroposterior views. Occasionally, patella alta may be identified on the lateral view, and tangential views of the patella at various knee flexion angles reveals a lack of contact of the medial facet of the patella with the medial facet of the trochlear groove of the femur. Lateral subluxation of the patellofemoral joint may also be observed.

This syndrome with a normal roentgenographic examination is frequently called chondromalacia patellae; with subluxation identified on radiograph, it is referred to as patellofemoral subluxation. A more accurate term would be patellofemoral arthralgia because patellofemoral subluxation was probably present prior to the onset of pain, and because chondromalacia patellae (softening of the patellar cartilage) is an arthroscopic or pathologic diagnosis. Patellofemoral arthralgia is a clinical diagnosis.



Initially, treatment is conservative, with the intent of improving quadriceps strength and stamina to stabilize the patellofemoral joint. Weight loss is prescribed to decrease the stress on the patellofemoral joint; reduction in loading the knee in the flexed position also accomplishes pressure reduction. Knee orthotics may be beneficial. When subluxation and fear of dislocation are major concerns, an orthotic that limits extension of the knee may be beneficial because the patella becomes inherently more stable with knee flexion. NSAIDs may be beneficial.


Only when conservative treatment is exhausted should surgical treatment be considered. Alteration in the alignment of the patellofemoral joint may be beneficial in patellofemoral arthralgia. Lateral retinacular release followed by a period of conservative treatment is beneficial in some cases. Distal realignment may be necessary to achieve appropriate alignment and reduction in pain in those cases with an abnormality such as valgus knee or increased femoral anteversion.


With lateral patellofemoral compression syndrome, there is tenderness along the lateral facet of the patella or along the femoral condyle. Without cartilage damage, an effusion is rarely present. Treatment includes decreasing the activity level, including avoiding hills or step aerobics. Ice-massage, quadriceps and hamstring stretching, and short-arc quadriceps exercises against resistance are recommended to strengthen the vastus medialis obliquus muscle without aggravating the pain. Patellar supports or neoprene sleeves may also be helpful. Most patients respond to this regimen and gradually resume their activities. The role of releasing a contracted lateral patellofemoral retinaculum is controversial.


Patellar tendinitis, or jumper's knee, is seen in basketball and volleyball players. Tenderness along the tendon, usually at the inferior pole of the patella, is noted. Treatment with ice and avoiding jumping usually suffices. In refractory cases, debridement of mucinous degenerative material from the tendon may be successful.


The prognosis for jumper's knee is quite good. The condition is often persistent but self-limiting. The patient can always alleviate the symptoms by avoiding the activities that cause the problem.

Csintalan R et al: Gender effects on the biomechanical properties of the peripatellar retinaculum. Clin Orthop Rel Res 2002;(402):260. [PMID: 12218492] 

Kettunen JA, Visuri T, Harilainen A et al: Primary cartilage lesions and outcome among subjects with patellofemoral pain syndrome. Knee Surg Sports Traumatol Arthrosc 2005;13:131. [PMID: 15756617] 

Witvrouw E, Werner S, Mikkelsen C et al: Clinical classification of patellofemoral pain syndrome: Guidelines for non-operative treatment. Knee Surg Sports Traumatol Arthrosc 2005;13:122. [PMID: 15703965] 

Lateral Knee Pain

Lateral knee pain that is not located on the joint line may result from iliotibial band friction syndrome. This is a form of bursitis caused by rubbing of the iliotibial band against the lateral epicondyle. Tenderness over the lateral epicondyle at approximately 30 degrees of flexion when the knee is extended is indicative of this diagnosis. Runners and cyclists are commonly afflicted. Crossover gait or running on banked terrain is thought to be a causative factor.

Treatment involves decreasing the athlete's activities, ice-massage, stretching of the iliotibial tract, and use of a lateral wedge orthotic in those patients with heel varus. Running on flat terrain and changing the gait pattern may be helpful. In cyclists, lowering the seat height so the full extension of the knee is not reached and adjusting the pedals so the toes are not internally rotated should help. Steroid injections are infrequently needed, and release of the inflamed portion of the iliotibial band is seldom necessary. As for other overuse syndromes of the knee, the prognosis is good.

Gunter P, Schwellnus MP: Local corticosteroid injection in iliotibial band friction syndrome in runners: A randomised controlled trial. Br J Sports Med 2004;38:269; discussion 272. [PMID: 15155424] 


Evaluation of foot and ankle injuries is described in Chapter 9. Injury specific to athletics includes chronic Achilles tendonitis, heel pain, plantar fasciitis and posterior tibial syndrome.

Clinical Findings

Achilles tendonitis, a frequent complaint in runners, may result from a contracted gastrocsoleus, or hyperpronation may cause overpulling of the medial insertion. Additionally, there may be a bony prominence on the superior-posterior aspect of the calcaneus, causing retrocalcaneal bursitis.

Heel pain is a common problem in runners and difficult to treat because of the uncertainty as to cause. Theories include painful heel spurs, bursitis, fat-pad atrophy, stress fracture, plantar fasciitis, or entrapment of the terminal branches of the posterior tibial nerve.

Many patients have pain localized in the posteromedial surface of the foot just distal to the attachment of the plantar fascia to the calcaneus (plantar fasciitis). This pain is often most severe on initially getting up in the morning and decreases as the day goes on.

Posterior tibial syndrome occurs in runners with hyperpronation. As the longitudinal arch flattens out, the posterior tibial musculotendinous unit elevates the flattened arch and has abnormal strain placed on it.


Treatment depends on the cause of the injury, but it includes decreasing running activities, using a heel lift, and performing stretching exercises. If hyperpronation is thought to be the cause, an orthotic may be used. Steroid injections are not recommended because they could lead to weakening and subsequent rupture of the tendon.

Surgical intervention for chronic Achilles tendinitis or retrocalcaneal bursitis is seldom needed. This would be done to remove areas of fibrosis or calcium within the tendon and possibly some bone from the posterior process of the calcaneus. The treatment for plantar fasciitis includes rest, ice-massage, and possibly antiinflammatory medications. A small shock-absorbing type of heel cup often is helpful, and a steroid injection may be given in recalcitrant cases. Acute rupture of the plantar fascia may occur. The pain is usually quite sharp and may cause significant disability for 6–12 weeks.

Hyperpronation may also cause fibular stress fractures. A semirigid orthosis may be recommended to decrease the amount and angular velocity of pronation. Using an orthosis while running actually increases the work of running, but if it decreases abnormal stresses in those who hyperpronate, it may be quite helpful.

Mizel MS et al: Evaluation and treatment of chronic ankle pain. Instr Course Lect 2004;53:311. [PMID: 15116624] 

Shalabi A et al: Eccentric training of the gastrocnemius-soleus complex in chronic Achilles tendinopathy results in decreased tendon volume and intratendinous signal as evaluated by MRI. Am J Sports Med 2004;25:149. [PMID: 15244320] 


Many disorders seen while caring for athletes may be difficult to diagnose with certainty. The differential diagnosis must be carefully made to rule out more severe injuries. A period of rest followed by gradual return to activities is often the best treatment. During convalescence, application of ice packs, stretching exercises, and gradual strengthening of the injured limb facilitate return to sports activities.


Many athletes, such as runners, cyclists, aerobics enthusiasts, volleyball players, and basketball players, develop painful disorders of the lower extremities without an acute injury. History taking is very important, and the examiner should ask specific questions about the circumstances in which the discomfort occurs. In a runner, for example, the examiner should ask whether there was an increase in the distance run or a change in the running surface, at what point the pain was felt, and what home remedies were tried before the runner sought advice from a physician.

The physical examination should include not only the affected area, but also evaluation of the back, pelvis, leg lengths, genu varum or valgum, femoral and tibial torsion, and cavus or flatfoot deformities. The presence of hamstring and heel cord contracture should be determined, and the gait pattern should be observed. Running shoes should be inspected for wear patterns, which may be quite helpful.

Muscle Strains

Muscle strains of the lower extremity are frequent, and disabling muscle injuries, with strain of the distal muscle tendon junction, are the most common. Muscles may stretch to approximately 125% of their resting length before tearing. Strains are graded as mild, moderate, and severe, based on the degree of pain, spasm, and disability that the strain causes. A severe strain would be complete disruption of the muscle, with a palpable defect and balling up of the muscle proximally.

In spite of the frequency of muscle strains and the disability they produce, there is little scientific information on their pathologic basis. Muscles susceptible to more stretching are more susceptible to strains. In the lower extremity, the muscles most frequently injured are the hamstring, quadriceps, and gastrocnemius muscles. These muscles all cross two joints, and they may be unable to resist full stretching across both joints. The most powerful muscles are more likely to be strained, and strains are more common in so-called explosive-type athletics. Eccentric contraction (muscle contraction while the muscle is lengthening) is often thought to be causative in muscle strains.

Clinical Findings

The diagnosis is relatively easy. Often the athlete feels the muscle "grab" while he or she is accelerating. There is localized tenderness over the muscle and pain on stretching of the muscle. Because the two joint muscles are most frequently involved, the muscles should be stretched over both of the joints during examination.

Treatment & Prognosis

The treatment of muscle strains should begin with ice in the immediate postinjury period. Flexibility and strength should be regained prior to return to activity. This may take many months, and if the patient returns to activity too early, there may be a setback to the level of the original injury.

Strengthening of the muscles might make them less susceptible to being torn. It is commonly believed that flexibility helps prevent muscle strains, but there are conflicting reports regarding this idea, and it is still unproved.

Askling C, Karlsson J, Thorstensson A: Hamstring injury occurrence in elite soccer players after preseason strength training with eccentric overload. Scand J Med Sci Sports 2005;15:65. [PMID: 15679576] 

Gabbe BJ, Finch CF, Bennell KL et al:. Risk factors for hamstring injuries in community level Australian football. Br J Sports Med 2005;39:106. [PMID: 15665208] 

Levine WN et al: Intramuscular corticosteroid injection for hamstring injuries. A 13-year experience in the National Football League. Am J Sports Med 2000;28(3):297. [PMID: 10843118] 

Shin Pain

Clinical Findings


The term shin splints is widely used for shin pain, but it is not a diagnostic term. A more specific diagnosis should be made if possible. Shin splints are usually defined as pain associated with activity in the beginning of training after a relatively inactive period. The pain and tenderness are usually located over the anterior compartment and disappear in 1–2 weeks as the athlete becomes conditioned to the exercise. Care must be taken to differentiate shin splints from stress fractures of the tibia, which cause more localized pain and have many more potential complications if not cared for properly.


Medial tibial syndrome is also seen in runners, occurring along the medial border of the distal tibia. After 3–4 weeks, some hypertrophy of the cortical bone and periosteal new bone formation may be seen on radiograph. It is thought to be either a periostitis or possibly an incomplete stress fracture. The pull of the tibialis posterior muscle from its origin on the tibia and posterior tibial tendinitis are also thought to be possible causes.


Treatment for shin splints and medial tibial syndrome is rest and resumption of athletic activities in a graduated fashion.

Stress Fractures

Stress fractures may occur in the pelvis, femoral neck, tibia, navicular, and metatarsals. They are usually the result of a significant increase in training and activity. In the female athlete, poor nutrition, low bone density, and a history of menstrual disturbance are associated with a higher prevalence of stress fractures. The history is important in differentiating these injuries from infection or neoplasm, particularly when there is a finding on radiographs. Plain radiographs are normal at first. MRI or technetium bone scans are the best diagnostic tests. If symptoms persist for over a month, radiographs may become positive.

Treatment of stress fractures involves rest and avoidance of high-impact activities until healing occurs. This includes resolution of the tenderness and signs of fracture healing on plain radiographs. Continuous activity with stress fractures may lead to complete fractures. Patients must be made aware of this and all the complications that may develop with a complete fracture.

Armstrong DW III, Rue JP, Wilckens JH et al: Stress fracture injury in young military men and women. Bone 2004;35(3):806. [PMID: 15336620] 

Perron AD, Brady WJ, Keats TA: Principles of stress fracture management. The whys and hows of an increasingly common injury. Postgrad Med 2001;110:115.

Exertional Compartment Syndromes

Exertional compartment syndromes may result from muscle hypertrophy within the confining osseofascial compartment. As the muscles hypertrophy and the amount of edema within the compartment increases, the blood supply to the nerves and muscles within the involved compartment is diminished, and the pressure continues to increase.

The syndrome presents as recurrent claudication during exertional activity and is relieved by rest. After exercise, the findings of localized pain, pain on passive motion, and hypesthesia are indicative.

Treatment consists activity modification including gradual onset of training. If unsuccessful, compartment pressures may be measured while the patient is exercising on a treadmill, and if the pressures are elevated, surgical fasciotomy is usually effective.

Shah SN, Miller BS, Kuhn JE : Chronic exertional compartment syndrome. Am J Orthop 2004;33:335. [PMID: 15344575] 


Contusion to the Quadriceps Muscle

Clinical Findings

A severe contusion to the quadriceps muscle (charley horse) is disabling and results in prolonged inactivity. It frequently occurs in football players. With significant bleeding into the muscle, there is inhibition of movement. Rarely, a compartment syndrome occurs.

Myositis ossificans may occur after these injuries. It may be apparent 2–4 weeks after the injury. Radiographically and histologically, myositis ossificans may be similar to osteogenic sarcoma; therefore, the history of contusion is very important. Radiographs should be obtained after such a contusion to minimize myositis ossificans being confused with cancer.

Treatment & Prognosis

Quadriceps contusions should be treated with elevation of the leg and the hip and knee flexed to tolerance to minimize bleeding. After a few days the knee can be moved with continuous passive motion or so-called drop-and-dangle gravity-assisted exercises. For the latter, the patient is seated on a table high enough to keep the feet off the floor. The patient then hooks the uninjured foot behind the ankle of the injured leg. The uninjured leg extends the knee of the injured leg, and gravity flexes the injured knee. Average length of disability for mild contusions is 2 weeks; for severe contusions, 3 weeks.

