Lee Kaplan MD
Nicholas Honkamp MD
Ryan Kehoe MD
Jonathon Tueting MD
Patrick J. McMahon MD
Knee Pain with Mechanical Symptoms
Injury to the knee from athletic activities, daily living, or trauma is becoming more common. Children continue to participate in athletics and more adults than ever remain active. As our society becomes increasingly active, injuries to knee cartilage, meniscus, ligament, or bone will continue to increase.
Our ability to accurately and acutely diagnose knee injuries is critical. There are many diagnoses for knee pain, but most involve one or a combination of the following: meniscal tear, cartilage damage, osteochondral fracture, or ligamentous injury. These injuries may present in a similar fashion, but with a precise history and physical examination combined with appropriate imaging tests, the correct diagnosis can be obtained.
Meniscal Tears
Anatomy
A thorough understanding of meniscal anatomy is required for both the recognition of meniscal injury as well as its treatment. Beginning in the late 1800s, the menisci were thought of as “functionless remnants” of leg muscles. However, the realization of the important function of menisci in the knee has since stimulated extensive study. Grossly, the medial meniscus is C-shaped whereas the lateral meniscus is more semicircular shaped. Both are composed of fibrocartilage with bony attachments at the anterior and posterior aspects of the tibial plateau. Additionally, the medial meniscus has an extensive attachment at its periphery to the capsule, referred to as the coronary ligament. The thickening of this midportion of its capsular attachment is the deep portion of the medial collateral ligament. This extensive attachment of the medial meniscus to the capsule and plateau makes it relatively less mobile compared to the lateral meniscus.
The lateral meniscus covers a larger portion of the lateral tibial articular surface and is more semicircular shaped than the medial meniscus. Variants of the lateral meniscus, which have broader coverage of the tibial plateau than normal, have been termed “discoid” variants and have been reported to have an incidence of 3.5–5%. The more semicircular shape of the lateral meniscus places the anterior and posterior bony attachments of the lateral meniscus closer together. The anterior cruciate ligament (ACL) attachment is just medial to the anterior horn of the lateral meniscus. Ligaments attaching the posterior horn of the lateral meniscus to the medial femoral condyle course in front of and behind the posterior cruciate ligament and are termed the ligaments of Humphrey and Wrisberg, respectively (Figure 3-1). Discoid menisci can be classified into complete (covering the entire lateral plateau), incomplete, and Wrisberg variants. A Wrisberg variant discoid meniscus has an absent posterior horn bony attachment, and the posterior meniscofemoral ligament of Wrisberg is the only stabilizing structure.
Posterolaterally, the popliteus tendon emerges in the joint via the popliteal hiatus. Small fasciculi attach the popliteus tendon to the meniscus and are thought to have a stabilizing effect. The capsular attachments to the lateral meniscus are much less developed than the medial side, causing increased translation of the lateral meniscus compared to its medial counterpart.
Collagen bundles make up the microstructure of the normal meniscus. These collagen bundles form both circumferential and less numerous, radial bundles within the menisci. The radial bundles are mainly found at the surface of the meniscus forming a crossed meshwork of fibers thought to be important in resisting surface sheer stresses. The circumferential bundles make up the majority of the midsubstance of the menisci, and their orientation allows them to disperse the compressive loads applied though the knee. Approximately 60–70% of the dry weight of the menisci is composed of collagen, with 8–13% noncell proteins and 0.6% elastin. The majority of the collagen is type I, with lesser amounts of types II, III, V, and VI.
At birth, the entire meniscus is vascularized, but by 9 months of age the inner third of the meniscus is
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avascular. By adult age, only the outer 10–30% of the meniscus is vascular, with the main blood supply arising from the medial and lateral genicular arteries. There is also a relative avascular zone of the meniscus occurring at the popliteal hiatus secondary to the entrance of the popliteal tendon into the joint. Cell nutrition to the inner two-thirds of the menisci occurs through diffusion and cell pumping of synovial fluid. The anterior and posterior horns as well as the periphery of the meniscus have neural elements present, and these are thought to play a role in proprioceptive feedback during knee range of motion.
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Figure 3-1. The anatomy of the tibial plateau showing the medial and lateral menisci with their associated intermeniscal ligaments. 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. St. Louis, Mosby-Year Book, 1991. ) |
The function of the meniscus involves load sharing, shock absorption, distribution of contact stresses, stabilization, limiting extremes of motion, and proprioception. Primary among these is its affect on loading sharing, shock absorption, contact stresses, and stabilization. The menisci transmit approximately 50–70% of the load in extension, and 85% of the load with 90° of knee flexion. A total medial menisectomy decreases the femoral contact area by 50–70% with a 100% increase in the contact stress. Similarly, a total lateral menisectomy decreases the femoral contact area by 40–50% and increases the contact stress by 200–300%. Such increases with menisectomy often lead to joint space narrowing, osteophytes, and squaring of the femoral condyles seen on radiographs. In addition, cartilage function is also affected with menisectomy. The menisci are 50% as stiff as cartilage and thereby function as significant shock absorbers in the knee. Loss of the meniscus leads to a loss of this shock absorbency and increased demands on the cartilage. Finally, the medial meniscus functions as a secondary stabilizer to anterior translation of the knee. In an ACL-competent knee, loss of the medial meniscus does little to affect the anterior to posterior motion of the knee. However, in an ACL-deficient knee, loss of the medial meniscus leads to a greater than 50% increase in anterior translation at 90° of flexion. In general, the inner two-thirds of the menisci are important for maximizing contact area and shock absorption, whereas the outer one-third is essential for load transmission and stability.
Pathogenesis
The incidence of meniscal tears is 60–70 per 100,000 persons, and affects males more frequently at a 2.5–4:1 ratio to females. The peak incidence of acute tears occurs in the 20- to 30-year-old age group, whereas degenerative chronic tears are more common in 40- to 60-year-old males. Female meniscal pathology is relatively constant after the second decade.
Younger patients often have an acute event as the cause of their meniscal tear. Approximately one-third of patients with an acute ACL tear will have a concomitant meniscal tear. Because of the relative increase in mobility of the lateral meniscus and lateral knee compartment, lateral meniscal tears are about four times as common as medial meniscal tears in ACL injuries. Because of its role as a secondary stabilizer to anterior translation in an ACL-deficient knee, medial meniscal tears are more prevalent in chronic ACL-deficient knees. Additionally, meniscal tears can occur in up to 47% of tibial plateau fractures, and are frequently observed in patients with a femoral shaft fracture and a concomitant knee effusion.
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Allen CR et al: Importance of the medial meniscus in the anterior cruciate ligament-deficient knee. J Orthop Res 2000;18:109.
Garrick JG (editor): Orthopaedic Knowledge Update: Sports Medicine 3. American Academy of Orthopaedic Surgeons, 2004.
Greis PE et al: Meniscal injury: I. Basic science and evaluation. J Am Acad Orthop Surg 2002;10:168.
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 often involves a large bucket-handle tear that has displaced into the femoral notch. In acute tears involving an associated ACL injury, the swelling may be more significant and acute. ACL injuries often involve a lateral meniscal 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 (>40 years old) with a 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. Symptoms of catching or locking may also derive from chondral or patellofemoral damage.
A thorough physical examination of the knee involving the entire leg is essential. Assessing hip range of motion and irritability is useful, especially in children, as 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. Any joint line swelling or deformity may be a clue to a meniscal cyst. Measurement of range of motion may reveal a loss of terminal extension seen in meniscal tears. Assessing for tenderness of the femoral condyles, joint lines, tibial plateaus, and patellofemoral joint may provide clues as to a possible osteochondral lesion, meniscal lesion, fracture, or chondrosis, respectively. Ligamentous testing including varus and valgus stress testing at full extension and 30° of flexion, Lachman, anterior drawer, and posterior drawer testing should be done to assess stability.
The most important physical examination finding in a patient with a meniscal tear is joint line tenderness. Other specialized tests including the McMurray, flexion McMurray, and Apley grind test have also been studied. The McMurray test is performed with the patient lying supine with the hip and knee flexed to about 90°. While one hand holds the foot and twists it from external to internal rotation, the other hand holds the knee and applies compression. A positive test elicits a pop or click that can be felt by the examiner when the torn meniscus is trapped between the femoral condyle and the tibial plateau (Figure 3-2). 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 is 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 involves placing the patient prone with the knee flexed to 90°. 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 (Figure 3-3).
Many studies have attempted to quantitate the reliability of various physical examination findings. In a prospective study comparing preoperative joint line tenderness to arthroscopic findings of meniscal tears, the sensitivity of joint line tenderness was found to be 86% and 92%, with an overall accuracy rate of 74% and 96% for the medial and lateral meniscus, respectively. Another study found similar results, with joint line tenderness having a sensitivity of 74%. The only significant McMurray sign to correlate with a meniscal injury was a “thud” elicited on the medial joint line with a medial meniscal tear. However, the McMurray and Apley tests were found by others to have less than 75% sensitivity for diagnosing meniscal tears.
In the setting of an acute ACL injury, joint line tenderness was found to be less useful in defining a meniscal injury preoperatively. In addition, misdiagnoses occurred with chondromalacia patella, plica, fat pad impingement, and chondral lesions.
Overall, joint line tenderness remains the most accurate finding by which to diagnose a meniscal tear. Despite the poor reliability of other examination findings taken individually, a thorough history and a physical examination using multiple tests combined with plain radiographs were 95% and 88% sensitive for detecting medial and lateral meniscal tears, respectively.
Eren OT: The accuracy of joint line tenderness by physical examination in the diagnosis of meniscal tears. Arthroscopy 2003;19(8):850.
The next step in the workup of a patient with mechanical knee symptoms involves obtaining weight-bearing plain radiographs of the knee, including 45° posteroanterior flexion views of both knees, a lateral view, and a patellofemoral view such as a Merchant view. The posterior femoral condyles often show earlier and more advanced wear, and corresponding joint space
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narrowing on a 45° weight-bearing view is often seen. This would not necessarily be seen on a non-weight-bearing radiograph, and is the principal reason that non-weight-bearing radiographs have no role in the workup of mechanical knee pain (Figure 3-4). Patients with knee pain and significant joint-space narrowing on radiographs should be cautioned that extensive meniscal and chondral damage may be present that is unlikely to respond to arthroscopic partial meniscectomy. A patellofemoral radiograph is essential to help exclude patellofemoral chondrosis as the source of knee pain. Additionally, plain radiographs will not make the diagnosis of a meniscal tear, but will help eliminate concurrent problems such as an osteochondral lesion, fracture, patellofemoral malalignment, or loose body.
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Figure 3-2. McMurray test. |
Magnetic resonance imaging (MRI) has contributed greatly to the accurate diagnosis of meniscal tears. Its advantages include the ability to image the meniscus in multiple planes and its lack of ionizing radiation. In addition, the ability to evaluate other articular and extraarticular structures is particularly useful in patients with a nondiagnostic history and physical examination, or in patients with associated injuries that make physical examination difficult. Its disadvantages include its high cost and the possibility of misinterpretation and a false-positive result leading to further evaluation. The normal meniscus has a uniform low-intensity signal on all pulse sequences. Because of increased vascularity in children, the appearance of a child's meniscus on MRI may have an increased intrameniscal signal. In older adults, an increased intrameniscal signal may be a sign of degeneration.
The appearance of the meniscus on MRI is done on a four-grade system. Grade 0 is a normal meniscus. Grade I has a globular increase in signal within the meniscus that does not extend to the surface. Grade II has a linear increase in signal within the meniscus that does not extend to the surface. Grade III has an increased signal that abuts the free edge of the meniscus. Only Grade III, where an increased signal reaches the
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meniscal surface, is considered a true meniscal tear. MRI is approximately 90–95% accurate in diagnosing a meniscal tear, particularly when two consecutive images show an increased meniscal signal touching the surface of the meniscus. The meniscal shape can also be important in the diagnosis of a meniscal tear. Generally, sagittal images through the meniscus give the meniscus a “bowtie” shape. Loss of the bowtie shape may indicate a meniscal tear. Also, the “double posterior cruciate ligament” sign indicates a torn and displaced meniscus that is adjacent to the posterior cruciate ligament in the femoral notch.
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Figure 3-3. Apley test. |
Common misinterpretations of normal structures include the popliteal hiatus posteriorly and the intermeniscal ligament anteriorly. There is often difficulty in determining a tear of the anterior horn of the meniscus, an uncommon finding. False-positive results of meniscal tears seen on MRI in asymptomatic patients do occur and the incidence increases with age. This emphasizes the importance of taking the entire clinical and radiographic picture into perspective when evaluating a patient. A recent study documented a 5.6% incidence of meniscal tears diagnosed by MRI in asymptomatic patients between the ages of 18 and 39 years with a normal physical examination. A second study found 13% of asymptomatic patients younger than 45 years old and 36% of those older than 45 years old had MRI scans read as positive for meniscal tears.
MRI has also been used to assess meniscal repair. It has been found to be equal or superior to contrast arthrography in assessing a repaired meniscus, as well as the ability to discriminate partial versus complete meniscal healing.
Fu FH et al (editors): Knee Surgery. Williams & Wilkins, 1998.
Kocabey Y et al: The value of clinical examination versus MRI in the diagnosis of meniscal tears and anterior cruciate ligament rupture. Arthroscopy 2004;20:696.
Meniscal tears can be classified either by etiology or by their arthroscopic and MRI appearance. Etiologic classification divides tears into either acute (excessive force applied to an otherwise normal meniscus) or degenerative (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 the location of the tear 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 as well as the associated healing rates decrease.
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 (Figures 3-5 and 3-6). Most acute tears in younger patients involve vertical longitudinal or oblique tears, whereas complex and degenerative tears occur more commonly in older patients. 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. This more commonly occurs in the medial meniscus, possibly due 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 older patients 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 sheer stresses and, when associated with meniscal cysts, occur in the medial meniscus and cause localized swelling at the joint line.
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Figure 3-4. Advantages of the Rosenberg x-ray. A: No joint space narrowing can be seen in a weight-bearing view with the knee straight. B: With flexion and weight bearing, significant narrowing of the medial compartment is demonstrated. (Reproduced, with permission, from Anderson J: An Atlas of Radiography for Sports Injuries. McGraw-Hill, 2000. ) |
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Treatment
Treatment options for meniscal tears include nonsurgical, meniscectomy (partial or complete), and meniscal repair. Advances in arthroscopy and technical skills have recently made meniscal transplant a more common procedure.
Nonsurgical treatment of meniscal tears is generally limited to smaller, incomplete tears involving the posterior horns. These tears may be painful but do not catch in the joint so the patient does not feel popping or catching. Such tears are usually found in stable knees. Treatment includes modification of activity to avoid cutting and pivoting sports that may aggravate symptoms, stretching, and quadriceps and hamstring strengthening. Such treatment often works best in older individuals as arthritis rather than the meniscal tear may be the cause of their symptoms. Small (<10 mm) stable longitudinal tears, partial-thickness tears on the superior or inferior surface, or small (<3 mm) radial tears may heal spontaneously or remain asymptomatic.
The indications for arthroscopic meniscal surgery are persistent pain with an effusion that does not respond to nonsurgical treatment, and catching or locking. Catching and locking are referred to as mechanical symptoms. These may interfere with activities of daily living. Physical examination should reveal joint effusion and joint line tenderness. Patients may also have limitations of knee motion and provocative signs such as pain with McMurray or Apley tests. Finally, other possible causes of knee pain should be ruled out through a thorough history, physical examination, and imaging studies.
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Figure 3-5. Types 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. Philadelphia: WB Saunders, 1990. ) |
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Open or arthroscopic removal of the entire meniscus, termed meniscectomy, was initially thought to be a benign procedure, but long-term outcome was poor and gender related: 75% of males and less than 50% of females had good or excellent results. But less than 50% of the males and only 10% of the females were symptom free. Results were poorer when surgery was done on younger compared to older individuals. Also, 75% of the patients had arthritis compared to only 6% of age-matched controls. The arthritis often did not manifest in many of the patients until more than 15 years after surgery. Lastly, degenerative changes occurred more rapidly after lateral compared to medial meniscectomy. With improved understanding of the importance of the knee menisci, advances in technique and instrumentation have allowed surgeons to perform a meniscal repair or a partial meniscectomy.
Deciding when to partially resect rather than repair a partially torn meniscus is difficult. There are many factors influencing outcome that need to be considered. For example, large partial meniscectomy that extends through the circumferential bands at the periphery of the meniscus yields poor results. Violation of these circumferential fibers significantly hinders the meniscus in distributing hoop stresses at its periphery. Also, when the mechanical axis of the knee joint falls within the side of the knee that has had a meniscectomy, there are poorer results. Lastly, associated pathology in the knee, specifically, the amount of chondral damage and the presence of associated ligamentous instability, is associated with poorer results. Other factors to consider include the patient's age, tear pattern (geometry, size), vascularity, tissue quality, and knee stability. New repair techniques and the technical skills of the surgeon may also influence the decision. Most importantly, the expected outcome and rehabilitation must fit the patient's individual goals. Partial meniscectomy has good or excellent results in nearly 90% of patients when there is no knee arthritis and the knee is stable. Results are satisfactory in only two-thirds of patients when arthritis or ACL injuries are present. Overall, radiographic progression of degenerative changes occurs with follow-up beyond 10 years, although radiographic changes do not necessarily correlate with patient symptoms. Again, medial meniscal tears generally have better results than lateral tears, and an intact meniscal rim and intact cartilage surfaces are associated with a better prognosis.