If heterotopic ossification is present, no specific treatment is recommended other than treatment for the contusion. Normal function may be obtained, but the recovery period is longer. Because early surgery may cause exacerbation of the heterotopic ossification, it should be avoided.

Cooper DE: Severe quadriceps muscle contusions in athletes. Am J Sports Med 2004;32:820. [PMID: 15090402] 

Diaz JA, Fischer DA, Rettig AC et al: Severe quadriceps muscle contusions in athletes. A report of three cases. Am J Sports Med 2003;3:289. [PMID: 12642267] 


Clinical Findings

Contusions about the pelvis and hip region may be very painful and disabling. Because of the subcutaneous location of the iliac crests and the greater trochanters, these regions are at risk in contact sports.

A contusion over the greater trochanter may cause persistent bursitis, tenderness directly over the greater trochanter, and increased pain with adduction of the leg. Females are more prone to trochanteric bursitis because of their broader pelvis.

A hip pointer is a very painful contusion over the iliac crest that occurs from many contact sports. It must be differentiated from an avulsion fracture in a child and a tear of the muscle aponeurosis in an adult. Profuse bleeding may occur and be very painful.

Treatment & Prognosis

For contusion over the greater trochanter, treatment consists of ice applications and decreased activities. Padding may be helpful to prevent recurrent injuries. The prognosis is good. For hip pointer injuries, initial treatment with ice is helpful. Protective pads are useful in preventing these injuries and returning the athlete to activities sooner.


Clinical Findings

Tibial tubercle avulsions occur in adolescent athletes, most often in males between 14 and 16 years of age. They result from a powerful contraction of the quadriceps muscle against a fixed tibia, as in jumping, or with forced passive flexion of the knee against a powerful quadriceps contraction, as in an awkward landing at the end of a jump or fall. Avulsion of the tubercle may occur with either a sudden acceleration or deceleration of the knee extensor mechanism. The patellar tendon must pull hard enough to overcome the strength of the growth plate, the surrounding perichondrium, and the adjacent periosteum.

Swelling and tenderness are located over the proximal anterior tibia. A tense hemarthrosis may be present. A palpable defect in the anterior tibia is associated with a much-displaced avulsion. Proximal migration of the patella occurs, and the patella may seem to float off the anterior aspect of the femur. The knee is held flexed; with displaced fractures, the patient is unable actively to extend the knee.

Watson-Jones defined three types of avulsion fractures, which were subsequently refined as the following three types (Figure 4–20): type 1 fracture, in which the fracture line lies across the secondary center of ossification at the level of the posterior border of the patellar ligament; type 2 fracture, in which a separation breaks out at the primary and secondary ossification centers of epiphysis; and type 3 fracture, in which the separation propagates upward through the main portion of the proximal tibial epiphysis. The degree of displacement depends on the severity of injury to the surrounding soft-tissue moorings. A lateral radiograph with the tibia slightly internally rotated is the best view to see the fracture and the degree of displacement.

Figure 4–20.


Classification of avulsion fractures of the tibial tubercle. Type 1 fracture (left) across the secondary ossification center at level with the posterior border of the inserting patellar ligament. Type 2 fracture (center) at the junction of the primary and secondary ossification centers of the proximal tibial epiphysis. Type 3 fracture (right) propagates upward across the primary ossification center of the proximal tibial epiphysis into the knee joint. This fracture is a variant of the Salter-Harris III separation and is analogous to the fracture of Tillaux at the ankle because the posterior portion of the physis of the proximal tibia is closing.

(Reproduced, with permission, from Odgen JA et al: Fractures of the tibial tuberosity in adolescents. J Bone Joint Surg Am 1980;62:205.)

Differential Diagnosis

Osgood-Schlatter disease, or osteochondrosis of the tuberosity of the tibia, should not be confused with acute avulsion of the tibial tubercle. In the former, the patient is usually between 11 and 15 years of age and involved in athletics. Pain is located at the tibial tubercle, and it has usually been present intermittently over a period of several months. Walking on a flat surface is not difficult, but ascending or descending stairs causes difficulty. Radiograph examination shows slight separation of the tibial tubercle with new bone formation beneath it (Figure 4–21).

Figure 4–21.


Development of Osgood-Schlatter lesion. (Left) Avulsion of osteochondral fragment that includes surface cartilage and a portion of the secondary ossification center of the tibial tubercle. (Right) New bone fills in the gap between the avulsed osteochondral fragment and the tibial tubercle.

(Reproduced, with permission, from Rockwood CA Jr (ed): Fractures in Children, 3rd ed. Lippincott, 1991.)

Treatment recommendations vary from decreasing the amount of running and jumping, but continuing participation in athletics, to cylinder cast immobilization for a short period of time. The long-term prognosis is excellent. Although symptoms are often present for 2 years, early short-term cast immobilization may shorten this period of discomfort to 9 months. In most children, casting is not necessary. Explaining the benign nature of the problem to both the patient and the parents, reassuring them that the long-term prognosis is good, and modifying activities usually allows continued participation in athletics. Hamstring stretching and ice-massage ideally decrease symptoms during the time needed for maturation of the tibial tubercle. The pain goes away when the tubercle unites with the tibia. In a very small number of cases, chronic pain is present if the ossicle fails to unite. Painful ossicles in the adult are treated successfully with simple excision.


Full function of the extensor mechanism is necessary, and therefore treatment of tibial tubercle avulsion fractures is aimed at this goal. If the fracture is minimally displaced, and the patient is able to extend the knee fully against gravity, nonoperative treatment is acceptable. A cylinder cast should be applied with the knee extended and worn for 4 weeks. Active range-of-motion and strengthening exercises should then commence. At 6 weeks, quadriceps exercises against resistance are initiated. For displaced fractures, open reduction and internal fixation are recommended, with screws if the piece or pieces are large enough. If rigid fixation of large fragments is obtained, early active flexion and passive extension may be initiated. If a tenuous repair is obtained, protection in a cast is advisable.


Because the injury occurs in children who are close to skeletal maturity, meaningful growth abnormalities at the proximal tibial physis do not occur. Return to activities is allowed after the athlete develops quadriceps mass and strength equal to the contralateral side.


Clinical Findings

In the skeletally immature athlete, the apophysis, or growth plate where the muscle attaches to bone, is the weak link in the bone-muscle-tendon unit. Therefore, just as the growth plate is prone to breaking in children's fractures, the bony origin of muscles may be pulled off. This most commonly occurs in athletes between 14 and 25 years of age. Comparison radiographs may be helpful to make sure the avulsion fracture is not just a normal anatomic variant. In the pelvis, this may occur at the iliac crest (abdominal muscles), anterior superior iliac spine (sartorius origin), anterior inferior iliac spine (rectus femoris origin), ischial tuberosity (hamstring origin), and lesser trochanter of the femur (iliopsoas insertion).

Treatment & Prognosis

Symptomatic care with a few days of rest followed by ambulation with crutches for approximately a month is recommended. It is usually 6–10 weeks before athletic activities may be resumed. Long-term athletic activity will probably not be affected. Open reduction and internal fixation do not show superior results, and therefore they are usually not warranted. Abundant calcification may occur in the ischial tuberosity region and may be the cause of chronic bursitis and pain. Excision of the exuberant callous should cure this problem. Another indication for surgery is a painful fibrous nonunion, which also may be cured with excision of the fragment.

Rossi F, Dragoni S: Acute avulsion fractures of the pelvis in adolescent competitive athletes: Prevalence, location and sports distribution of 203 cases collected. Skeletal Radiol 2001;30:127. [PMID: 11357449] 


The shoulder is the third most commonly injured joint during athletic activities, after the knee and the ankle. Sports-related injuries of the shoulder may result from a direct traumatic event or repetitive overuse. Any activity that requires arm motion, particularly overhead arm motion such as throwing, may stress the soft tissues surrounding the glenohumeral joint to the point of injury. The shoulder is the most mobile joint in the body, partly as a result of minimal containment of the large humeral head by the shallow and smaller glenoid fossa. The trade-off for this mobility is less structural restraint to undesirable and potentially damaging movements. Thus, a fine balance must be struck to maintain full range of shoulder motion and normal glenohumeral joint stability.

Kim DH et al: Shoulder injuries in golf. Am J Sports Med 2004;32(5):1324. [PMID: 15262661] 



The glenohumeral joint is a modified ball-and-socket joint. The glenoid fossa is a shallow inverted, comma-shaped, articular surface one fourth the size of the humeral head. The articular surface of the humeral head is retroverted approximately 30 degrees relative to the transverse axis of the elbow. Because the scapula is oriented anterolaterally approximately 30 degrees on the thorax, relative to the coronal plane of the body, the face of the glenoid fossa matches the humeral head retroversion. The scapula rotates to direct the glenoid superiorly, inferiorly, medially, or laterally to accommodate changing humeral head positions. As a result, the humeral head is centered in the glenoid throughout most shoulder motions. When this centered position is disturbed, instability may result.


The clavicle articulates medially with the sternum at the sternoclavicular joint and laterally with the acromion of the scapula at the acromioclavicular joint. The clavicle rotates on its long axis and acts as a strut to stabilize the glenohumeral joint, serving as the only bone connecting the appendicular upper extremity to the axial skeleton.


The capsule of the glenohumeral joint may be the most lax of all the major joints, yet in certain positions it makes an important contribution to stability. The capsuloligamentous structures and the glenoid labrum share a common insertion. The anterior capsule is composed of the coracohumeral and superior glenohumeral ligaments, the middle glenohumeral ligament, and the inferior glenohumeral ligament (Figure 4–22). There is a variable relationship between the anterior capsuloligamentous structures and the labrum, such that certain anatomic variations may be associated with joint instability more often than others. For example, an anterosuperior sublabral hole is variably present within the glenohumeral joint, connecting with the subscapularis bursa that lies between the subscapularis tendon and the capsule.

Figure 4–22.


Ligaments about the shoulder girdle.

The glenoid labrum not only acts as an attachment site for the capsuloligamentous structures but also as an extension of the articular cavity. Its presence deepens the glenoid socket by nearly 50%, and removal of the labrum decreases joint stability to shear stress. In this way, the triangular cross section of the labrum acts as a chock-block to help prevent subluxation.


The muscles around the shoulder may be divided into three functional groups: glenohumeral, thoracohumeral, and those that cross both the shoulder and elbow.

Glenohumeral Muscles

Four muscles compose the rotator cuff: the supraspinatus, subscapularis, infraspinatus, and teres minor. The supraspinatus has its origin on the posterosuperior scapula, superior to the scapular spine. It passes under the acromion, through the supraspinatus fossa, and inserts on the greater tuberosity with an extended attachment of fibrocartilage. The supraspinatus is active during the entire arc of scapular plane abduction; paralysis of the suprascapular nerve results in an approximately 50% loss of abduction torque. The infraspinatus and the teres minor muscles originate on the posterior scapula, inferior to the scapular spine, and insert on the posterior aspect of the greater tuberosity. Despite their origin below the scapular spine, their tendinous insertions are not separate from the supraspinatus tendon. These muscles function together to externally rotate and extend the humerus. Both account for approximately 80% of external rotation strength in the adducted position. The infraspinatus is more active with the arm at the side; the teres minor activates mainly with the shoulder in 90 degrees of elevation. The subscapularis muscle arises from the anterior scapula and is the only muscle to insert on the lesser tuberosity. The subscapularis is the sole anterior component of the rotator cuff and functions to rotate and flex the humerus internally. The tendinous insertion of the subscapularis is continuous with the anterior capsule so that both provide anterior glenohumeral stability.

The deltoid is the largest of the glenohumeral muscles. It covers the proximal humerus on a path from its tripennate origin at the clavicle, acromion, and scapular spine to its insertion midway on the humerus at the deltoid tubercle. Abduction of the joint results from activity of the anterior and middle portions. The anterior portion is also a forward flexor. The posterior portion does not abduct the joint but instead adducts and extends the humerus. The deltoid is active throughout the entire arc of glenohumeral abduction; paralysis of the axillary nerve results in a 50% loss of abduction torque. The deltoid muscle can fully abduct the glenohumeral joint with the supraspinatus muscle inactive.

The teres major muscle originates from the inferior angle of the scapula and inserts on the medial lip of the bicipital groove of the humerus, posterior to the insertion of the latissimus dorsi. The axillary nerve and the posterior humeral circumflex artery pass superior to it through the quadrilateral space also bordered by the teres minor, the triceps, and the humerus. It contracts with the latissimus dorsi muscle, and the two muscles function as a unit in humeral extension, internal rotation, and adduction.

Thoracohumeral Muscles

The pectoralis major and the latissimus dorsi muscles are powerful movers of the shoulder and hence contribute to the joint force that in turn usually stabilizes the glenohumeral joint. The pectoralis major muscle arises as a broad sheet of two distinct heads with the lowermost fibers of the sternal head inserting most proximally on the humerus.

Muscles that have origin on the thorax contribute to glenohumeral stability and may have roles in instability as well. When the shoulder is placed in horizontal abduction, similar to the apprehension position, the lowermost fibers of the sternal head of the pectoralis major muscle are stretched to an extreme. Because anterior instability also occurs from forcible horizontal abduction of the shoulder, the humeral head can be pulled out of the glenoid by passive tension in the pectoralis major and latissimus dorsi muscles.

Biceps Brachii Muscle

Both heads of the biceps brachii muscle have their origin on the scapula. The short head originates from the coracoid and with the coracobrachialis muscle forms the conjoined tendon. The long head of the biceps has its origin just superior to the articular margin of the glenoid from the posterosuperior labrum and the supraglenoid tubercle, and it is inside the synovial sheath of the glenohumeral joint. It traverses the glenohumeral joint, passing over the anterior aspect of the humeral head to the bicipital groove where it exits the joint under the transverse humeral ligament.