Aglietti P et al: Arthroscopic meniscectomy for discoid lateral meniscus in children and adolescents: 10-year follow-up. Am J Knee Surg 1999;12:83.
Anderson-Molina H et al: Arthroscopic partial and total meniscectomy: long-term follow-up study with matched controls. Arthroscopy 2002;18:183.
Chatain F et al: The natural history of the knee following arthroscopic medial meniscectomy. Knee Surg, Sports Trauma, Arthrosc 2001;9(1):15.
Chatain F et al: A comparative study of medial versus lateral arthroscopic partial meniscectomy on stable knees: 10 year minimum follow-up. Arthroscopy 2003;19(8):842.
Because of the importance of the meniscus in knee stability and protection of chondral surfaces, surgeons often recommend meniscal repair in young, active individuals and those undergoing ACL or chondral reconstruction. Commonly accepted criteria for meniscal repair include a complete, vertical, longitudinal tear greater than 10 mm in length, a tear of the peripheral 10–30% of the meniscus or within 3–4 mm of the meniscocapsular junction, a peripheral tear that can be displaced toward the center of the plateau by probing, the absence of secondary degeneration of the meniscus, and a tear in an active patient or one undergoing concurrent ligament or chondral reconstruction.
Multiple factors affect the success of meniscus repair. Although no absolute age limit exists, patients younger than 40 years old are thought to have a better chance of 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.
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Acute tears located in the peripheral red/red or red/white zone have better healing ability 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), tears 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 employed. 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.
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Figure 3-6. Meniscal tears. A: Meniscal degeneration should not be mistaken for a tear. This is a common finding of doubtful clinical significance, appreciated on MRI as an area of high signal that does not extend to the auricular surface. B: Complex tear of the posterior horn of the medial meniscus. C: Vertical peripheral tear in the posterior horn of the medial meniscus. D: Bucket-handle tear with flipping of the loose meniscal fragment into the intercondylar notch, producing a “double posterior cruciate ligament” sign on this sagittal MR image. E: The same bucket-handle tear in D shown in coronal section. (Reproduced, with permission, from Anderson J: An Atlas of Imaging in Sports Medicine. McGraw-Hill, 1999. ) |
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 done 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 edges to ensure good healing potential.
Greis PE et al: Meniscal injury: II. Management. J Am Acad Orthop Surg 2002;10:177.
Medvecky MJ, Noyes FR: Surgical approaches to the posteromedial and posterolateral aspects of the knee. J Am Acad Orthop Surg 2005;13:121.
Noyes FR, Barber-Westin SD: Arthroscopic repair of meniscal tears extending into the avascular zone in patients younger than twenty years of age. Am J Sports Med 2002;30(4):589.
Noyes FR, Barber-Westin SD: Arthroscopic repair of meniscus tears extending into the avascular zone with or without anterior cruciate ligament reconstruction in patients 40 years of age and older. Arthroscopy 2000;16:822.
Open repair of meniscus tears has had successful long-term results. The technique involves making a small incision through the subcutaneous tissue, capsule, and synovium to directly visualize the tear. Open repair is most useful in peripheral or meniscocapsular tears, often performed in conjunction with open repair of a collateral ligament injury or a tibial plateau fracture. Follow-up studies of 10 years or longer have shown 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.
Muellner T et al: Open meniscal repair. Am J Sports Med 1999;27:16.
(1) Inside-out
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 have consistently shown rates of success 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 mid-posterior horn tears. There is difficulty in passing needles in mid- to anterior horn meniscus tears.
Elkousy H, Higgins LD: Zone-specific inside-out meniscal repair: technical limitations of repair of posterior horns of medial and lateral menisci. Am J Orthop 2005;34:29.
Spindler KP et al: Prospective comparison of arthroscopic medial meniscal repair technique: inside-out versus entirely arthroscopic arrows. Am J Sports Med 2003;31:929.
(2) Outside-in
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 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 have shown complete or partial healing in 74–87% of meniscus repairs. As expected, results were not as good for posterior horn tears and tears in unstable knees.
Rodeo SA: Arthroscopic meniscal repair with use of the outside-in technique. J Bone Joint Surg A 2000;82:127.
Yiannakopoulos CK et al: A simplified arthroscopic outside-in meniscus repair technique. Arthroscopy 2004;20:183.
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(3) All-inside
The popularity of the all-inside repairs has increased as numerous devices and techniques have been introduced in the past few years. This is due in part to the fact that these repairs 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. 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, including 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 that 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 and RapidLoc devices.
It is difficult to compare studies for these updated first- 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 have shown 60–90% clinical success rates using either second-look arthroscopy or clinical examination evaluations. Some have even been 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 have also been recently published. A follow-up to the initial T-Fix device, the second-generation FasT-Fix suture device, has shown 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 various meniscus arrows or screws have biomechanical performance equivalent 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 as 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. Most 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, 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 have shown that (1) vertical are superior to horizontal mattress sutures, (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) suture devices such as the FasT-Fix have biomechanical profiles similar to vertical mattress sutures. What remains to be determined, 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; this results in a higher rate of success than if the knee is left unstable.
Anderson K et al: Chondral injury following meniscal repair with a biodegradable implant. Arthroscopy 2000;16:749.
Barber FA, Herbert MA: Load to failure testing of new meniscal repair devices. Arthroscopy 2004;20(1):45.
Borden P et al: Biomechanical comparison of the FasT-Fix meniscal repair suture system with vertical mattress and meniscal arrows. Am J Sports Med 2003;31(3):374.
Klimkiewicz J, Shaffer B: Meniscal surgery 2002 update. Arthroscopy 2002;18(suppl 2):14.
Miller MD et al: Pitfall associated with FasT-Fix meniscal repair. Arthroscopy 2002;18(8):939.
Miller MD et al: All-inside meniscal repair devices. Am J Sports Med 2004;32(4):858.
Petsche T et al: Arthroscopic meniscus repair with bioabsorbable arrows. Arthroscopy 2002;18:246.
Sgaglione NA et al: Current concepts in meniscus surgery: resection to replacement. Arthroscopy 2003;19(10; suppl 1):161.
Shaffer B et al: Preoperative sizing of meniscal allografts in meniscus transplantation. Am J Sport Med 2000;28:524.
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Rath E et al: Meniscal allograft transplantation: two to eight-year results. Am J Sports Med 2001;29:410.
Zantop T et al: Initial fixation strength of flexible all-inside meniscus suture anchors in comparison to conventional suture technique and rigid anchors: biomechanical evaluation of new meniscus refixation systems. Am J Sports Med 2004;32(4):863.
Meniscal transplantation is now a viable option for selected patients with meniscal-deficient knees. Recent advances in surgical technique and clarification in the indications for the procedure have improved the clinical outcome. Meniscal transplantation is indicated for patients with symptoms referable to a meniscal-deficient tibiofemoral compartment. Contraindications to meniscal transplant include patients with advanced articular cartilage degeneration, instability, or malalignment of the lower limb.
Fresh-frozen, cryopreserved, and irradiated allografts have all been used. Based on early reports, fresh-frozen grafts may give superior results. Graft sizing is a critical factor in the success of meniscal transplantation. Currently, more sophisticated techniques such as MRI have not proved more accurate than plain radiographic tibial plateau measurements. Improved techniques to accurately size meniscal allografts to within 2 mm of the actual meniscal dimensions are still needed.
Lateral meniscal transplants are usually done using a common bone bridge that connects the anterior and posterior horn insertions, whereas medial meniscal transplants typically use separate anterior and posterior bone plugs. The reason for the differing techniques involves the close proximity of the anterior and posterior horns of the lateral meniscus, which makes the placement of a common bone bridge technically easier. The medial or lateral meniscal allograft is then sutured to the surrounding capsule. The use of both capsular sutures as well as bone plugs has been shown to be biomechanically superior to capsular sutures alone.
The long-term success (>10 years) of meniscal transplantation, particularly with the use of fresh-frozen allografts, is promising. Successful results have been shown in both isolated meniscal transplants as well as transplants combined with ACL reconstruction. Functional scores in activities of daily living after surgery have shown significant improvements over scores before surgery. Currently, it is not recommended that meniscal transplant patients return to high-level athletic activities.
Allen CR et al: Importance of the medial meniscus in the anterior cruciate ligament-deficient knee. J Orthop Res 2000;18:109.