Its origin on the scapula and insertion of the radius leaves the long head of the biceps brachii muscle with potential for function at both the shoulder and the elbow. Its function at the elbow is well established to include both flexion and supination. Long considered a depressor of the humeral head, the role of the active biceps was questioned because electromyographic studies showed little or no activity of the biceps when elbow motion was controlled. This does not preclude a passive role or an active role associated with elbow motion because tension in the tendon may then contribute to glenohumeral joint stability.


The axillary artery traverses the axilla, extending from the outer border of the first rib to the lower border of the teres minor muscle, forming the brachial artery. The axillary artery lies deep to the pectoralis muscle but is crossed in its midregion by the pectoralis minor tendon, just before the tendon inserts on the coracoid process. The axillary vein travels with the axillary artery, and branches of the axillary artery supply most of the shoulder girdle. The brachial plexus consists of the ventral rami of the fifth through eighth cervical nerves and the first thoracic nerve. This network of nerve fibers begins with the joining of the ventral rami proximally in the neck and continues anteriorly and distally, crossing into the axillary region obliquely underneath the clavicle at about the junction area of the distal one third and proximal two thirds. Clavicular fractures in this area have the potential of injuring the brachial plexus. The plexus then lies inferior to the coracoid process, where its cords form the peripheral nerves that continue down the arm. Muscles of the shoulder girdle are supplied by the nerves arising at all levels of the brachial plexus.

Eberly VC, McMahon PJ, Lee TQ: Variation in the glenoid origin of the anteroinferior glenohumeral capsulolabrum. Clin Orthop 2002;400,26. [PMID: 12072742] 

Enad JG: Bifurcate origin of the long head of the biceps tendon. Arthroscopy 2004;20:1081. [PMID: 15592239] 

Price MR et al: Determining the relationship of the axillary nerve to the shoulder joint capsule from an arthroscopic perspective. J Bone Joint Surg Am 2004;86-A:2135. [PMID: 15466721] 

History & Physical Examination


The history of shoulder complaints must include age, arm dominance, location, intensity, duration, temporal occurrence, aggravating and alleviating factors, radiation of discomfort, physical activity level, occupation, and the mechanism of injury. These responses, combined with the physical findings (Table 4–3) and imaging studies, can lead to accurate diagnosis of shoulder problems. Previous responses to treatment help to characterize their efficacy and establish a pattern of disease or injury progression. The physical examination begins with the patient undressing so both shoulders are fully exposed. Patients should be examined first in the standing position. The surface anatomy should be checked for asymmetry, atrophy, or external lesions. The supraspinatus and infraspinatus fossae are especially important to examine for atrophy. The area of pain should be pointed out by the patient prior to the physician manipulating the shoulder to avoid hurting the patient unnecessarily. A thorough neurovascular examination of the upper extremity should be performed.

Table 4–3. History and Physical Examination of the Shoulder.



Physical Examination

Cuff tendonitis

Pain over the lateral shoulder with overhead activity

Neer and Hawkin impingement signs


Night pain

Normal ROM


Mild weakness

Mild weakness



Pain relieved with lidocaine injection into the subacromial space

Cuff tear

Pain over the lateral shoulder with overhead activity

Neer and Hawkin impingement signs


Night pain

Loss of active ROM





Loss of ROM

Pain relieved with lidocaine injection into the subacromial space


Joint "slips" out

Apprehension of instability with shoulder abduction and external rotation (anterior instability only)


Pain and feelings of instability with shoulder abduction and external rotation (anterior instability only)

Apprehension of instability with shoulder abduction and external rotation relieved by relocation test (if anterior instability only)


Asymptomatic with the shoulder at rest


AC joint instability (separation)

History of fall onto the "point" of the shoulder

Tenderness at AC joint


Pain on top of the shoulder

Deformity at AC joint: acromion displaced inferior to the distal clavicle


Pain with cross-body movements

Pain with cross-body movements


Bump at the AC joint

Pain relieved with lidocaine injection into the AC joint

AC joint arthritis

Pain on top of the shoulder

Tenderness at AC joint


Pain with cross-body movements

Pain with cross-body movements



Pain relieved with lidocaine injection into the AC joint


Decreased ROM

Decreased active and passive ROM


Pain with shoulder at rest but worse at the limits of ROM

Pain relieved with lidocaine injection into the glenohumeral joint


Decreased ROM

Decreased active and passive ROM


Pain with shoulder at rest but worse with motion

Crepitus with motion


Crepitus with motion

Pain relieved with lidocaine injection into the glenohumeral joint

Biceps tendonitis

Pain over the anterior shoulder with activity

Speed and Yerguson tests



Tenderness at the bicipital groove



Pain relieved with a lidocaine injection into the bicipital groove


AC = acromioclavicular; ROM = range of motion.


Types of Movement

Many terms may be used to describe movements of the shoulder joint (Figure 4–23). Flexion occurs when the arm begins at the side and elevates in the sagittal plane of the body anteriorly. Extension occurs when the arm starts at the side and elevates in the sagittal plane of the body posteriorly. Adduction occurs when the arm moves toward the midline of the body, with abduction occurring as the arm moves away from the midline of the body. Internal rotation occurs when the arm rotates medially, inward toward the body, and external rotation occurs as the arm rotates laterally or outward from the body. Horizontal adduction occurs as the arm starts at 90 degrees of abduction and adducts forward and medially toward the center of the body, and horizontal abduction happens as the arm starts at 90 degrees of abduction and moves outward, away from the body. Elevation is the angle made between the thorax and arm, regardless if it is in the abduction plane, flexion plane, or in between.

Figure 4–23.


Description of shoulder motion.

Evaluation of Movement

Range of motion of the injured shoulder should be compared with the opposite shoulder, along with the strength during abduction and rotation. This should be done both passively and actively. The shoulder should be inspected for any changes in synchrony, such as scapular winging, elevation of the scapula, muscle fasciculations indicating abnormal function, and any other irregular or asymmetric movements of the scapula. Information may be gained on loss of flexibility and instability resulting from muscle imbalance, fibrosis, and tendon, capsular, or ligament contractures. Loss of flexibility usually occurs in the capsular tissues of the glenohumeral joint. Sudden pain or clicking may indicate an intraarticular problem. Loss of motion in either internal or external rotation is suggestive of a chronic anterior or posterior dislocation, respectively.

Provocative Tests

Specific tests are then performed that aid in making the correct diagnosis. The specific tests for instability, impingement syndrome, bicipital tendonitis, and superior capsulolabral/biceps anchor lesions are discussed later.

Imaging & Other Studies

Many varieties of radiologic views and projections are available to examine shoulder injuries. An initial radiographic evaluation of the shoulder should consist of an anteroposterior view of the glenohumeral joint in both internal and external rotation, and an axillary lateral. Additional plain radiographic views depend on the underlying pathology. MRI may be indicated in evaluation of rotator cuff disorders recalcitrant to conservative treatment. An MR arthrogram may be useful in detecting labral pathology. Traditional arthrography is rarely indicated because it is invasive and has little or no advantage over MRI. Ultrasonography is also useful in diagnosis of rotator cuff injury, but it is operator dependent. Electromyographic examination can be useful in identifying shoulder pain of cervical origin.

Arthroscopic Evaluation


Indications for arthroscopic examination of the shoulder include the following:


1. impingement syndrome including subacromial bursitis, rotator cuff tendonitis, and rotator cuff tears;

2. acromioclavicular joint osteoarthritis;

3. loose bodies;

4. chronic synovitis;

5. glenohumeral instability;

6. superior capsulolabral/biceps anchor lesions; and

7. adhesive capsulitis (frozen shoulder).


With the patient either in the lateral decubitus or the beach chair position, the arthroscope is inserted into a posterior portal, medial and inferior to the posterolateral corner of the acromion. With visualization of the glenohumeral joint, an anterior portal immediately lateral to the coracoid allows additional inflow and entrance of additional instruments. Distal clavicle excision, removal of loose bodies, and capsular release of adhesive capsulitis can be performed. An additional anterior portal inferior to the first is required for instability repair with an arthroscopic technique. The arthroscope is then removed from the joint and placed into the subacromial bursa. Portals lateral to the acromion allow subacromial decompression and rotator cuff repair to be carried out with arthroscopic techniques.


Examination of shoulder range of motion and stability with the patient under anesthesia is helpful in the diagnosis and treatment of shoulder injuries. This should be performed in the operating room prior to arthroscopy. The steps in arthroscopic examination should then include the following:


1. glenohumeral articular surfaces;

2. rotator cuff from inside the joint;

3. labrum including the biceps anchor;

4. anterior capsuloligamentous structures;

5. rotator cuff from the subacromial bursal space;

6. coracoacromial ligament;

7. acromion; and

8. acromioclavicular joint

Applegate GR et al: Chronic labral tears: Value of magnetic resonance arthrography in evaluating the glenoid labrum and labral-bicipital complex. Arthroscopy 2004;20:959. [PMID: 15525929] 

Kaplan LD et al: Internal impingement: Findings on magnetic resonance imaging and arthroscopic evaluation. Arthroscopy 2004;20:701. [PMID: 15346111] 

Lee DH et al: The double-density sign: A radiographic finding suggestive of an os acromiale. J Bone Joint Surg Am 2004;86-A:2666. [PMID: 15590851] 

Lindauer KR et al: MR imaging appearance of 180–360 degrees labral tears of the shoulder. Skeletal Radiol 2005;34:74. [PMID: 15668822] 

Magee T, Williams D, Mani N: Shoulder MR arthrography: Which patient group benefits most? AJR Am J Roentgenol 2004;183:969. [PMID: 15385288] 

Middleton WD, Teefey SA, Yamaguchi K: Sonography of the rotator cuff: Analysis of interobserver variability. Am J Roentgenol 2004;183:1465. [PMID: 15505321] 

Porcellini G et al: Arthroscopic treatment of calcifying tendinitis of the shoulder: Clinical andultrasonographic follow-up findings at two to five years. J Shoulder Elbow Surg 2004;13:503. [PMID: 15383805] 


Rotator Cuff Tendon Injuries

Injury to the rotator cuff, a common cause of shoulder pain and disability, has a high prevalence during athletic activities. Injury of the rotator cuff may result in pain, weakness, and decreased range of motion. Symptoms are often worsened by activity, especially when the hand is positioned overhead. Night pain is also common, and many complain of awakening after rolling onto the affected shoulder. Although shoulder weakness and decreased range of motion usually result from a rotator cuff tendon tear, pain alone from subacromial bursitis or rotator cuff tendonitis may also be the cause. Each of these entities most often results from impingement syndrome.

Impingement Syndrome

Any prolonged repetitive overhead activity such as tennis, pitching, golf, or swimming may cause compromise of the space between the humeral head and the coracoacromial arch that includes the acromion, coracoacromial ligament, and the coracoid process. Impingement causes microtrauma to the rotator cuff, resulting in local inflammation, edema, cuff softening, pain, and poor function. These problems may even cause greater impingement, producing a continuous vicious cycle (Figure 4–24). This cycle may be precipitated by acute injury to the rotator cuff tendon itself. Blood supply to this tendon is precarious, thus decreasing its capacity for healing.

Figure 4–24.


The cycle of injury and reinjury resulting from rotator cuff impingement.

Subacromial Bursitis

Clinical Findings

Bursitis of the shoulder refers to the inflammation of the subacromial bursa. It has the mildest signs and symptoms of shoulder impingement. Pain is present with overhead activity, and there is usually no or mild pain with the arm at the side.

Active range of shoulder motion is limited by pain. No atrophy of the shoulder muscles is present, and manual muscle testing demonstrates mild weakness. Passively, when the internally rotated shoulder is moved into forward flexion, the patient experiences discomfort. This is called the Neer impingement sign (Figure 4–25). Injection of 10 mL of lidocaine into the subacromial space resolves the pain, and there is a dramatic increase in strength and range of motion with the Neer impingement test.

Figure 4–25.


Evaluating for impingement of the supraspinatus tendon with the "empty can" test.


Radiographic views of the subacromial space, such as the supraspinatus outlet view, may show a spur on the undersurface of the acromion, causing narrowing of the subacromial space. Advances in imaging methods, such as ultrasonography and MRI, now aid in diagnosis of subacromial bursitis, rotator cuff tendonitis, and rotator cuff tendon tear (Figure 4–26).

Figure 4–26.


MRI demonstrating (A) normal shoulder anatomy and (B) cystic changes at the greater tuberosity with rotator cuff tear (arrow).

Treatment & Prognosis

Treatment for impingement syndrome starts with conservative measures such as activity modification, physical therapy, and oral antiinflammatory medications. Activity modification is necessary to minimize overhead arm motion and effect a return to normal overhead throwing biomechanics. Modalities such as heat and cold, iontophoresis or phonophoresis, and microelectric nerve stimulation may also be helpful. Only with normal function of the rotator cuff tendons do glenohumeral mechanics improve and the impingement syndrome cease. If this treatment fails, a subacromial injection of corticosteroids may be helpful.

Surgical intervention is indicated only after failure of a prolonged conservative treatment program (a minimum of 3 months). If the subacromial space is narrow, release of the coracoacromial ligament combined with shaving the undersurface of the acromion (known as acromioplasty or subacromial decompression) may result in relief of symptoms. This can be done with an arthroscopic technique to decrease postoperative discomfort and minimize the complication of deltoid muscle injuries.

Never has there been more controversy about this surgical procedure. It has been used since the 1930s to diminish symptoms associated with rotator cuff injury. The classic rationale for its efficacy is that any prolonged repetitive overhead activity, such as tennis, pitching, golf, or swimming, may cause compromise of the space between the humeral head and the coracoacromial arch, which includes the acromion, coracoacromial ligament, and the coracoid process. Known as impingement syndrome, microtrauma to the rotator cuff results in local inflammation, edema, cuff softening, pain, and poor function. These problems may even cause greater impingement, producing a continuous vicious cycle. This cycle may also be precipitated by acute injury to the rotator cuff tendon itself. Blood supply to this tendon is precarious, thus decreasing its capacity for healing. Removing subacromial spurs as well as increasing the size of the subacromial space may release pressure on the cuff tendons, ending the vicious cycle and allowing for healing.