Fukushima K et al: Meniscus allograft transplantation using posterior peripheral suture technique: a preliminary follow-up study. J Orthop Sci 2004;9(3):235.
Rijk PC: Meniscal allograft transplantation—-part I: background, results, graft selection and preservation, and surgical considerations. Arthroscopy 2004;20(7):728.
Osteochondral Lesions
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 may 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. 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 OCLs. 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 majority of adult OCLs are thought to have arisen from a persistent juvenile OCL, 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 OCLs 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%. 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 OCLs.
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 enters the room. An effusion may be variably present, but generally crepitus or pain with range of motion is absent in
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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. 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 a plain radiographic evaluation is to exclude any bony pathology, evaluate the physes, and localize the lesion (Figure 3-7). Lesion location and an estimation of size should also be determined.
An MRI is frequently obtained once the diagnosis has been confirmed on plain radiographs. MRI can provide 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. The high signal line was the most common sign in patients found to have unstable lesions; for these patients nonsurgical treatment was most likely to fail. Patient maturity and lesion size were also important predictors of failure of nonsurgical treatment.
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Figure 3-7. Osteochondritis dissecans. A: Fragmentation has occurred at the lateral aspect of the medial femoral condyle. A loose body has separated from the condyle and lies within the intercondylar notch. B: A subchondral bone defect at the medial femoral condyle shows a good cortical margin at its rim and appears healed. A displaced ossicle lies in the intercondylar notch. (Reproduced, with permission, from Anderson J: An Atlas of Imaging in Sports Medicine. McGraw-Hill, 1999. ) |
Equivocal prognostic value has been found in the use of intravenous gadolinium in the diagnosis of OCLs. Technetium bone scans were initially proposed to monitor the presence of healing. However, MRI eliminates ionizing radiation and is fast, so bone scans are no longer widely used.
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Treatment
Nonoperative management should be pursued in children with open physes who present with a stable OCL. The goal of nonoperative treatment is to obtain a healed lesion before physis closure so as to prevent osteoarthritis. Even if patients are within 6–12 months of physeal closure, a trial of nonoperative treatment is warranted. Because failure of the subchondral bone precedes failure of the overlying articular cartilage, most orthopedists recommend some modification of activity. Debate exists as to whether this should include immobilization with a cast or brace. The tenet of nonoperative treatment is to reduce the activity level to a point at which pain-free activities of daily living are possible.
Patients should at least be non-weight bearing 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, which may be initiated once patients are pain free, should focus on low-impact quadriceps and hamstring strengthening. If patients remain asymptomatic during this phase, up to at least 3 months postdiagnosis, they may slowly advance 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 of the non-weight-bearing period and possible immobilization for a longer period. Obvious patient frustration and lack of compliance, especially in adolescents, are 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), or (4) near or complete epiphyseal closure. Goals of operative treatment should include 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 have shown radiographic healing and relief of symptoms in 80–90% of patients with open physes. This decreases to 50–75% in patients with closed physes.
Management of patients with flap lesions or partially unstable lesions should depend on the status of the subchondral bone. Fibrous tissue between the lesion and subchondral bone should be debrided. If significant subchondral bone loss has occurred, packing of the autogenous bone graft into 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 have been described including Herbert or cannulated screws and bioabsorbable screws or pins. Complications, however, have been associated with these treatments.
Simple excision of the larger fragments has shown 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 have also shown inferior results. Results also tend to deteriorate with time as indicated by worsening radiographic changes. For these larger lesions, transplantation of autologous osteochondral plugs or autologous chondrocyte implantation has been tried. Disadvantages of autologous osteochondral plugs or mosaicplasty include donor site morbidity and incongruent articular fit. Advantages include biological fixation of autogenous material. Longer-term results in young adult patients show successful clinical outcomes in up to 90%. However, additional larger and longer-term follow-up studies are needed.
Bentley G et al: A prospective, randomized comparison of autologous chondrocyte implantation versus mosaicplasty for osteochondral defects in the knee. J Bone Joint Surg B 2003; 85:223.
Flynn JM et al: Osteochondritis dissecans of the knee. J Pediatr Orthop 2004;24:434.
Friederichs MG et al: Pitfalls associated with fixation of osteochondritis dissecans fragments using bioabsorbable screws. Arthroscopy 2001;17:542.
Kocher MS et al: Diagnostic performance of clinical examination and selective magnetic resonance imaging in the evaluation of intra-articular knee disorders in children and adolescents. Am J Sports Med 2001;29:292.
Kocher MS et al: Functional and radiographic outcome of juvenile osteochondritis dissecans of the knee treated with transarticular arthroscopic drilling. Am J Sports Med 2001;29:562.
Peterson L et al: Treatment of osteochondritis dissecans of the knee with autologous chondrocyte transplantation: results at two to ten years. J Bone Joint Surg A 2003;85(suppl 2):17.
Pill SG et al: Role of magnetic resonance imaging and clinical criteria in predicting successful nonoperative treatment of osteochondritis dissecans in children. J Pediatr Orthop 2003;23: 102.
Weakness About the Knee
The differential diagnosis of weakness about the knee is vast and often overwhelming. It is helpful to think of the various causes in a systematic way, thereby simplifying the approach. The causes of weakness about the
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knee may be subdivided into those stemming from muscular (strains, contusions, tears), ligamentous (sprains, partial or complete tears), tendinous, neurologic (central or peripheral), vascular, and bony sources. This section will focus on muscular, tendinous, and bony causes of weakness about the knee.
Quadriceps Contusion
Traumatic contusion of muscle is one of the most common causes of soft-tissue injury and weakness. Up to 90% of all sports injuries are contusion or strain injuries. Muscle contusion injuries can occur from direct trauma, including laceration or blunt force, and indirect trauma or tensile overload. Tensile overload typically causes muscle failure at the musculotendinous junction or tendon insertion, whereas blunt force trauma is the most common cause of muscle contusion. The quadriceps is the most common site for muscle contusion, and this discussion will be limited to injuries sustained in this muscle from blunt force trauma.
Muscles are known to work optimally within a set temperature range. Additionally, fatigued muscle is known to decrease the ability of stretched muscle to withstand injury. Therefore, adequate rest and a warm-up period prior to exertion reduce the incidence of injury.
Clinical Findings
Quadriceps muscle contusions are common after being struck from the front or side with the muscle compressed against the femur. Patients will often have a history of direct trauma, which is common in many sports including football, hockey, lacrosse, rugby, soccer, and the martial arts. The injury is associated with acute swelling, pain, and a decreased active and passive range of motion of the hip and knee. Patients may or may not be able to continue with their activity. If seen late, bruising may be evident on the skin overlying the quadriceps.
Tenderness to palpation over the quadriceps and a decreased range of motion of the hip and/or knee are the most common findings on examination. If severe, a palpable mass may be present indicating a possible hematoma. Also, a palpable gap may be present if significant muscle tearing has occurred.
Quadriceps contusion injuries may be a diagnosis of exclusion, but are usually readily apparent given a history of direct trauma and the associated clinical findings. Plain radiographs may be obtained to rule out associated fracture, although this is uncommon. Ultrasound or measuring the size of any muscle gap and associated hematoma can differentiate acute hematoma from diffuse swelling. The use of MRI in diagnosing and following contusion injuries is not well defined.
If the patient exhibits pain out of proportion to the clinical findings or the clinical findings show severe swelling in a thigh compartment, compartmental pressure monitoring may be indicated. Pressures greater than 30 mm Hg have been suggested as thresholds for emergent fasciotomies.
Metaplasia of the severely contused muscle may result in ossification within the muscle, termed myositis ossificans. The risk of developing myositis ossificans is directly related to the severity of the injury, and has been reported to be as high as 9% following deep thigh contusions. Serial plain radiographs or computed tomography (CT) may be needed to follow the progression of ossification within the muscle. Generally, surgery is not recommended for this condition unless the ossification is severely limiting. A delay of at least 6 months after injury is recommended to allow the abnormal bone formation to mature, thereby limiting further surgery-induced ossification.
Treatment
The goal of treatment for quadriceps contusion injuries focuses on symptomatic pain relief, maintenance of knee motion and quadriceps strength, and prevention of myositis ossificans. Protocols have been developed for optimal rehabilitation and treatment. This includes an initial immobilization period not to exceed 48 hours, followed by progressive leg and gravity-assisted range of motion exercises. Decreased quadriceps muscle contraction has been found to occur when patients are immobilized with the hip and knee in flexion according to pain tolerance. Indomethacin or other nonsteroidal antiinflammatory drugs (NSAIDs) have been advocated to decrease the risk of myositis ossificans. These medications may have beneficial short-term effects on pain modulation, but their effect on early and late muscle healing and regeneration is not clear.
Beiner JM, Jokl P: Muscle contusion injuries: current treatment options. J Am Acad Orthop Surg 2001;9:227.
Diaz JA et al: Severe quadriceps contusions in athletes. Am J Sports Med 2003;31:289.
Patellar Tendon Ruptures
Rupture of the patellar tendon is a rare but serious knee injury with a peak incidence in males during the third or fourth decade. It is typically seen in more active patients, and the injury may be the end result of repetitive microtraumatic injuries. A typical healthy adult tendon
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is extremely resistant to rupture. Patients who rupture their patellar tendons typically exhibit some form of tendinopathy clinically or pathologically. Dysfunction of the patellar tendon may exist across a degenerative spectrum, with younger patients exhibiting clinical symptoms of “jumpers knee” or patellar tendinitis and older patients exhibiting pathologic changes resulting in an end-stage tendon rupture due to a degenerative tendinopathy. Although unilateral ruptures are more common, bilateral ruptures have been described. Risk factors for bilateral ruptures include systemic diseases that weaken collagenous tissues such as rheumatoid arthritis, diabetes mellitus, chronic renal failure, or systemic lupus erythematosus. Chronic steroid use or previous major knee surgery, such as total knee arthroplasty or anterior cruciate reconstruction with patellar tendon autograft, is also a risk factor.
The patellar tendon should more accurately be named the patellar ligament, as it is a continuation of the quadriceps expansion over the patella distally to the tibial tubercle. For this discussion, however, it will be referred to as the patellar tendon. The quadriceps consists of the rectus femoris, vastus intermedious, vastus lateralis, and vastus medialis muscles. Portions of the vastus medialis and lateralis muscles extend distally to contribute to the quadriceps tendon and, ultimately, the patellar tendon. Tendinous expansions of the vastus lateralis and medialis, however, extend past the patellar to the proximal tibia and are referred to as the lateral and medial reticulum, respectively. Blood supply to the patellar tendon arises from the infrapatellar fat pad as well as the reticular structures through anastomoses from the inferior genicular arteries. The proximal and distal aspects of the patellar tendon attachment are watershed areas of vascularity where many ruptures typically occur.
With increasing knee flexion, the contact point of the patella within the femoral trochlear groove moves proximally, giving the patellar tendon a longer lever arm and a greater mechanical advantage with respect to the quadriceps tendon. Additionally, the greatest strain or tensile load deformation occurs at the insertion sites as opposed to the mid-tendon substance. Therefore, most ruptures occur with deep knee flexion at the distal pole of the patella.
Clinical Findings
Patellar tendon ruptures typically occur in patients 40 years of age or younger, often during athletic activities. Although a patient of any age can sustain a patellar tendon rupture, patients older than 40 years typically tear their quadriceps tendon. The history is that of a sudden, forceful quadriceps eccentric contraction on a flexed knee such as landing from a jump or stumbling on a stair. Patients describe a sudden pain and a popping or tearing sensation in the knee which leads to an inability to continue their activity. Weight bearing is often difficult and requires assistance.
Patients usually present with a knee effusion or a hemarthrosis. In a complete tear through the tendon and adjacent reticula, the patella is displaced proximally by the pull of the quadriceps tendon. Extensor function is absent or greatly decreased, with patients unable to actively extend their knee or passively maintain an extended knee position. In incomplete patellar tendon tears or complete patellar tendon tears with sparing of the reticula, patients may have some active extension against gravity. However, maintenance of extension against force is not possible. A palpable gap may be present.
In a patient with a delayed presentation, organizing hematoma or fibrosis may obscure the tendon defect. These patients, however, will typically have a classic history and will often have quadriceps atrophy, weakness in knee extension, and an antalgic gait.
Plain radiographs consisting of anteroposterior and lateral views are essential. The lateral view may show patella alta, with the entire patella located proximal to Blumensatt's line. The Insall–Salvati ratio (the length of the patella tendon divided by the length of the patella) will be greater than 1.2 signifying patella alta. An avulsed bone fragment in the distal pole of the patella may be seen. A patellar view and a flexed knee view may be helpful to rule out other intraarticular pathology such as patella fractures or osteochondral injuries. Comparison views of the contralateral knee may also be helpful to compare patellar height.
High-resolution ultrasonography has been utilized as an effective means of imaging the patellar tendon. Its advantages include its relatively low cost, lack of ionizing radiation, and quick availability and results. Its main disadvantage is that it is highly operator and reader dependent, which makes it unavailable or unreliable in many areas. MRI is very accurate in diagnosing patellar tendon tears. It is particularly helpful in patients with chronic tears and questionable partial versus complete tears, and in patients suspected of having additional intraarticular pathology. For most acute cases, MRI is not necessary for diagnosis.
Treatment
No widely accepted classification system exists for patellar tendon ruptures. Various classification schemes based on the chronicity of diagnosis and treatment, the tear
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configuration, and the level of tendon rupture have been described. The only classification system that has been found to have a correlation with clinical outcome is that of Siwek and Rao, who grouped their patients into two categories: immediate repair (defined as less than 2 weeks) and delayed repair (defined as greater than 2 weeks). Subsequent studies have shown that patellar rupture repairs done acutely (2–4 weeks) generally have a better prognosis than repairs done on a delayed or chronic basis (>4–6 weeks). Repairs performed on a delayed basis are hampered by quadriceps contraction and fibrous adhesions that make restoration of tendon length and repair more difficult.
Thus, surgical restoration is necessary to reestablish the extensor mechanism in most patients, both athletes and nonathletes, with complete tears. Surgical repair should be done in a timely fashion, making accurate diagnosis essential. Nonoperative treatment is ineffective and has few indications.
The knee is approached anteriorly through a longitudinal incision from the mid-patella to the tibial tubercle. To avoid complications to wound healing, thick flaps of tissue are maintained during the exposure. The ruptured tendon ends and reticula are identified and debrided. Often, the rupture occurs so close to the patella that sufficient soft tissue on the patella is not present. If the tendon rupture is more mid-substance, primary end-to-end repair of both the tendon and reticula is done using heavy, nonabsorbable sutures. A strong stitch such as a Bunnell or Krackow is used. Typically, as the tendon rupture is adjacent to the inferior pole of the patella, the repair is accomplished by passing the suture from the patella tendon through two or three longitudinal, transpatellar drill holes. A circumferential reinforcing suture is often added to the repair. This suture is passed through a drill hole in line with and posterior to the tibial tubercle, and then brought proximally and passed transversely through the quadriceps tendon. Prior to tying, the sutures are tensioned, and a single lateral radiograph of the knee is obtained to assess patellar height. A contralateral radiograph is used for comparison. Once the appropriate patellar height is recreated by proper tensioning of the sutures, the sutures are tied over the superior pole of the patella. The circumferential reinforcing suture is then also tied. The knee flexion angle at which sufficient tension is present across the repair can be assessed to help guide postoperative physical therapy rehabilitation. The suture line can be oversewn with a smaller nonabsorbable suture depending on surgeon preference.
Careful attention to restoring the patellofemoral alignment can improve patellofemoral tracking and clinical outcome. Restoration of patellar tendon length and patellar height has been shown to improve results and diminish later patellofemoral symptoms. This can cause difficulty in the repair in delayed or chronic cases. Such cases may require preoperative traction on the patella to restore length, intraoperative lysis of adhesions around the extensor mechanism, and the use of allograft or autograft tissue augmentation.
Initially, most patients were immobilized in extension postoperatively for 6 weeks in either a brace or cylinder cast. This was thought to allow tendon healing without tension, and good results were reported. As evidence mounted that controlled movement after repair positively influenced tendon nutrition and healing, use of early range of motion has been reported to produce comparable results. A common protocol involves starting isometric quadriceps/hamstring exercises on the first postoperative day, with active flexion and passive extension added at 2 weeks postoperatively and active knee extension added at 3–4 weeks postoperatively. Patients are allowed toe-touch weight bearing immediately postoperatively, and are advanced to full weight bearing without crutches by 6 weeks postoperatively as quadriceps function and leg control return.
The most common complications following this injury are persistent loss of quadriceps strength and loss of full knee flexion. This is thought to be associated with the injury itself. This emphasizes the need for an aggressive postoperative physical therapy protocol emphasizing range of motion and strengthening. Manipulation under anesthesia and arthroscopic lysis of adhesions are typically not needed when such a protocol is instituted.
Complications
Surgical complications are infrequent, but include wound infection or dehiscence, a persistent hemarthrosis, rerupture, and patellofemoral pain. In a circumferential repair, breakage of the wire cerclage has also been reported. Wound complications can be reduced by maintaining thick skin flaps and using a slightly lateral incision away from the tibial tubercle. Rerupture is typically seen in patients who return to sport prior to obtaining full knee motion and adequate (85–90%) quadriceps and hamstring strength. Assessing the alignment and height of the patella on a lateral radiograph in comparison to the contralateral side can help in restoring proper patellofemoral mechanics.