Other rationales are proposed for the efficacy of subacromial decompression in treating rotator cuff injuries. The subacromial space, including the subacromial bursa and the subacromial periosteum, is richly innervated, primarily by branches of the suprascapular nerve. Subacromial decompression results in denervation of the subacromial space. Others have found increased inflammatory factors in the subacromial bursa of shoulders with rotator cuff injury that may normalize after subacromial decompression.

Rotator cuff pathology is associated with the shape and geometry of the acromion, especially if there is acromial encroachment onto the supraspinatus tendon. Bigliani and Morrison introduced a commonly used classification to describe the shape of the acromion in 1986. They found a higher incidence of rotator cuff tears in hooked (type III) acromions than in flat (type I) and curved (type II) acromions. However, several studies show poor to moderate interobserver reliability of this classification, regardless if the clinicians used radiographs, MRI, or cadaveric scapulas to classify the acromions. Routine use of subacromial decompression in the treatment of rotator cuff tears is now questioned. A newer prospective, randomized study of rotator cuff repair found no statistical difference in outcome whether or not a subacromial decompression was done. To confuse matters even more, a study of nearly a hundred patients followed for nearly a decade found subacromial decompression may not prevent progression of impingement syndrome to a tear.

Rotator Cuff Tendonitis

Clinical Findings

Of the four rotator cuff muscles, the supraspinatus tendon is most often initially involved. Rotator cuff tendonitis also results from impingement syndrome and is characterized by pain with overhead activity. The patient may occasionally be awakened by pain at night. Active shoulder range of motion is limited by pain. Typically, no atrophy of the shoulder muscles is present and manual muscle testing demonstrates mild weakness. The Neer impingement sign is positive and the pain resolves with subacromial injection of lidocaine.

Treatment & Prognosis

Radiographic evaluation and treatment are similar to subacromial bursitis management. An exception is the athlete less than 40 years old with glenohumeral instability and secondary tendonitis. In this case, the instability should be treated first and the rotator cuff tendonitis then resolves.

Rotator Cuff Tendon Tear

Clinical Findings

A rotator cuff tendon tear is characterized by pain with overhead activity. However, the patient is often also awakened at night with pain. The athlete with a chronic rotator cuff tear may describe a gradual loss of strength. Pain may be persistent, occurring even with the arm at the side.

Active range of shoulder motion is limited, and if the tear is severe, there will be atrophy of the shoulder muscles. Manual muscle testing demonstrates weakness. The Neer impingement sign is positive, and the pain resolves with subacromial injection of lidocaine.

Treatment & Prognosis

Radiographic evaluation and treatment are similar to subacromial bursitis management. Unlike acute tears, chronic rotator cuff tears often present insidiously, with slow progression from subacromial bursitis to rotator cuff tendonitis and eventual tendon tear. Differentiating severe rotator cuff tendonitis from partial or small full-thickness chronic rotator cuff tears may be a difficult task.

Tears are most common at the humeral insertion site of the supraspinatus tendon, where stress is greatest with the joint in abduction. Tears may be partial thickness or involve the full thickness of the tendon. The size may be small (less than 1 cm), medium (1–3 cm), large (3–5 cm), or massive (more than 5 cm). Chronic rotator cuff tears may result partly from degeneration within the rotator cuff tendon. Poor vascularity and repetitive activity, especially in the athlete with a restricted subacromial space, may be contributing factors. A minor traumatic event may also cause a full-thickness tear in an athlete with mild or moderate tendon degeneration.

If the tear is small, a prolonged period of rest, lasting 4–9 months, may relieve symptoms. Range-of-motion exercises are also recommended, unless they cause significant discomfort. If this fails to control the symptoms, surgical repair of the tear is recommended. The thin degenerated tissue of a chronic rotator cuff tear makes surgical repair more difficult than repair of an acute tear. Surgical decompression of the subacromial space to remove spurs should also be considered.

Rehabilitation lasts from 6 months to a year with gradual exercise progression needed to restore normal, or near-normal function, and strength. This varies with the tear size repaired and type of surgery performed. Typically, immediately after the procedure, passive motion and isometric strengthening exercises start, along with elbow, hand, and grip strengthening exercises. At 6 weeks, the athlete may be able to begin low-intensity active strengthening exercises against gravity. The goals are to bring the athlete to normal strength with a functional, pain-free range of motion.

Although the lesion location and size are helpful in describing the rotator cuff tear, symptoms do not correlate with these factors alone. Both epidemiologic and imaging studies indicate a high incidence of partial-thickness rotator cuff tears at younger ages and a high incidence of full-thickness rotator cuff tears at older ages. Small full-thickness rotator cuff tears may be asymptomatic as long as the force couple of the anterior and posterior rotator cuff is preserved. Instead, a number of other factors influence the severity of symptoms, including acute/chronic nature of injury, patient age, activity level, humeral head superior migration, shoulder muscle strength, arthritis, pain tolerance, and workers' compensation status.

Partial-Thickness Rotator Cuff Tear

A partial articular sided tendon avulsion is much more common than a bursal side tear of the rotator cuff. As with other rotator cuff injuries, symptoms may resolve with appropriate physical therapy and analgesics. Yet some individuals with a partial-thickness tear have persistent or recurrent symptoms. If a conservative program of exercises and gradual return to activity does not lead to steady improvement, then further diagnostic evaluation with ultrasonography, MRI, or arthroscopy may be helpful. Arthroscopic debridement of the abnormal cuff may promote healing in athletes with partial-thickness posttraumatic tears. Following debridement, immediate resumption of range-of-motion and muscle-strengthening exercises begins. Typically, it requires 6–12 months for a throwing athlete to return to athletics following arthroscopic debridement of a partial-thickness rotator cuff tear.

Gartsman GM, O'Connor DP: Arthroscopic rotator cuff repair with and without arthroscopic subacromial decompression: A prospective, randomized study of one-year outcomes. J Shoulder Elbow Surg 2004;13:424. [PMID: 15220883] 

Hyvonen P, Lohi S, Jalovaara P: Open acromioplasty does not prevent the progression of an impingement syndrome to a tear. Nine-year follow-up of 96 cases. J Bone Joint Surg Br 1998;80:813. See comment as well in J Bone Joint Surg Br 1999;82:743. [PMID: 9768891] 

Klepps S et al: Prospective evaluation of the effect of rotator cuff integrity on the outcome of open rotator cuff repairs. Am J Sports Med 2004;32:1716. [PMID: 15494338] 

Lam F, Mok D: Open repair of massive rotator cuff tears in patients aged sixty-five years or over: is it worthwhile? J Shoulder Elbow Surg 2004;13:517. [PMID: 15383807] 

Millstein ES, Snyder SJ: Arthroscopic evaluation and management of rotator cuff tears. Orthop Clin North Am 2003;34:507. [PMID: 14984190] 

O'Holleran JD et al: Determinants of patient satisfaction with outcome after rotator cuff surgery. J Bone Joint Surg Am 2005;87-A:121. [PMID: 15634822] 

Rebuzzi E et al: Arthroscopic rotator cuff repair in patients older than 60 years. Arthroscopy 2005;21:48. [PMID: 15650666] 

Romeo AA et al: Shoulder scoring scales for the evaluation of rotator cuff repair. Clin Orthop 2004;(427):107. [PMID: 15552145] 

Sperling JW, Cofield RH, Schleck C: Rotator cuff repair in patients fifty years of age and younger. J Bone Joint Surg Am 2004;86-A:2212. [PMID: 15466730] 


Bicipital Tendinitis

Clinical Findings

The long head of the biceps muscle is an intraarticular structure deep in the rotator cuff tendon as it passes under the acromion to its insertion at the top of the glenoid. The same mechanism that initiates impingement syndrome symptoms in rotator cuff injuries may inflame the tendon of the biceps in its subacromial position, causing bicipital tendinitis. Tendinitis may also result from subluxation of the tendon out of its groove in the proximal humerus, which occurs with rupture of the transverse ligament. The symptoms of bicipital tendinitis, whether the result of impingement or tendon subluxation, are essentially the same. Pain is localized to the proximal humerus and shoulder joint, with resisted supination of the forearm aggravating the pain. Pain may also occur on manual testing of the elbow flexors and on palpation of the tendon itself. The Yergason test is used to test for instability of the long head of the biceps in its groove.

Treatment & Prognosis

If the tendinitis is associated with shoulder impingement, therapy aimed at treating the impingement syndrome relieves the bicipital tendinitis. If subluxation of the tendon within its groove is the cause of the irritation, conservative therapy includes NSAIDs and restriction of activities, followed by a slow resumption of activities after a period of rest. Strengthening of the muscles that assist the biceps in elbow flexion and forearm supination is also beneficial. Steroid injections into the sheath of the biceps tendon are helpful, but they may be hazardous if placed into the substance of the tendon because they promote tendon degeneration. Persistent symptoms may warrant tenodesis of the biceps tendon directly into the humerus. Recovery from this procedure is difficult, and it is doubtful if a competitive athlete could return to peak performance after such a procedure.

Biceps Tendon Rupture

Clinical Findings

The long head of the biceps tendon may rupture proximally, either from the supraglenoid tubercle of the scapula at the entrance of the bicipital groove proximally or at the exit of the tunnel at the musculotendinous junction. The muscle mass moves distally, producing a bulging appearance to the arm. Rupture of the long head of the biceps is predictive of a rotator cuff tear. Rupture of the biceps distally at its insertion involves both heads, and the muscle mass moves proximally. The mechanism is usually a forceful flexion of the arm and is more common in older athletes (greater than 50 years old) or with direct trauma. Microtears probably serve to render the tendon vulnerable to an acute tearing event. The degree of ecchymosis depends on the location of the tear, with avascular areas having less and the musculotendinous junction producing quite a noticeable amount of ecchymosis. Diagnosis is usually easily obvious because the deformity is evident.

Treatment & Prognosis

Surgical treatment of proximal ruptures, if indicated, is usually reserved for patients less than 40 years old. Open surgical repair leaves a long scar and usually does not completely restore the underlying anatomy. The coiled-up distal end of the tendon is usually found beneath the attachment of the pectoralis major. A correlation exists between proximal biceps tendon rupture and rotator cuff tears in middle-age and older athletes (more than 50 years old). Rupture of the distal biceps tendon often warrants surgical repair because of loss of forearm flexion and supination strength. In this case, the tendon is usually found approximately 5–6 cm above the elbow joint, and care must be taken to avoid damage to the lateral antebrachial cutaneous nerve.

Cope MR, Ali A, Bayliss NC: Biceps rupture in body builders: Three case reports of rupture of the long head of the biceps at the tendon-labrum junction. J Shoulder Elbow Surg 2004;13:580. [PMID: 15383821] 

Vidal AF, Drakos MC, Allen AA: Biceps tendon and triceps tendon injuries. Clin Sports Med 2004;23:707. [PMID: 15474231] 


Rupture of the pectoralis major tendon is an uncommon injury, usually occurring during bench press exercises in weight lifting caused by sudden unexpected muscle contraction during pulling or lifting. The athlete usually experiences sudden pain and develops local ecchymosis and swelling. As the swelling subsides, a sulcus and deformity may be visible, and the patient notices weakness of the arm in adduction and internal rotation. The rupture may be partial or complete, and nonoperative treatment usually results in satisfactory function for the activities of daily life. Surgery may be considered if the athlete wishes to return to heavy weight lifting.

Aarimaa V et al: Rupture of the pectoralis major muscle. Am J Sports Med 2004;32:1256. [PMID: 15262651] 


To make the correct diagnosis, the glenohumeral joint must be tested for anterior, posterior, and inferior instability. Different classifications of glenohumeral joint instability are proposed, based on etiology, the direction of the instability, or on various combinations. TUBS is an acronym describing instability caused by a traumatic event, which is unidirectional, associated with a Bankart lesion, and often requires surgical treatment. AMBRI refers to atraumatic, multidirectional instability that may be bilateral and is best treated by rehabilitation. In this classification, the etiology of multidirectional instability is thought to be enlargement of the capsule from genetic or microtraumatic origin.

The positive sulcus sign is used as the diagnostic hallmark for multidirectional instability, but we now know that the sulcus sign is sometimes found in asymptomatic shoulders of individuals with increased laxity. Laxity or joint play is a trait of body constitution that differs from one individual to another. Individuals may be loose or tight jointed. A shoulder is hyperlax if the examiner can easily subluxate the humeral head out of the glenoid in the anterior, posterior, and inferior directions without eliciting symptoms. Unfortunately, this makes classification of instability based on etiology, or direction alone, extremely difficult. Instead, classification is best based on the direction of instability that elicits symptoms and the presence or absence of hyperlaxity (Table 4–4).

Table 4–4. Classification of Glenohumeral Instability Based on the Direction of Instability and the Presence or Absence of Hyperlaxity.




UDI (Unidirectional Instability)

MDI (Multidirectional Instability)

Normal laxity

Very common 60%

Very rare 3%

Increased laxity

Common 30%

Rare 7%


Adapted, with permission, from Gerber C: Observations of the classification of instability. In Warner JJP et al eds: Complex and Revision Problems in Shoulder Surgery. Lippincott-Raven, 1997:9–18.

Gerber C, Nyffeler RW: Classification of glenohumeral instability. Clin Orthop 2002;400:65. [PMID: 12072747] 

Glenohumeral Joint Instability Evaluation


The apprehension test is performed to assess anterior instability. The test applies an anterior directed force to the humeral head from the back with the arm in abduction and external rotation (Figure 4–27). A positive test results from the patient's apprehension that the joint will dislocate. This maneuver mimics the position of subluxation, or dislocation, and causes reflex guarding. Conversely, the relocation test is positive if relief is obtained by applying a posterior directed force to the humeral head (Figure 4–28).

Figure 4–27.


The apprehension test for anterior instability.


Figure 4–28.


The relocation test is positive if relief is obtained by applying a posterior directed force to the humeral head.


No single test has high sensitivity and specificity for posterior instability. The posterior apprehension test is performed by applying a posterior directed force to the forward flexed and internally rotated shoulder. To perform the circumduction test, the patient is instructed to move the shoulder actively in a large circle starting from a flexed, internally rotated and cross-body position, then to forward flexion, then to an abducted and externally rotated position, and lastly to the arm at the side. The examiner stands behind the patient and palpates the posterior shoulder. If positive, the joint subluxes in the flexed, internally rotated, and cross-body position, and it reduces as the shoulder is moved. For the Jahnke test, a posteriorly directed force is applied to the forward flexed shoulder. The shoulder is then moved into the coronal plane as an anterior directed force is applied to the humeral head. A clunk occurs as the humeral head reduces from the subluxed position (Figure 4–29).

Figure 4–29.


The Jahnke test for posterior instability. A: A posterior directed force applied to the forward flexed shoulder (in the upper left column). B: The shoulder is then moved into the coronal plane as an anterior directed force is applied to the humeral head (in the lower left column). A clunk occurs as the humeral head reduces from the subluxed position.

(Reprinted, with permission, from Hawkins RJ, Bokor DJ: Clinical evaluation of shoulder problems. In Rockwood CA et al (eds): The Shoulder. WB Saunders, 1998, p. 186.)


The sulcus sign is used to evaluate laxity and inferior instability. The test is performed with the athlete in a sitting position with the arm at the side. A distraction force is applied longitudinally along the humerus. If positive, discomfort or apprehension of instability are experienced as the skin just distal to the lateral acromion hollows out (Figure 4–30).

Figure 4–30.


The sulcus test for inferior instability.

(Reprinted, with permission, from Hawkins RJ, Bokor DJ: Clinical evaluation of shoulder problems. In Rockwood CA et al (eds): The Shoulder. WB Saunders, 1998, p. 189.)

Glenohumeral Dislocation

When the shoulder is forced beyond the limit of its normal range of motion, the articular surface of the humeral head may displace from the glenoid to varying degrees. The majority of glenohumeral dislocations, or subluxations, are in the anteroinferior direction.

Anterior Dislocation


Anterior glenohumeral dislocation occurs from either an external rotation or abduction force on the humerus, a direct posterior blow to the proximal humerus, or a posterolateral blow on the shoulder large enough to displace the humeral head. The anterior capsule is either stretched or torn within its attachment to the anterior glenoid. The head may be displaced into a subcoracoid, subglenoid, subclavicular, or intrathoracic position. Two major lesions are typically seen in patients with recurrent anterior dislocations (Figure 4–31). First is the Bankart lesion, an anterior capsular injury associated with a tear of the glenoid labrum off the anterior glenoid rim. The Bankart lesion may occur with fractures of the glenoid rim. Such fractures are often minimally displaced, and treatment is usually dictated by the joint instability. The second major lesion associated with recurrent anterior dislocations is the Hill-Sachs lesion, a compression fracture of the posterolateral articular surface of the humeral head. It is created by the sharp edge of the anterior glenoid as the humeral head dislocates over it. When large, both the Bankart and the Hill-Sachs lesions predispose to recurrent dislocations when the arm is placed in abduction and external rotation. If the glenoid rim fracture involves greater than 20% of the glenoid diameter, the joint becomes prone to instability and treatment with open reduction and internal fixation is indicated. If the fracture is old or the glenoid rim is worn to a similar level, corticocancellous bone grafting of the glenoid rim is indicated.

Figure 4–31.


Anatomic lesions producing shoulder instability.

Other injuries associated with anterior dislocation may occur. These include avulsion of the greater tuberosity from the humerus, caused by traction from the rotator cuff, and injury to the axillary nerve, which may be stretched or torn. Permanent loss of axillary nerve function results in denervation of the deltoid muscle and loss of sensation over the proximal lateral aspect of the arm. Axillary nerve palsy may also occur during reduction of the dislocation, and therefore it should be tested both before and after reduction. The deltoid extension lag sign, described later in the section on axillary nerve injuries, may be the best way to assess function of this nerve. Lastly, the dead arm syndrome may occur after anterior joint instability. For example, a pitcher may report sudden inability to throw, with the arm going numb and becoming extremely weak after the ball release. The symptoms are transient, resolving within a few seconds to minutes.

Athletes who sustain a shoulder dislocation try to hold the injured extremity at the side, gripping the forearm with the opposite hand. Most athletes know their shoulder is dislocated, and they seek help immediately. On physical examination of an anterior dislocation, the examiner notes a space underneath the acromion where the humeral head should lie and a palpable anterior mass representing the humeral head in the anterior axilla.


One must distinguish between acute and recurrent anterior glenohumeral dislocations because an acute dislocation sustains severe trauma with the increased probability of associated injuries. The recurrent dislocation may occur with minimal trauma, and reduction may be accomplished with much less effort. Anterior dislocations may be reduced by one of several techniques. Longitudinal traction may be exerted on the affected arm with external rotation, followed by internal rotation of the arm. Care must be taken to avoid direct pressure on the neurovascular structures. Another method is to have the patient lie face down on the table and tie or tape a bucket to the injured arm and slowly fill it with water. This allows the musculature around the shoulder to relax from the force of the weight and effects the spontaneous reduction.

Following reduction of an initial dislocation, the shoulder should be immobilized in internal rotation for 2–6 weeks. Healing generally takes at least 6 weeks. Before returning to athletics, the patient should have normal range of motion without pain, and normal strength in the shoulder. Emphasis must be placed on strengthening the rotator cuff muscles to compensate for the laxity of the ligamentous support. When weight training is begun, military press, fly exercises, a narrow grip while bench pressing, and deep shoulder dips must be excluded until considerable time elapses and complete healing is realized.

Recurrent dislocations should be treated with minimal immobilization until the pain subsides, followed by range-of-motion and muscle-strengthening exercises. Many restraining devices are available to help prevent recurrent dislocations during sporting activities, focusing on keeping the arm from going into abduction and external rotation. These orthotics may be effective, but because they limit the athlete's range of shoulder motion, their use is limited for certain competitive activities.

If an athlete has sustained multiple dislocations and is unresponsive to conservative treatment, surgical reconstruction of the shoulder joint may be indicated. There are a wide variety of procedures to correct the instability, with most involving repair of the labral defect and tightening of the anterior capsule and ligamentous structures through an anterior incision (Table 4–5).

Table 4–5. Repair of Capsule and Labrum Back to the Glenoid Rim.

  Bankart procedure

  duToit procedure

  Viek procedure

  Eyre-Brook procedure

  Moseley procedure

Muscle and capsule plication 

  Putti-Platt procedure

  Symeonides procedure

Muscle and tendon sling procedures 

  Magnuson-Stack procedure

  Bristow-Helfet-Latarjet procedure modifications

  Boytchev procedure

  Nicola procedure

  Gallie-LeMesurier procedure

  Boyd transfer of long head of biceps (for posterior dislocation)

Bone block 

  Eden-Hybbinette procedure

  DeAnquin procedure (through a superior approach to the shoulder)


  Weber (humeral neck)

  Saha (humeral shaft)


For most surgical procedures, aggressive range-of-motion exercises do not start until at least 3 weeks postoperatively. The goal is to have full abduction and 90 degrees of external rotation. By 12 weeks, patients are often progressing well into their initial programs and may begin a variety of weight training exercises, avoiding exercises that strain the anterior capsule.

Posterior Dislocation


Posterior glenohumeral dislocations result from the posterior capsule being torn, stretched, or disrupted from the posterior glenoid. A reverse Hill-Sachs lesion (Figure 4–31) may appear on the anterior articular surface of the humerus. With a posterior dislocation, the subscapularis, or its insertion on the lesser tuberosity, may be injured. Posterior dislocations are often difficult to diagnose because the patient may have a normal contour to the shoulder or the deltoid of a well-developed athlete may mask signs of a displaced humeral head. The patient holds the injured shoulder in internal rotation and the examiner cannot rotate it externally. Anteroposterior radiographs can be misleading, and axillary views must be obtained to diagnose a posterior dislocation.


Applying traction in the line of the adducted humerus, with an anterior directed force to the humeral head, reduces a posterior dislocation. Anesthesia often helps decrease the trauma of reduction. Following reduction, the shoulder is immobilized for 2–6 weeks in external rotation and a small amount of abduction. Surgical treatment should be considered if these measures fail to provide the desired results.

Multidirectional Instability


Some patients have instability in both the anterior and posterior directions, most often subluxation and not dislocation. This situation may result in a painful shoulder, especially if rotator cuff strength decreases. The pain is often primarily a result of rotator cuff inflammation, likely from attempts to stabilize the humeral head during activity.


A rotator cuff strengthening program is often successful treatment.

Brophy RH, Marx RG: Osteoarthritis following shoulder instability. Clin Sports Med 2005;24:47. [PMID: 15636776] 

Good CR, Macgillivray JD: Traumatic shoulder dislocation in the adolescent athlete: Advances in surgical treatment. Curr Opin Pediatr 2005;17:25. [PMID: 15659959] 

Kim SH et al: Loss of chondrolabral containment of the glenohumeral joint in atraumatic posteroinferior multidirectional instability. J Bone Joint Surg Am 2005;87-A:92. [PMID: 15634818] 

Kim SH et al: Painful jerk test: A predictor of success in nonoperative treatment of posteroinferior instability of the shoulder. Am J Sports Med 2004;32:1849. [PMID: 15572311] 

Kirkley A et al: Prospective randomized clinical trial comparing the effectiveness of immediate arthroscopic stabilization versus immobilization and rehabilitation in first traumatic anterior dislocations of the shoulder: Long-term evaluation. Arthroscopy 2005;21:55. [PMID: 15701612] 

Krishnan SG et al: A soft tissue attempt to stabilize the multiply operated glenohumeral joint with multidirectional instability. Clin Orthop 2004;(429):256. [PMID: 15577496] 


Clinical Findings

The glenoid labrum is a fibrocartilaginous rim around the glenoid fossa that deepens the socket and provides stability for the humeral head. It also is a connection for the surrounding capsuloligamentous structures. Glenoid labrum tears may occur from repetitive shoulder motion or acute trauma. In the athlete with repeated anterior subluxation of the shoulder, tears of the anteroinferior labrum may occur, leading to progressive instability.

Weight lifters may also develop glenoid labrum tears from repetitive bench pressing and overhead pressing. Weakness in the posterior rotator cuff may aggravate this condition. Tears of the glenoid labrum may also occur from acute trauma such as falling on an outstretched arm, but they are also seen in the leading shoulders of golfers and batters when they ground their clubs or bats.

Patients with glenoid labrum injuries may describe their pain as interrupting smooth functioning of the shoulder during their specific activity. On examination, they may have discomfort on forced external rotation at 90 degrees of abduction, with the pain typically not increasing as the arm goes into further abduction. Frequently, a labrum disruption may be felt as a pop or click on forced external rotation. The patient may also experience discomfort on forced horizontal adduction of the shoulder. Manual muscle testing may show associated weakness in the rotator cuff muscles. Diagnostic tests such as a CT scan and MRI following injection of contrast dye into the shoulder joint may allow early detection of glenoid labrum lesions.

Treatment & Prognosis

Range-of-motion exercises and gradual return to activity are often successful in relieving symptoms. However if nonoperative management fails, arthroscopic intervention may be indicated to debride a torn symptomatic labrum. During arthroscopy, care must be taken not to debride the inferior labrum because this may result in increased anterior shoulder instability, escalating the probability of anterior shoulder dislocation. Immediately following surgery, range-of-motion exercises and strengthening training begin. Usually within 2–3 weeks following surgery, the athlete may begin a throwing program. Baseball pitchers may be ready to throw 3 months postoperatively.


The use of shoulder arthroscopy in the diagnosis and treatment of shoulder disorders has led to increased awareness of superior labrum anterior posterior (SLAP) lesions. SLAP lesions involve the origin of the long head of the biceps brachii (biceps anchor) and the superior capsulolabral structures. A type I lesion has degeneration or fraying of the labrum without instability. Type II lesions are most common, accounting for more than 50% of patients with a SLAP lesion, and they involve detachment of the superior labrum from the glenoid. A type III lesion has a bucket-handle tear of the superior labrum with firm attachment of the remainder of the labrum. Type IV lesions also remain attached to the labrum, but they have an associated bucket-handle tear of the labrum that extends into the biceps tendon (Figure 4–32).

Figure 4–32.


The five types of the SLAP lesion include fraying of the superior capsulolabrum (type 1), detachment of the superior capsulolabrum and the biceps anchor (type 2), bucket-handle tearing of the superior capsulolabrum (type 3), detachment of the superior capsulolabrum and tearing into the biceps anchor (type 4), and combinations of these (type 5).

Types V through VII SLAP lesions were later added to this initial four-part classification. A type V lesion is an anterior-inferior Bankhart lesion that continues superiorly to include separation of the biceps tendon. A type VI lesion includes a biceps separation with an unstable flap tear of the labrum. Finally, a type VII is a superior labrum-biceps tendon separation that extends anteriorly beneath the middle glenohumeral ligament.

Clinical Findings

Patients present with nonspecific shoulder pain associated with activity. A complicating factor in making the diagnosis is that the majority of SLAP lesions are associated with other shoulder pathology, such as rotator cuff tears, acromioclavicular joint pathology, and instability. Less than 28% of SLAP lesions are isolated.

No single test is both sensitive and specific for diagnosis of SLAP lesions. magnetic resonance arthrography (MRA) can be helpful. However, diagnostic arthroscopy remains the best means to diagnose SLAP lesions definitively. The active compression test may prove to be the most useful single provocative maneuver. The internally rotated shoulder is forward flexed to 90 degrees and then brought across the body in horizontal abduction of approximately 10 degrees. The test is positive if the patient has pain with resisted forward flexion that is relieved by external rotation of the shoulder.