Prognosis
Multiple studies detailing the results of patellar tendon rupture repairs have been reported in the literature. To date, the only factor correlated with a positive clinical outcome is acute repair. Additionally, younger and more athletic patients with an isolated injury tend to have better results compared to older or multitrauma patients. Siwek and Rao compared acute (<7 days)
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versus delayed (>7 days) repairs and found that acute repairs did significantly better in terms of range of motion and strength. Although some quadriceps atrophy and slight motion loss (<10°) may persist postoperatively, good and excellent reports have been shown to occur in 66–100% of patients, although a smaller percentage of recreational athletes return to their preinjury athletic level. Most studies reported use of some circumferential augmentation in the form of either a suture or wire. A retrospective comparison of polydioxanone suture to wire augmentation found no significant differences.
Patellofemoral arthritis or incongruity has not been shown to be associated with outcome. Although most patients with poorer outcomes tend to have patellofemoral complications, many patients without symptoms also have radiographic findings of incongruity or arthrosis. Thus, articular incongruity may not alone be the cause of poor outcomes. Despite evidence indicating the benefits of early motion, no study has found significant improvement in outcome in patients undergoing delayed versus immediate postoperative therapy. Overall, patients with acute treatment, higher level athletes or those involved in diligent postoperative rehabilitation, and athletes without significant quadriceps atrophy seem to achieve better postoperative outcomes.
There are only a few case reports or case series on the results of delayed reconstruction. Multiple reconstructions have been described including primary repair augmented with autogenous fascia lata or hamstring grafts; allografts have also been used. Patients repaired on a delayed basis who require preoperative traction or the use of allograft or autograft augmentation seem to have inferior results.
Kasten P et al: Rupture of the patellar tendon: a review of 68 cases and a retrospective study of 29 ruptures comparing two methods of augmentation. Arch Orthop Trauma Surg 2001; 121:578.
Quadriceps Tendon Ruptures
Rupture of the quadriceps tendon typically occurs in patients over 40 years of age. Injuries usually occur from indirect mechanisms and require a previously weakened tendon prior to rupture. As in patellar tendon ruptures, bilateral ruptures do occur and are more likely in patients with underlying systemic conditions such as chronic steroid use, systemic lupus erythematosus, diabetes, or chronic renal failure.
The quadriceps tendon is formed by a convergence of the tendons of the rectus femoris, vastus intermedius, vastus lateralis, and vastus intermedius muscles approximately 3 cm proximal to the patella. Portions of the vastus medialis and lateralis extend adjacent to the patella and insert directly into the proximal tibia, forming the medial and lateral reticulum, respectively. The anatomic location of the muscles contributing to the quadriceps tendon is reflected in the distinct planes that make up the tendon. The superficial plane is composed of fibers from the rectus femoris, the middle plane from the vastus lateralis and medialis muscles, and the deep plane from the vastus intermedius. Adherent to the deep surface of the tendon is the capsule and synovial lining of the knee joint, which often tears with complete rupture of the quadriceps tendon, causing the acute hemarthrosis seen with such an injury.
A tendon from a normal, healthy adult is extremely resistant to rupture. When subjected to supramaximal loads, the extensor mechanism will fail at other weaker points such as the osteotendinous or musculotendinous junctions. Thus, for a rupture of the quadriceps tendon to occur, it is generally believed that a weakened tendon state must be involved. Alternations in the normal collagen structure of tendons do occur normally with age; however, despite this, quadriceps rupture is still a rare event. Other concurrent pathologic processes must be present to alter the structure of the tendon. Such processes may accelerate fatty or mucoid degeneration, decrease the collagen content, or disrupt the vascular supply. Conditions such as chronic renal failure, rheumatoid arthritis, gout, systemic lupus erythematosus, steroid use, or hyperparathyroidism have all been implicated as causative factors.
Clinical Findings
In older patients traumatic ruptures of the quadriceps tendon generally occur during daily activities with the knee in a semiflexed state and the quadriceps firing in an eccentric fashion. Typical mechanisms include stumbling while walking, stair climbing, or, less likely, exertion during an athletic event. Patients typically complain of rapid swelling, an inability to ambulate, and lack of knee extension after such an injury. They may also describe a tearing sensation or pop in their knee with pain.
The diagnostic hallmarks of a quadriceps tendon rupture are an inability to actively extend the knee and a suprapatellar gap. Although active knee flexion remains intact, patients are typically unable to actively extend the knee or maintain extension in a passively flexed knee (ie, demonstrate an extension lag sign). Patients with partial ruptures or complete tendon ruptures with intact retinacula may demonstrate some active extension, but typically still demonstrate an extension lag. A palpable depression superior to the patella, known as the suprapatellar gap sign, is pathognomonic.
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Failure to diagnose the injury, observed in up to 50% of cases, delays subsequent treatment. In patients with an acute hemarthrosis, the suprapatellar gap may be obscured. A helpful maneuver to elicit this sign involves having the patient actively flex the hip, which shortens the rectus femoris muscle thereby drawing the quadriceps tendon more proximally and widening the defect at the rupture site. Additionally, comparison with the contralateral leg for both palpation as well as active extension is essential.
Anteroposterior and lateral radiographs should be obtained on any patient suspected of having a quadriceps tendon injury. Four radiographic signs may be present in plain radiographs in patients with quadriceps tendon ruptures: obliteration of the quadriceps tendon shadow, a suprapatellar mass (retraction of the ruptured tendon), suprapatellar calcific densities (dystrophic calcifications or avulsed bone fragments), and an inferiorly displaced patella.
Ultrasound is highly sensitive and specific in assessing partial and complete quadriceps ruptures. It can also be used to assess the tendon after repair. It is a relatively cheap modality and spares the patient ionizing radiation. Ultrasound is, however, highly operator dependent and therefore is not available in all areas. MRI is also highly sensitive and specific in the diagnosis of quadriceps tendon ruptures. It is particularly helpful in patients with massive swelling, which may preclude a good physical examination, as well as in patients suspected of having additional intra-articular injuries. Because of its cost, MRI is generally not used in straightforward, acute cases of quadriceps tendon rupture.
Treatment
Management and treatment of quadriceps ruptures should initially be based on whether the rupture is partial or complete, as determined by physical examination and/or additional imaging. Partial ruptures can generally be managed nonoperatively with the knee braced or casted in near full extension for 6 weeks, followed by progressive range-of-motion and strengthening exercises. There are no data, however, concerning the percentage of tendon ruptures that can be effectively treated nonoperatively.
Complete rupture of the quadriceps tendon is an indication for surgical treatment. The nonoperative management of complete ruptures results in long-term disability secondary to quadriceps weakness and extensor lag. In cases of delayed patient presentation or diagnosis, the repair can be more difficult due to retraction of the torn tendon ends making apposition difficult. Early intervention (less than 72 hours if possible) is recommended to optimize results.
Multiple methods of repair have been described, and no published data are available comparing the results of different types of repairs. Generally, repair proceeds in a similar fashion as described below. For midsubstance tears in which there is ample tendon tissue on both ends of the rupture, a primary end-to-end repair may be done. Typically, two heavy nonabsorbable sutures are placed in a running fashion (eg, Krakow or Bunnell) in each end. Similarly, smaller nonabsorbable sutures are placed in apposition to the torn reticula ends. These are opposed but not tied until the tendon sutures are tied. In ruptures near the osteotendinous junction of the superior patellar pole (a common place for rupture), a similar suture technique is used to secure the tendon end. The superior pole of the patella is debrided of remaining soft tissue and roughened to bleeding bone in preparation for tendon approximation. Three 2-mm longitudinal drill holes are then placed through the patella, and the free ends of the sutures are passed through the holes with a Keith needle and tied distally over the inferior pole of the patella with the knee in near full extension.
Circumferential augmentation, similar to what is done in patellar tendon ruptures, can be added. Options include wire, Mersilene tape, or a nonabsorbable suture. Another option to repair or augment acute ruptures includes the Scuderi technique, in which a partial-thickness triangular flap is excised from the anterior surface of the proximal quadriceps tendon, approximately 2 inches wide and 3 inches on each side. This flap is then folded down distally over the rupture site and sutured into place.
Bilateral ruptures should be treated in a similar fashion to unilateral ruptures. Additionally, an evaluation for known systemic diseases that cause tendon degeneration should be conducted. These patients are at increased risk for delayed presentation as they are often seen by nonorthopedists or their disabilities are attributed to other causes such as various arthritides or neurologic disorders.