Treatment of SLAP lesions can be simplified by noting whether or not the lesion contributes to detachment of either the biceps anchor or the anterosuperior capsulolabrum. Lesions producing meaningful detachment of the anterior capsuloligamentous structures generally require repair of these structures back to the bony glenoid rim. Lesions producing significant defects extending into the biceps tendon may require biceps tenotomy, with or without tenodesis.

Holtby R, Razmjou H: Accuracy of the Speed's and Yergason's tests in detecting biceps pathology and SLAP lesions: comparison with arthroscopic findings. Arthroscopy 2004;20:231. [PMID: 15007311] 

Musgrave DS, Rodosky MW: SLAP lesions: Current concepts. Am J Sports Med 2001;30:29. [PMID: 11198828] 

Parentis MA, Mohr KJ, El-Attrache NS: Disorders of the superior labrum: Review and treatment guidelines. Clin Orthop 2002;400:77. [PMID: 12072748] 


Clinical Findings

Often called adhesive capsulitis or frozen shoulder, shoulder stiffness is a painful condition characterized by significant restriction in both active and passive range of motion. The shoulder is characterized as being stiff when the articular surfaces are normal and the joint is stable, yet there is a restriction in range of motion. Stiffness may also result from pathologic connections between the articular surfaces, soft-tissue contracture, bursal adhesions, or a shortened muscle–tendon unit. Often of uncertain etiology, the restrictions of shoulder motion are global. That is, none of the shoulder planes of motion is spared.

Shoulder stiffness may be separated into idiopathic and posttraumatic etiologies. Idiopathic shoulder stiffness is most common in older individuals, especially women between 40 and 60 years of age. Other factors that predispose to idiopathic shoulder stiffness include cervical, cardiac, pulmonary, neoplastic, neurologic, and personality disorders. Patients with diabetes mellitus are also at a high risk of developing shoulder stiffness, with 10–35% of diabetics having restriction of shoulder motion. Diabetics who have been insulin dependent for many years have the greatest incidence and bilateral involvement. The pathophysiology of idiopathic shoulder stiffness remains uncertain, but the pathoanatomy is commonly limited to contracture of the glenohumeral capsule (Figure 4–33). Most prominently involved is the rotator interval that includes the coracohumeral ligament.

Figure 4–33.


Adhesive capsulitis of the shoulder. Note the small irregular joint capsule with addition of contrast material.

Although all patients can recall some traumatic event that preceded their shoulder stiffness, those with distinct trauma such as a prior fracture, rotator cuff tear, or surgical procedure have a posttraumatic etiology. Stiffness after shoulder surgery is typical and usually resolves with time and appropriate rehabilitation. But the shoulder should not be neglected after any surgery about the shoulder girdle. This includes axillary or cervical lymph node dissections, especially when combined with radiation therapy, cardiac catheterization in the axilla, coronary artery bypass grafting with sternotomy, and thoracotomy. All surgeons should be aware that these procedures may result in restricted shoulder motion.

The clinical presentation of idiopathic shoulder stiffness is classically described as having three phases. The first phase is the painful, freezing phase. The pain is typically achy, and sudden jolts or attempts at rapid motion exacerbate the chronic discomfort. The pain may begin at night, and shoulder motion becomes progressively limited. Patients often hold their arm at their side and in internal rotation with the forearm across the belly. They may also be treated for nonspecific shoulder pain with a sling in this position. This inflammatory phase often lasts between 2 and 9 months.

The second phase of progressive stiffness lasts between 3 and 12 months. Stiffness progresses to the point where shoulder motion is restricted in all planes. Essentially, the shoulder has undergone fibrous arthrodesis. Fortunately, pain progressively decreases from the initial inflammatory phase. With time, patients are able to use the shoulder with little or no pain, within the restricted range of motion, but attempts to exceed this range are accompanied by pain. The patient's symptoms then plateau. Unfortunately, this phase may be persistent with symptoms lasting for extended periods. In the resolution, or thawing phase, the shoulder slowly and progressively becomes more supple. It can be as short as a month but typically lasts 1–3 years.

On clinical examination, there is loss of both active and passive range of shoulder motion. Often the first motion to be affected is internal rotation demonstrated by an inability to bring the arm up the back to the same level as the normal shoulder. Radiographic confirmation of adhesive capsulitis may be done by arthrography, which demonstrates marked reduction in the capacity of the joint. Often the affected shoulder does not take more than 2–3 mL of dye, although normal capacity is 12 mL.

Treatment & Prognosis

Treatment varies, but conservative modalities and progressive range-of-motion exercises seem effective. Range-of-motion exercises for external rotation and abduction help minimize the length of restriction in motion and dysfunction. Manipulation under anesthesia, long the mainstay of intervention, is being replaced by selective arthroscopic capsular release. Short-term results indicate a quicker return of motion. Whether treated with rehabilitation alone or with capsular release, a return of approximately 80% shoulder range of motion is usual.

Ide J, Takagi K: Early and long-term results of arthroscopic treatment for shoulder stiffness. J Shoulder Elbow Surg 2004;13:174. [PMID: 14997095] 

Nicholson GP: Arthroscopic capsular release for stiff shoulders: Effect of etiology on outcomes. Arthroscopy 2003;19:40. [PMID: 12522401] 

Wolf JM, Green A: Influence of comorbidity on self-assessment instrument scores of patients with idiopathic adhesive capsulitis. J Bone Joint Surg Am 2002;84-A:1167. [PMID: 12107317] 


The clavicle is one of the most commonly fractured bones in the body, with direct trauma being the usual cause in athletic events (Figure 4–34). Football, wrestling, and ice hockey are the sports most commonly involved in clavicular fractures, which is not surprising because all three are associated with high-speed contact between players.

Figure 4–34.


Analysis of 1603 shoulder girdle injuries, showing the frequency and location of fractures and dislocations.

Clinical Findings

Despite the proximity of vital structures, clavicular fractures that occur during athletic activities are rarely associated with neurovascular damage, and accompanying soft tissue disorders are uncommon. The patient usually gives a history of falling in the area of the shoulder or receiving a blow to the clavicle, experiencing immediate pain and inability to raise the arm. Radiography usually confirms the clinical impression and must show the entire clavicle, including the shoulder girdle, upper third of the humerus, and sternal end of the clavicle. Midclavicular fractures account for 80% of clavicular fractures, with distal fractures at 15% and proximal fractures at 5%. Most fractures of the shaft of the clavicle heal well. The potential for a rare but serious neurovascular complication, such as a tear of the subclavian artery or brachial plexus injury, must be kept in mind when evaluating and treating clavicular fractures, and a neurovascular examination on initial evaluation is very important. Pulses in the distal part of the upper extremity, strength, and sensation must be carefully evaluated.

Because the clavicle is the single bone structure that fixes the shoulder girdle to the thorax, a fracture through the clavicle causes the shoulder to sag forward and downward. The pull of the sternocleidomastoid muscle may displace the proximal fragment superiorly. These forces tend to hinder the initial reduction and maintenance of reduction. In addition, distal fractures, which are more common in older age groups (more than 50 years old), may involve tears in the coracoclavicular ligament, which allows the proximal clavicle to ride up superiorly mimicking an acromioclavicular dislocation. Delayed union in this type of fracture is a much greater possibility than with other clavicular fractures.

Treatment & Prognosis

Mid and proximal clavicular fractures are usually treated with a short period of rest, and a sling may be used on the affected side to support the extremity. Immobilization is usually discontinued at 3–4 weeks, and once the clavicular fracture heals, range-of-motion and strengthening exercises should begin. Onset of exercises prior to healing may result in nonunion. Athletes should not be allowed to return to play until achieving their preinjury shoulder strength and range of motion. Generally, no special braces or pads are required when the athlete returns to play.

Grassi FS, Tajana MS, D'Angelo F: Management of midclavicular fractures: Comparison between nonoperative treatment and open intramedullary fixation in 80 patients. J Trauma 2001;50:1096. [PMID: 11426125] 

Robinson CM, Cairns DA: Primary nonoperative treatment of displaced lateral fractures of the clavicle. J Bone Joint Surg Am 2004;86-A:778. [PMID: 15069143] 

Robinson CM, Court-Brown CM, McQueen MM et al: Estimating the risk of nonunion following nonoperative treatment of a clavicular fracture. J Bone Joint Surg Am 2004;86-A:1359. [PMID: 15252081] 


Fractures of the proximal humerus, which represent approximately 4–5% of all fractures, are a relatively uncommon sports injury. They most often present in the early adolescent with open growth plates or in elderly (more than 70 years old) osteoporotic patients. When they do occur in the athlete, they are typically the result of a high-energy impact injury or are secondary to an underlying pathologic bone condition.

Clinical Findings

The proximal humerus consists of four major bony components: the humeral head, the greater tuberosity, the lesser tuberosity and the humeral shaft. Fractures can occur between any or all of these regions, and they are traditionally defined by the location and displacement of the fracture fragments (see Figure 3–15). The patient with a proximal humerus fracture usually is able to report the mechanism of injury and complains of pain, swelling, and inability to use the shoulder. Physical examination often reveals loss of the normal contour of the shoulder, tenderness about the shoulder, ecchymosis that may extend down to the elbow, and crepitus on attempted range of motion. A thorough neurovascular exam is essential because brachial plexus and axillary nerve injuries are reported in association with proximal humerus fractures. Because the axillary nerve is the most commonly injured nerve in these cases, sensation to light touch and pinprick over the lateral aspect of the upper arm and deltoid muscle function must be tested. Accurate radiographic evaluation is necessary to confirm the type and severity of the fracture and is essential in determining the treatment plan. Necessary views include anteroposterior and lateral views in the plane of the scapula as well as an axillary view to rule out an associated glenohumeral dislocation.

Treatment & Prognosis

Most proximal humerus fractures are minimally displaced and can be treated nonoperatively with sling immobilization and early passive range of motion. However, an estimated 20% of these fractures should be treated operatively. Many factors contribute to this decision-making process, including fracture type and degree of displacement, bone quality, activity level, and associated injuries. Surgical options range from closed reduction and percutaneous pinning to open reduction with internal fixation to humeral head replacement.

For minimally displaced fractures, the prognosis is generally good. Loss of motion is the most common complication. It can take 12–18 months to attain the maximal result, so range-of-motion exercises should be continued for an extended period of time.

Fankhauser F et al: A new locking plate for unstable fractures of the proximal humerus. Clin Orthop 2005;430:176.

Iannotti JP, Ramsey ML, Williams GR et al: Nonprosthetic management of proximal humeral fractures. J Bone Joint Surg Am 2003;85:1578. [PMID: 15116630] 

Robinson CM, Aderinto J: Posterior shoulder dislocations and fracture-dislocations. J Bone Joint Surg Am 2005;87-A(3):639.


In skeletally immature athletes, epiphyseal fractures of the proximal humerus may occur. The separate growth centers of the articular surface, greater tuberosity, and lesser tuberosity coalesce at approximately 7 years of age, with the remaining growth plates closing at 20–22 years of age. Therefore, fracture separations may occur at any age until the growth plates close. Fortunately, fractures in this area usually do not arrest growth.

Injury can occur to the shoulder of the growing musculoskeletal system from overhead throwing sports. Proximal humerus pain, especially while throwing and associated with widening of the proximal humerus epiphysis, is termed little league shoulder. Although widening of the proximal humerus epiphysis can be an adaptive change to throwing, when painful it may represent an overuse fracture.

Dobbs MB et al: Severely displaced proximal humeral epiphyseal fractures. J Pediatr Orthop 2003;23:208. [PMID: 12604953] 

Karatosun V et al: Treatment of displaced, proximal, humeral, epiphyseal fractures with a two-prong splint. J Orthop Trauma 2003;17:578. [PMID: 14504580] 


Clinical Findings

Acromioclavicular dislocations or subluxations, commonly referred to as separations, vary in severity depending on the extent of injury to the stabilizing ligaments and capsule. The typical mechanism of injury is a direct downward blow to the tip of the shoulder. Clinically, pain at the top of the shoulder over the acromioclavicular joint is the predominant symptom, with varying decreases in motion depending on the severity of the injury. The athlete who has sustained this type of injury typically leaves the field holding the arm close to the side.

When checking for instability of the acromioclavicular joint, the examiner should manipulate the midshaft of the clavicle, rather than the acromioclavicular joint, to rule out pain from contusion to the acromioclavicular area. For milder acromioclavicular injuries, the patient should put the hand of the affected arm on the opposite shoulder, and the examiner may then gently apply downward pressure at the patient's affected elbow, noting if this maneuver causes pain at the acromioclavicular joint.

Acromioclavicular joint injuries were initially divided into grades I through III (Figure 4–35). Grade I injuries are typically produced by a mild blow causing a partial tear of the acromioclavicular ligament. When the acromioclavicular ligament is completely torn, but the coracoclavicular ligament remains intact, a grade II injury that involves subluxation or partial displacement results. When the force of injury is severe enough to tear the coracoclavicular and acromioclavicular ligaments in addition to the capsule, a grade III injury occurs.

Figure 4–35.


Grades of acromioclavicular joint separations.

Three additional injuries were later added to the classification. In grade IV injuries, the clavicle is displaced posteriorly and buttonholed through the fascia of the trapezius muscle. Grade V injuries demonstrate severe inferior displacement of the glenohumeral joint, with the clavicle often 300% superior to the acromion. Lastly, in grade VI injuries, the distal end of the clavicle is locked inferior to the coracoid.

Acromioclavicular joint displacement is often obvious on physical examination, but it is best classified by radiography. An anteroposterior radiograph that is aimed 10 degrees cephalad allows visualization of the acromioclavicular joint. A radiograph of the entire upper thorax allows the vertical distance between the coracoid and the clavicle on both the involved and uninvolved sides to be compared. Anteroposterior radiographs with weights applied to the upper extremities are usually unnecessary. An axillary lateral radiograph is also essential for proper classification.