Chronic ruptures of the quadriceps tendon can involve more difficult repairs, particularly when tendon retraction has occurred. Retraction typically requires lysis of adhesions between the tendon and underlying femur to gain appropriate length. When tendon ends can be reapproximated, a standard repair as described previously can be used. When significant gapping exists despite maximal mobilization of the tendon ends, a Codivilla lengthening procedure may be required. This involves making a partial thickness, V-shaped cut from the distal aspect of the proximal quadriceps tendon stump. The apex of the V-shaped cut points cephalad. The flap is then reflected distally on its attached base
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and sewn to the distal tendon stump. The upper portion is then sutured closed in a side-to-side fashion.
The knee is splinted or braced in extension until the wound has sealed and any drains placed intraoperatively have been removed. Although data have shown improved tendon healing with gentle early range of motion, a comparison of patients immobilized in extension for 6 weeks versus those started on early range-of-motion exercises did not show a difference. For patients immobilized for 6 weeks, immediate weight bearing in extension is allowed. Range-of-motion exercises are started at 4–6 weeks and slowly advanced. Once adequate quadriceps function and leg control are obtained, the brace can be discontinued at 6–12 weeks. Patients on more aggressive rehabilitation protocols may start isometric quadriceps/hamstring contractions with active flexion and passive extension at 2–3 weeks, and progress to active extension at 6 weeks postoperatively. Complete range of motion should be seen at 12 weeks, with most patients returning to full activities by 4–6 months postoperatively.
Complications
The most common complications following quadriceps tendon repair are an inability to regain full knee flexion and continued quadriceps weakness. An extensor lag is also a known complication, but can usually be overcome with appropriate physical therapy. Other less common but known complications include wound infection or dehiscence, persistent hemarthrosis, and patella baja or patellar incongruity. Wound complications can be minimized by placing sutures or wires away from the incision, and maintaining thick skin flaps during surgical dissection. Postoperative drains may decrease the rate of hemarthrosis. Finally, attention to the patellar height and congruity of the patellofemoral articulation intraoperatively may help decrease patellofemoral complications.
Prognosis
Several studies have shown improved results of acute repair over chronic repair, although other studies have not shown such a correlation. In general, acute repairs result in excellent clinical outcomes in 83–100% of patients. No differences have been found in repair technique or postoperative protocols. Range of motion is generally within 5–10° of the uninjured side, with strength losses of approximately 10% or less. Over 90% of patients are generally satisfied, although one study showed only 51% were able to return to their presurgery level of recreational activity. Perhaps the high satisfaction rating and good clinical results may be attributable to the older age group and subsequent lower activity demands.
Ilan DI et al: Quadriceps tendon rupture. J Am Acad Orthop Surg 2003;11:192.
O'Shea K, Kenny P: Outcomes following quadriceps tendon ruptures. Injury 2002;33:257.
Shak MK: Outcomes in bilateral and simultaneous quadriceps tendon rupture. Orthopedics 2003;26(8):797.
Avulsion of the Tibial Tubercle
Developmentally, the tibial tubercle begins proximal on the tibia, and descends distally to a point just distal to the proximal tibial growth plate. A vertical component of the tibial growth plate appears under the tubercle. Progressive replacement of the immature fibrocartilage to mature bone occurs in a proximal-to-distal direction. Complete epiphysiodesis occurs in boys at about 17 years of age and in girls at about 15 years of age.
Clinical Findings
Acute tibial tubercle avulsions occur almost exclusively in boys between the ages of 12 and 17 years. The history is often that of a sudden, forceful quadriceps contraction (eg, jumping) or an eccentric quadriceps contraction against a passively flexing knee (eg, landing from a jump). Competitive jumping sports such as basketball or high jumping or contact sports such as football are commonly involved.
Patients present with focal proximal tibial swelling and anterior knee pain. They may or may not be able to extend their knee against gravity, but all have some form of knee weakness. An audible pop may have been heard at the time of injury.
Patients with a tibial tubercle fracture have focal anterior tibial tenderness. Those with an intraarticular extension of their fracture will have an associated knee effusion or hemarthrosis. Patients demonstrate weakness or complete absence of knee extension. Associated injuries may also occur. A thorough knee examination should be performed looking for associated joint line tenderness or ligamentous instability indicative of a meniscal tear or intraarticular ligament tear, respectively.
A true lateral radiograph of the tibial tubercle is essential to accurately diagnose a tibial tubercle avulsion. Anteroposterior and oblique radiographs should also be obtained. Because the tubercle lies lateral to the midline, slight internal rotation of the knee prior to shooting the lateral film will help visualize the tibial tubercle. Although uncommon, an MRI may be obtained if suspicion exists for an associated intraarticular injury.
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Treatment
The Ogden modification of the Watson–Jones classification is used to categorize these injuries and guide treatment. There are three types, each with an A and B subtype. Type I is a fracture distal to the normal junction of the ossification centers of the proximal end of the tibia and tuberosity. Type II is a fracture at the junction of the ossification centers of the proximal end of the tibia and tuberosity. Type III fractures extend into the joint. Further subtyping is used to describe the absence (subtype A) or presence (subtype B) of displacement and comminution (Figure 3-8).
Treatment goals include anatomic fracture reduction, maintenance of articular congruency, and restoration of the extensor mechanism.
Nondisplaced type I fractures (IA) can be successfully treated with a cylinder cast or long leg cast in extension for 4–6 weeks. Some displaced type I (IB) and IIA fractures may similarly reduce anatomically with extension in a cast.
Those type IB and IIA fractures that do not reduce, as well as most type IIB and III injuries, are best treated with open reduction and internal fixation.
The approach is typically directly anterior or slightly off midline, with dissection carried down adjacent or posterior to the patellar tendon insertion. Any interposed soft tissue or periosteum is removed and an anatomic reduction is obtained. The use of intraoperative fluoroscopy is helpful. Fixation may be accomplished with the use of cannulated screws and/or a tension band construct. Grade III injuries should be evaluated for associated ligamentous or meniscal injury.
Whether operative or nonoperative treatment is chosen, a cast is typically worn for 4–6 weeks, at which time progressive knee range-of-motion exercises are started. Quadriceps strengthening is typically started at approximately 6 weeks or when full range of motion has been obtained. Patients may return to regular activities after quadriceps strength has returned to 85% of the contralateral leg. Return to full sports activities is expected by 3–6 months.
Complications & Prognosis
The prognosis for tibial tubercle avulsion fractures is very good with few complications. Genu recurvatum has not been reported, likely due to the fact that these patients are at or near skeletal maturity when their injury occurs. Loss of motion, patellar malposition, and compartment syndrome have been observed. Careful attention to anatomic alignment of the fracture and comparison to the contralateral knee is helpful to avoid patellar complications. Compartment syndrome due to laceration of a small recurrent artery is possible, and patients should be carefully observed postoperatively. The institution of an early, aggressive therapy protocol can help to obtain full knee range of motion. Nonunion is rare.
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Figure 3-8. Avulsion fractures of the tibial tubercle. A: Type I fracture across the secondary ossification center at a level with the posterior border of the inserting patellar ligament. B: Type II fracture at the junction of the primary and secondary ossification centers of the proximal tibial epiphysis. C: Type III fracture 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. ) |
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McKoy BE, Stanitski CL: Acute tibial tubercle avulsion fractures. Orthop Clin North Am 2003;34(3):397.
Mosier SM, Stanitski CL: Acute tibial tubercle avulsion fractures. J Pediatr Orthop 2004;24(2):81.
Zionts LE: Fractures around the knee in children. J Am Acad Orthop Surg 2002;10:345.
Knee Instability
Anatomy
Knee instability entails four primary ligaments as stabilizing structures of the knee. These ligaments include the anterior cruciate ligament (ACL), the posterior cruciate ligament (PCL), the medial collateral ligament (MCL), and the lateral collateral ligament (LCL). There are also several accessory or secondary stabilizers of the knee, including the menisci, iliotibial band, and biceps femoris. These secondary stabilizers become more important when a primary stabilizer is injured.
The MCL, the primary static medial stabilizer against valgus stress at the knee, originates from the central sulcus of the medial epicondyle (Figure 3-9). 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: the superficial MCL, the posterior oblique ligament, and the deep capsular ligament.
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Figure 3-9. Medial capsuloligamentous complex. (Reproduced, with permission, from Feagin JA Jr: The Crucial Ligaments. New York: Churchill Livingstone, 1988. ) |
The LCL, the primary static lateral stabilizer against varus stress at the knee, 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 that statically and dynamically controls varus angulation and external tibial torsion (Figure 3-10). The iliotibial band and biceps femoris also contribute to stability on the lateral aspect of the knee.