Treatment & Prognosis

Management of acromioclavicular joint injuries depends on their severity. Grade I and grade II injuries may be treated with a sling until discomfort dissipates, usually within 2–4 weeks. Next, a rehabilitation program starts, and normal range of motion and strength to the upper extremity begins to be restored. The treatment of grade III injuries or complete dislocations in athletes is controversial. Most feel that grade III injuries are best managed nonoperatively; others advocate operative treatment. Grade IV through VI injuries are best treated with open reduction and internal fixation along with reconstruction of the coracoclavicular ligament.

Nonsurgical treatment may either be a sling for comfort or an acromioclavicular sling to try to achieve reduction. The fit of the device must apply pressure to the distal clavicle sufficient to afford reduction, but not great enough to compromise the skin. Ice and other modalities are used for the acute acromioclavicular injury to reduce soreness and swelling. Pain is the limiting factor in beginning range-of-motion and isometric muscle strengthening exercises. It should be used as a guide for gradual initiation and escalation of these physical therapy regimes. Isotonic exercises may then follow because isometric exercises are more effective earlier when range of motion is limited.

Before resuming athletic activities, the patient must have full range of pain-free motion and no tenderness upon direct palpation of the acromioclavicular joint or pain when manual traction is applied. Athletes who do not require elevation of the arm, such as soccer or football players, tend to return to sports earlier than players who require overhead arm activity, such as tennis, baseball, and swimming athletes.

Fractures of the coracoid process are rare, usually seen in professional riflemen and skeet shooters, although they are also reported in baseball and tennis players. They are identified radiographically, and conservative treatment, including cessation of activity, usually results in uncomplicated healing after 6–8 weeks.

Dumonski M et al: Evaluation and management of acromioclavicular joint injuries. Am J Orthop 2004;33:526. [PMID: 15540856] 

Su EP et al: Using suture anchors for coracoclavicular fixation in treatment of complete acromioclavicular separation. Am J Orthop 2004;33:256. [PMID: 15195920] 


In the skeletally mature adult athlete, injury to the sternoclavicular joint usually consists of the surrounding soft tissue and capsule tearing, leading to subluxation or dislocation. The mechanism of injury is either a blow to the point of the shoulder, which predisposes to anterior dislocation, or a direct blow to the clavicle or chest with the shoulder in extension, which predisposes to posterior dislocation. The injury may range from a symptomatic sprain to a complete sternoclavicular dislocation with disruption of the capsule and its restraining ligaments.

Anterior Dislocation

The most common type of sternoclavicular dislocation is anterior dislocation, which is recognized clinically by an anterior prominence of the proximal clavicle on the involved side. Radiographic documentation of an anterior sternoclavicular dislocation is difficult because of overlapping of the rib, sternum, and clavicle at the joint, but it may be confirmed by oblique views. A CT scan is usually very sensitive and should be done if radiographic appear normal but the diagnosis is suspected.

Although dislocation of the anterior sternoclavicular joint may cause considerable distress initially, the symptoms usually subside rapidly, with no loss of shoulder function. A variety of surgical and nonsurgical approaches are advocated, but most feel that surgery for anterior dislocations results in significant complications. Closed treatment modalities vary from a sling alone to attempted closed reduction, which may be successful initially but is difficult to maintain.

Posterior Dislocation

Posterior sternoclavicular dislocation is much less common but has more complications because of the potential for injury to the esophagus, great vessels, and trachea. Presenting symptoms range from mild to moderate pain in the sternoclavicular region to hoarseness, dysphagia, severe respiratory distress, and subcutaneous emphysema from tracheal injury.

In most instances, closed reduction of posterior dislocations, if performed early, are successful and stable. To effect reduction, a pillow is placed under the upper back of the supine patient and gentle traction is applied with the shoulder held in 90 degrees of abduction and at maximum extension (Figure 4–36). Rarely, closed reduction under general anesthesia or open reduction is required.

Figure 4–36.


Method for reducing (A): anterior sternoclavicular dislocation and (B): posterior sternoclavicular dislocation.

After reduction, the patient is put in an immobilization splint, instructed to use ice and antiinflammatory agents. Once the joint heals sufficiently, usually within 2–3 weeks, range-of-motion exercises may begin. Elevation of the arm should not be attempted until 3 weeks after injury.

Medial Clavicular Epiphyseal Fracture

In athletes younger than 25 years, sternoclavicular injuries may not result in true dislocations but rather in fractures through the growth plate of the proximal clavicle. These clavicular epiphyseal fractures may appear clinically as dislocations, especially if some displacement is present, and they may be treated conservatively. Typically, these are not associated with growth deformities, and reduction of the fracture is not needed unless there is severe displacement. Symptomatic treatment for pain usually suffices. Sometimes an adolescent presents with an enlarging mass at the sternoclavicular joint and parents are worried about cancer. A careful history reveals trauma several weeks earlier, and the mass represents the callus of a healing clavicular epiphyseal fracture that can be demonstrated radiographically.

Battaglia TC et al: Interposition arthroplasty with bone-tendon allograft: A technique for treatment of the unstable sternoclavicular joint. J Orthop Trauma 2005;19:124. [PMID: 15677929] 


Brachial Plexus Injury

Brachial plexus injuries are typically caused by a fall on the shoulder as seen in acromioclavicular joint injuries. Most brachial plexus injuries do not involve motor loss and exhibit paresthesias, which resolve in a period of minutes to weeks, although some cases may persist for months or years. Early in the course of the injury, a transient slowing of conduction across the plexus or a mild prolongation of nerve latency possibly is seen. The "burner" or "stinger" is one of the most common brachial plexus injuries encountered in athletes. The key to diagnosis is short duration of upper extremity paresthesias and shoulder weakness, with pain-free range of motion of the cervical spine. Players may return to competition after shoulder strength and full pain-free range of motion returns.

Rarely, a severe injury occurs (eg, from motorcycle racing). Chronic injuries result in instability of the shoulder that may be treated with trapezius transfer. Arthrodesis is an alternative, initially or after failed muscle transfer.

Peripheral Nerve Injury


Traction incidents may cause a long thoracic nerve palsy, with subsequent serratus anterior paralysis and winging of the scapula. Traction and blunt trauma may also cause injury to the spinal accessory nerve, another cause of winging of the scapula. These can be differentiated on physical examination by the position of the scapula. With serratus anterior palsy, the inferior portion of the scapula tends to go medially, whereas the opposite occurs with spinal accessory nerve palsy. Treatment is usually conservative, with return of function in weeks if the nerve is not divided.

Safran MR: Nerve injury about the shoulder in athletes, part 2: Long thoracic nerve, spinal accessory nerve, burners/stingers, thoracic outlet syndrome. Am J Sports Med 2004;32:1063. [PMID: 15150060] 


Entrapment of the suprascapular nerve is often associated with activities such as weight lifting, baseball pitching, volleyball, and backpacking. Traction and repetitive shoulder use are the mechanisms of injury. Compression of the nerve may occur from entrapment at the anterior suprascapular notch of the scapula or at the level of the spinoglenoid notch. The latter occurs in volleyball players and baseball players likely caused by rapid overhead acceleration of the arm. Compression is associated with poorly localized pain and weakness in the posterolateral aspect of the shoulder girdle. This may be followed by atrophy of the supraspinatus or infraspinatus muscles. Eventually, there is weakness of forward flexion and external rotation of the shoulder. The diagnosis is confirmed by electromyography and nerve conduction studies.

Conservative therapy consists of rest, antiinflammatory medication, and physical therapy designed to increase muscular tone and strength. If this is unsuccessful, then surgical exploration is indicated, which may reveal hypertrophy of the transverse scapular ligament, anomalies of the suprascapular notch, and ganglion cysts. Results of surgery vary with the lesion discovered, but many patients return to full function postoperatively.

Safran MR: Nerve injury about the shoulder in athletes, part 1: Suprascapular nerve and axillary nerve. Am J Sports Med 2004;32:803. [PMID: 15090401] 


The musculocutaneous nerve is susceptible to damage from direct frontal blows or surgical procedures. Injury is associated with numbness in the lateral forearm to the base of the thumb and weak to absent biceps muscle function. Most injuries seen in sports are transient and respond to conservative treatment in a matter of days to weeks.

Lo IK, Burkhart SS, Parten PM: Surgery about the coracoid: neurovascular structures at risk. Arthroscopy 2004;20:591. [PMID: 15241309] 


The usual mechanism of injury is trauma either by direct blow to the posterior aspect of the shoulder or following dislocation of the shoulder or fracture of the proximal humerus. Axillary nerve injury occurs in many sports, such as football, wrestling, gymnastics, mountain climbing, rugby, and baseball. The degree of injury to the nerve varies because the initial presentation may be mild weakness during elevation and abduction of the arm with or without numbness of the lateral arm. The deltoid extension lag sign is indicative of axillary nerve injury. To perform this test, the examiner elevates the arm into a position of near full extension and then releases the arm while asking the patient to hold the arm in this position. If there is complete deltoid paralysis, the arm drops. For partial nerve injuries, the magnitude of the angular drop, or lag, is an indicator of deltoid strength. Approximately 25% of all dislocated shoulder injuries are associated with axillary nerve traction injuries, which respond well to rest, physical therapy, and time. If recovery is not complete within 3–6 months, surgical intervention is recommended with exploration, utilizing neurolysis or grafting, or both, as necessary. Results of surgery are usually favorable, with sensory recovery occurring before motor recovery.

Hertel R et al: The deltoid extension lag sign for diagnosis and grading of axillary nerve palsy. J Shoulder Elbow Surg 1998;7:97. [PMID: 9593085] 


The symptoms resulting from thoracic outlet compression may be neurologic, venous, or arterial. Obstruction of the subclavian vein may lead to stiffness, edema, and even thrombosis of the limb. Arterial obstruction may be the result of direct compression and manifests with pallor, coolness, and forearm claudication. Doppler examination reveals changes in arterial and venous flow. Electromyography and nerve conduction studies are also helpful in diagnosis.

Nonoperative treatment is recommended for less severe forms of this syndrome, and once the pain subsides, an exercise program to strengthen the pectoral girdle muscles is beneficial. Special exercises to strengthen the upper and lower trapezius, along with the erector spinae and serratus anterior muscles, yields good results. Correcting poor posture and an ongoing maintenance program are mandatory once improvement is reached. Progression of symptoms or failure of nonoperative treatment are indications for surgical exploration and correction of the pathologic factors encountered.

Degeorges R, Reynaud C, Becquemin JP: Thoracic outlet syndrome surgery: Long-term functional results. Ann Vasc Surg 2004;18:558. [PMID: 15534735] 


Tennis elbow is the term given to many painful conditions about the elbow. An anatomic location may usually be found and specific diagnosis made.

Lateral Epicondylitis

Lateral tennis elbow involves the common tendon to the extensor muscles of the wrist and hand. Patients who perform repetitive wrist extension against resistance (such as the backhand stroke in tennis) are at risk. Their pain is usually chronic and more bothersome than disabling. Tenderness is located over the lateral humeral epicondyle, and pain is produced by extending the wrist against resistance. The tendon of the extensor carpi radialis brevis is identified as the most common site of the lesion. Other causes for lateral elbow pain should be considered, including radiocapitellar arthritis and posterior interosseous nerve compression. Radiographs only rarely reveal soft-tissue calcification near the lateral humeral epicondyle, and MRI is of questionable aid in making the diagnosis.

Treatment includes decreasing specific activities and using a tennis elbow band to distribute the tension of the muscular pull over a larger area, thereby decreasing the force per unit area. A lighter racquet, smaller grip on the racquet, and correcting backhand technique are also helpful. Exercises to strengthen the wrist extensor muscles should be included in the treatment plan. If this approach fails, an injection of local anesthetic and cortisone into the most tender region is often curative. Surgical treatment is needed in recalcitrant cases. Multiple procedures are described to take care of this malady. Commonplace in all procedures is release of the common extensor origin. Histologic studies of the afflicted tendon show degenerative changes with angiofibroblastic proliferation. These are thought to be similar to the pathologic changes of the torn rotator cuff, with diminished vascularity, an altered nutritional state, and tearing of the susceptible tendon.

Medial Epicondylitis

Medial epicondylitis involves the common flexor pronator origin. Treatment is similar to the management of lateral tennis elbow. Ulnar nerve compression at the elbow may occur in conjunction with medial tennis elbow. In approximately 60% of the cases treated surgically, ulnar nerve compression was present. The common flexor origin is an important medial stabilizer of the elbow, so if surgical treatment is indicated, the debrided tendon should be reattached rather than released from the medial epicondyle.

Ciccotti MC, Schwartz MA, Ciccotti MG: Diagnosis and treatment of medial epicondylitis of the elbow. Clin Sports Med 2004;23:693 [PMID: 15474230] 

Jobe FW, Ciccotti MG: Lateral and medial epicondylitis of the elbow. J Am Acad Orthop Surg 1994;2:1. [PMID: 10708988] 


Rupture of the collateral ligaments of the elbow occurs most commonly from elbow dislocation. This can result from excessive valgus force, and initially the ulnar collateral ligament ruptures. Excessive posterolateral rotatory force may also result in rupture of the lateral ulnar collateral ligament. In either case, the elbow may dislocate, and typically the direction is posterior. Treatment after relocation and brief immobilization consists of active range-of-motion exercises. Recurrent instability is rare, and instead a small loss of elbow extension, usually less than 10 degrees, commonly results.

Valgus Instability

Valgus instability may result from overuse in overhead throwing sports, such as baseball, football, and javelin throwing. With acute medial collateral ligament rupture, a pop may be felt during a throw. Tenderness is present on the medial side of the elbow, usually just distal to the medial epicondyle. Instability can then be appreciated when a valgus force is applied to the elbow. This must be done with the elbow flexed 20 degrees because failure to unlock the olecranon from within the olecranon fossa in full extension creates a false sense of stability. Comparison to the contralateral side aids in making the correct diagnosis. If the ulnar collateral ligament was injured but remains intact, the valgus stress test may elicit pain but no instability. Then the so-called milking maneuver (Figure 4–37) also elicits pain along the medial side of the elbow. Eliciting pain while moving the elbow in flexion and extension with valgus stress during the milking maneuver may be the best test for diagnosing medial collateral ligament injuries in the elbow.

Figure 4–37.


The valgus stress and milking maneuver tests for medial ulnar collateral ligament injury.

(Reprinted, with permission, from Chen FS et al: Medial elbow problems in the overhead-throwing athlete. J Am Acad Orthop Surg 2001;9(2):102.)

A stress radiograph may aid in making the diagnosis. An anteroposterior radiograph can be taken while the examiner performs the valgus stress test. Alternatively, gravity can be used to apply the valgus stress. For this, an anteroposterior radiograph of the elbow is taken with the shoulder externally rotated at 90 degrees with the elbow flexed at approximately 20 degrees. When instability is present, there will be a wider medial opening than on the contralateral normal side. MRI may also be useful, especially if an arthrogram is performed concurrently, because dye leaking through the ulnar collateral ligament is diagnostic of a rupture.

Surgical repair may be indicated in overhead throwing athletes who suffer an acute rupture of their ulnar collateral ligament and still want to continue to participate in their sport. Soccer players, basketball players, and other athletes participating in nonoverhead throwing may be treated with a program of early active range-of-motion exercises with expectation of full return to their sport. Chronic ulnar collateral ligament injuries resulting from overuse are best treated with rehabilitation, NSAIDs, and avoidance of throwing for as long as 3 months. Only those with residual pain and instability after participation in such a program should undergo reconstruction of the anterior band of the ulnar collateral ligament. In this surgery, pioneered by Dr. Frank Jobe, the palmaris longus tendon is woven through drill holes in the medial humeral epicondyle and olecranon. Nearly 70% of athletes are able to return to highly competitive throwing after such surgery.

Chen FS, Rokito AS, Jobe FW: Medial elbow problems in the overhead-throwing athlete. J Am Acad Orthop Surg 2001;9(2):99.

O'Driscoll SW, Lawton RL, Smith AM: The "moving valgus stress test" for medial collateral ligament tears of the elbow. Am J Sports Med 2005;33:231. [PMID: 15701609] 

Thompson WH et al: Ulnar collateral ligament reconstruction in athletes: Muscle-splitting approach without transposition of the ulnar nerve. J Shoulder Elbow Surg 2001;10:152. [PMID: 11307079] 

Posterolateral Rotatory Instability

Posterolateral rotatory instability of the elbow may result from a fall on the outstretched upper extremity, surgery of the lateral side of the elbow, or chronic varus stress as may occur in long-term crutch walkers. The instability covers a spectrum of severity from mild subluxation to recurrent dislocation. Those with mild forms complain of intermittent symptoms on the lateral side of the elbow associated with supination of the forearm, such as pain, snapping, or catching. More severe symptoms include locking or sensations of elbow instability. To perform the posterolateral rotatory instability test, a valgus stress is applied to the supinated elbow with the patient supine and the upper extremity over the head (Figure 4–38). Subluxation of the radial head occurs with the elbow in extension and resolves when the elbow is flexed. This maneuver also reproduces the patient's symptoms. A lateral stress radiograph, done with the elbow in extension as described for the posterolateral rotatory instability test, may also demonstrate the instability (see Figure 4–38). Treatment for acute cases consists of an elbow brace to hold the forearm in pronation and restricted terminal elbow extension for 6 weeks. Chronic cases are best treated with reconstruction of the lateral ulnar collateral ligament. Postoperatively the patient is put in the same brace as used for acute posterolateral rotatory instability for 6–12 weeks.

Figure 4–38.


The posterolateral rotatory instability test reproduces the patient's symptoms.

Olsen BS, Sojbjerg JO: The treatment of recurrent posterolateral instability of the elbow. J Bone Joint Surg Br 2003;85:342 [PMID: 12729105] 

Sanchez-Sotelo J, Morrey BF, O'Driscoll SW: Ligamentous repair and reconstruction for posterolateral rotatory instability of the elbow. J Bone Joint Surg Br 2005;87:54. [PMID: 15686238] 


Posterior Elbow Impingement

Impingement may result from mechanical abutment of bone and soft tissues in the posterior elbow, which may or may not be associated with injury of the ulnar collateral ligament. Hyperextension injuries with an intact ulnar collateral ligament occur in gymnasts, football linemen, weight lifters, and others. The lesion is usually located in the center of the posterior elbow, and the pain is reproduced by forcible extension of the elbow. If there is insufficiency of the ulnar collateral ligament, as is often the case when there is posterior elbow impingement in overhead athletes, the lesion is posteromedial. In this case, the impingement is between the medial aspect of the olecranon and the lateral side of the medial wall of the olecranon fossa (Figure 4–39). Pain may be reproduced with the valgus stress test as described earlier for valgus instability, but the pain is posteromedial and medial. Radiographs may demonstrate osteophytes of the olecranon of the olecranon fossa.

Figure 4–39.


Mechanism of posteromedial impingement between the medial aspect of the olecranon and the lateral side of the medial wall of the olecranon fossa.

(Reprinted, with permission, from Chen FS et al: Medial elbow problems in the overhead-throwing athlete. J Am Acad Orthop Surg 2001;9(2):105.)

As with most injuries caused by repetitive trauma, treatment begins with prevention. The number of innings pitched is probably the most important factor relating to injury. If symptoms persist, removal of osteophytes is successful treatment, providing no ulnar collateral ligament injury is present. Treatment of the valgus instability is also required for successful outcome.

Moskal MJ, Savoie FH III, Field LD: Arthroscopic treatment of posterior elbow impingement. Instr Course Lect 1999;48:399. [PMID: 10098066] 

Fatigue Fracture of the Medial Epicondyle

In children, fatigue fractures of the medial epicondyle cause pain and swelling. This was blamed on throwing curve balls, but some studies show that a properly thrown curve ball causes no more injuries than the traditional fastball. Prevention or minimization of damage involves several steps. First, it is important to maintain proper conditioning by continuing pitching practice in the off-season or beginning the baseball season in a slow progressive fashion. Second, pain and inflammation should be avoided, and if the elbow becomes painful, the athlete should stop throwing immediately. An accurate pitching count should be kept during a game, and a stopping point should be planned in advance. If the pitcher begins having pain or shows loss of control, pitching should be temporarily terminated, and treatment to decrease the swelling and inflammation should begin. No competitive throwing is allowed until full range-of-motion returns and no pain or tenderness is associated with throwing.

Osteochondritis Dissecans of the Capitellum

Osteochondritis dissecans of the capitellum usually affects pitchers older than 10 years (Figure 4–40). Changes in the radiocapitellar joint are very worrisome because of possible permanent loss of function. If fragmentation occurs, loose bodies may require excision.

Figure 4–40.


AP view of an elbow with osteochondritis dissecans of the capitellum.

Stubbs MJ, Field LD, Savoie FH: Osteochondritis dissecans of the elbow. Clin Sports Med 2001;20:1. [PMID: 11227698] 


Cervical spine injuries in athletes are relatively infrequent, but the potential for serious injury to the nervous system exists. If spine injury is suspected, it is wise to be extremely cautious until a proper diagnosis can be made. This is the best way to prevent conversion of a repairable injury to a catastrophic outcome. Most often, a spine injury results from a collision, and sometimes it includes associated head injuries. The head and neck must be immobilized right away, and ease of breathing and level of consciousness ascertained immediately.

Brachial Plexus Neurapraxia

The most common cervical injury is pinching or stretching neurapraxia of the nerve root and brachial plexus. The injury is of short duration, and the patient has a full pain-free range of motion of the neck. These injuries are commonly called "stinger" or "burner" injuries. They result from lateral impact of the head and neck with simultaneous depression of the shoulder. This may cause stretching and pinching of the nerves of the brachial plexus, with burning pain, numbness, and tingling extending from the shoulder down into the hand and arms. Symptoms frequently involve the C5 and C6 root levels. Recovery is usually spontaneous within a few minutes after the acute episode.

Patients who demonstrate full muscle strength of the intrinsic muscles of the shoulder and upper extremity and have full pain-free range of motion of the cervical spine may return to their activities. If they have residual weakness or numbness, they should not be allowed to re-enter the game. Absence of neck pain should alert one to the possibility of a cervical spine injury, as neck pain is not part of the syndrome.

Persistence of paresthesia or weakness requires further evaluation before returning to play. This includes neurologic, electromyographic, and radiographic evaluation. The athlete should not participate in contact sports until full muscle strength is achieved and a repeat electromyogram shows evidence of axonal regeneration, usually at least 4–6 weeks.

Prevention of so-called stinger injuries is chiefly through correct head and neck techniques and strengthening of the neck musculature. Additionally, the use of cervical rolls may eliminate extremes of motion during impact.

Cervical Strain

Acute strains of the muscles of the neck are probably the most frequent cervical injuries in athletes. The word strain implies injury to a muscle, whereas a sprain is a ligamentous injury. A strain happens when a muscle tendon unit is overloaded or stretched. The clinical picture is common to all musculotendinous injuries. Motion of the neck becomes painful, reaching a peak after several hours or the next day. NSAIDs, heat, massage, and other modalities are beneficial.

Cervical Sprain

With cervical sprain, there is damage to the ligamentous and capsular structure connecting the facet joints and vertebra. It is often difficult to differentiate from a strain. There is limited motion and pain in the area of the injury and along the muscle groups overlying the area of the injury. Ligamentous disruption may be extensive enough to result in instability with associated neurologic involvement. Routine cervical spine radiographs are indicated. In those athletes with diminished motion as well as pain, stability of the cervical spine should be documented, which may be done with flexion and extension radiographs.

Treatment of a cervical sprain consists of immobilization, rest, support, and antiinflammatory therapy. Return to participation is permitted when motion and muscle strength normalize.

Cervical Spinal Cord Neurapraxia with Transient Tetraplegia

The phenomenon of cervical spinal cord neurapraxia with transient tetraplegia is a distinct clinical entity. Sensory changes include a burning pain, numbness, tingling, or loss of sensation. Motor changes include weakness or complete paralysis, which is usually transient, with complete recovery occurring in 10–15 minutes, although in some cases gradual resolution occurs over 36–48 hours. Complete motor function and full pain-free cervical motion returns. Routine radiographs of the cervical spine are negative for fractures or dislocations. Some radiographic findings include spinal stenosis, congenital fusions, cervical instability, and intervertebral disk disease. To determine whether cervical spinal stenosis is present, the anteroposterior diameter of the spinal canal is measured, and this figure is divided by the anteroposterior diameter of the vertebral body (Figure 4–41). If the ratio is less than 0.80, stenosis is present.

Figure 4–41.


The ratio of the spinal canal to the vertebral body is the distance from the midpoint of the posterior aspect of the vertebral body to the nearest point on the corresponding spinolaminar line (A) divided by the anteroposterior width of the vertebral body (B).

(Reproduced, with permission, from Torg JS et al: Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 1986;68:1354.)

Athletes who have suffered transient tetraplegia are not known to be at any greater risk for permanent tetraplegia. Patients who have this syndrome and associated instability of the cervical spine or cervical disk disease should be precluded from further participation in contact sports. Those who have spinal stenosis alone should be treated on an individual basis.

More severe injuries, including fractures and dislocation of the cervical spine, may occur. Treatment of these begins on the playing field, with immobilization of the spine. A face mask, if worn, may be cut off with bolt cutters. After thoroughly stabilizing the spine, the patient is moved to a spine board. Sandbags are used to immobilize the head and neck. The patient may then be transported to a local emergency room for further evaluation and treatment. Fractures and dislocations with or without permanent neurologic injury are treated like other spine injuries.

Torg JS et al. Cervical cord neurapraxia: Classification, pathomechanics, morbidity, and management guidelines. J Neurosurg 1997;87:843. [PMID: 9384393] 

Torg JS et al: Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 1986;68:1354. [PMID: 3782207] 


Clinical Findings

Spondylolysis is a disruption of the pars interarticularis, whereas spondylolisthesis involves anterior slippage of one vertebral body over the next. Spondylolysis is most often found at L5 and L4 but may occasionally be seen at L3 and L2. It is believed to result from repeated stress around the pars interarticularis during hyperextension of the lumbar spine. If continued hyperextension activity occurs, spondylolysis may become spondylolisthesis. Sports in which spondylolisthesis is commonly found include gymnastics, football, and weight lifting. Female teenage gymnasts, for example, often have back pain but normal early radiographs. Approximately 3–6 weeks later, a stress response may be seen around the pars interarticularis, with increased density developing. At this time, the bone scan is positive, indicating an impending stress fracture that will show up on plain radiographs in 2–4 weeks. A physician who is aware of which sports put stress on the pars interarticularis should consider a bone scan to rule out spondylolisthesis.

Treatment & Prognosis

The treatment of spondylolisthesis involves cessation of all aggravating sports and other actions producing spinal hyperextension. A certain percentage of these fractures heal spontaneously. Healing time for spondylolysis of the lumbar spine is usually approximately 6 months. If after that period of time no significant signs of healing are apparent, it is unlikely that spontaneous healing will take place. At this point, spinal fusion should be considered, or the patient should be willing to confine activities to less stressful pain-free sports.

Many patients with spondylolisthesis engage in high-level sporting activities without significant pain or neurologic deficit. Only a small percentage actually present for evaluation and care. Complete evaluation and treatment recommendations for spondylolisthesis and spondylolysis are found in the section on the spine.

Bono CM: Low-back pain in athletes. J Bone Joint Surg Am 2004;86-A:382. [PMID: 14960688] 

Miller SF, Congeni J, Swanson K: Long-term functional and anatomical follow-up of early detected spondylolysis in young athletes. Am J Sports Med 2004;32:928. [PMID: 15150039] 

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