The ACL, the primary static stabilizer of the knee against anterior translation of the tibia with respect to the femur, originates from the posteromedial surface of the lateral femoral condyle in the intercondylar notch (Figure 3-11). It inserts on the tibial plateau just medial to the anterior horn of the lateral meniscus about 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 intraarticular and extrasynovial.
The PCL, the primary static stabilizer of the knee against posterior translation of the tibia with respect to the femur, originates from the posterior aspect of the lateral surface of the medial femoral condyle in the intercondylar notch (Figure 3-12). It 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 the posteromedial. 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
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component of the PCL. The meniscofemoral ligaments travel from the posterior horn of the lateral meniscus to the posteromedial femoral condyle.
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Figure 3-10. The lateral supporting portions of the knee. (Reproduced, with permission, from Rockwood CA Jr et al: Fractures in Adults. New York: Churchill Livingstone, 1984. ) |
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Figure 3-11. 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 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. ) |
Fu FH et al: Current trends in anterior cruciate ligament reconstruction. Part 1: Biology and biomechanics of reconstruction. Am J Sports Med 1999;27:821.
Differential Diagnosis
The differential diagnosis of acute or chronic knee instability can involve any of the following structures: the ACL, the PCL, the MCL, the LCL, and the other structures of the posterolateral corner. Of course there are often combinations of the above ligamentous injuries in addition to injuries of secondary stabilizing structures such as the menisci that produce an unstable knee. The history and mechanism of injury are valuable pieces of information if available. Similarly, the location of pain with palpation can help to narrow the diagnosis. Clearly, however, a thorough physical examination helps to distinguish which ligaments are responsible for knee instability. Additionally, imaging studies are often obtained to confirm clinical suspicions and to evaluate for occult injuries in the setting of a suspected multiligamentous knee injury.
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Figure 3-12. 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. (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. ) |
Medial Collateral Ligament Injuries
Essentials of Diagnosis
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Prevention
Prevention of MCL injury can be achieved by a variety of methods. Increased strength of the thigh muscles and proprioceptive training can help protect from knee injuries. Hinged knee braces may provide some protection from excessive valgus stresses.
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.
How and when the patient was hurt are important parts of the history. Lower grade MCL injuries typically involve a noncontact external rotational injury whereas higher grade injuries generally involve lateral contact to the thigh or upper leg. Other important information includes 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 (grade III) MCL injuries. Immediate swelling may indicate 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.
MCL injuries are evaluated with a complete knee examination to determine the presence of any coexisting injuries. This is especially important with ACL and PCL evaluations because an injury to either of these ligaments would significantly change the course of 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. MCL ligament sprains are graded on a scale ranging from mild (grade I) to moderate (grade II) and severe (grade III) sprains. Laxity to valgus stresses is assessed by the amount of medial joint space opening that occurs at 30° of flexion (Figure 3-13). It is important to stress the knee at 30° of flexion because with the knee in full extension the posterior capsule and PCL will stabilize the knee to valgus stress, which in full extension could lead 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, in grades I and II, injuries typically have a firm end point, whereas in grade III, the injury tends to have a soft end point to valgus stress.
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 (Segond's fracture—see ACL imaging), loose bodies, Pellegrini–Stieda lesion (MCL calcification) (Figure 3-14), and evidence of patellar dislocation. Stress radiographs should be obtained in patients prior to skeletal maturity to rule out an epiphyseal fracture.
MRI is most useful for confirming the site of MCL injury and identifying meniscal and other coexisting 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 a conventional physical examination is thought to be unreliable secondary to patient guarding. Diagnostic arthroscopy can also be used to evaluate for coexistent pathology. However, both of these diagnostic methods have largely been replaced by MRI as a first line diagnostic test.
Treatment
Treatment of an isolated MCL injury is generally nonoperative and involves protection against valgus stress and early motion. Classically, MCL injuries were treated with surgical repair. However, the results of nonoperative treatment paralleled operative intervention.
Grade I and grade II injuries can be treated by placing the knee in either a cast or a brace with weight bearing 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.
Treatment of grade III injuries is more controversial. Increased instability has been shown in grade III tears treated nonoperatively, although in most instances knees with multiligamentous injuries were not excluded. Comparing isolated grade III MCL tears treated with surgical reconstruction versus conservative management, the conservative treatment group enjoyed better results in both subjective scoring and earlier return to activity.
The exception to the current trend of nonoperative treatment of grade III injuries involves multiligamentous knee injury. In this group, particularly with a distal tibial avulsion of the MCL, nonoperative treatment has not fared nearly as well as in isolated MCL injuries.
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Surgical 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 if needed 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 conservative 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 in-creases accordingly.
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Figure 3-13. The collateral ligament being tested in extension and 30° of flexion with the foot between the examiner's elbow and hip. (Reproduced, with permission, from Feagin JA Jr: The Crucial Ligaments. New York: Churchill Livingstone, 1988. ) |
Complications
With nonoperative treatment becoming the standard of care, the amount of complications associated with an MCL injury has significantly decreased. The main potential complication of nonoperative therapy is residual valgus laxity or medial knee pain. Radiographs may also show residual calcification of the MCL (Pelligrini–Steida lesion). Potential surgical complications include arthrofibrosis, infection, damage to the saphenous nerve or vein, or recurrent valgus laxity.
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Figure 3-14. Pellegrini–Steida lesion. There is a curvilinear calcification at a site of the previous medial collateral ligament injury. (Reproduced, with permission, from Anderson J: An Atlas of Imaging in Sports Medicine. McGraw-Hill, 1999. ) |
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Prognosis & Return to Play
In general, in isolated MCL injuries good outcomes can be achieved with conservative treatment and rehabilitation. A 98% return to professional football after nonoperative treatment of isolated MCL injuries has been shown.
Gardiner JC et al: Strain in the human medial collateral ligament during valgus loading of the knee. Clin Orthop Related Res 2001;391:266.
Mazzocca AD et al: Valgus medial collateral ligament rupture causes concomitant loading and damage of the anterior cruciate ligament. J Knee Surg 2003;16(3):148.
Nakamura N et al: Acute grade III medial collateral ligament injury of the knee associated with anterior cruciate ligament tear. The usefulness of magnetic resonance imaging in determining a treatment regimen. Am J Sports Med 2003;31(2):261.
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 B 2004;86(5):674.
Sawant M et al: Valgus knee injuries: evaluation and documentation using a simple technique of stress radiography. Knee 2004;11(1):25.
Wilson TC et al: Medial collateral ligament “tibial” injuries: indication for acute repair. Orthopedics 2004;27(4):389.
Lateral Collateral Ligament Injuries
Essentials of Diagnosis
Prevention
Bracing has not been shown to be effective in prevention of LCL injuries.
Clinical Findings
Because this is a relatively rare injury seen in combination with other ligamentous injuries, the clinical findings of an LCL and posterolateral corner injury can frequently go unnoticed. Subtle findings such as lateral and posterolateral pain and ecchymoses should be noted and investigated further.
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, level of patient activity, overall limb alignment, and other associated knee injuries. For example, a sedentary individual with minimal laxity and overall valgus alignment will have few if any symptoms. However, if LCL laxity is combined with overall varus alignment, hyperextension, and an increased level of activity, symptoms will be quite pronounced. These patients may complain of lateral joint line pain and a varus thrust of their leg with everyday activities, often described as the knee buckling into hyperextension with normal gait.
Patients with an LCL and/or posterolateral corner injury often 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
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should be performed as the incidence of neurovascular injury, particularly peroneal nerve injury, in posterolateral knee injuries has been reported to be 12–29%.
The integrity of the LCL is assessed with a varus stress with the knee in full extension and 30° of flexion. Baseline varus opening is widely variable and should be compared to the contralateral leg. The average baseline for varus opening is 7°. Examination findings with an isolated LCL injury should include varus laxity at 30° of flexion and no instability in full extension. This is due to the stabilizing effect that the intact cruciate ligaments provide in full extension.
It is important to 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, performed by externally rotating each tibia and noting the angle subtended between the thigh and the foot. The dial test is performed at 30° and 90° of flexion with a significant difference being an angle 5° or greater than the contralateral leg.
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's fracture—see ACL imaging), loose bodies, fibular head avulsions (Figure 3-15), 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 to 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 previously mentioned, 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.
This test involves starting with the knee flexed to 90°. With the knee extended, the leg is loaded axially with a valgus stress applied to the knee and the foot is held in external rotation. A palpable shift is noted as the tibia reduces from its posteriorly subluxed position as the knee is extended.
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 occur with adequate quadriceps relaxation in a patient with posterolateral instability.
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 will be greatest with external tibial rotation.
An examination while the patient is relaxed under a 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.
Treatment
Isolated LCL ligament injuries, as noted above, are rare. 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 will usually yield good results. Grade III injuries will often not respond as well with conservative treatment. A combination of delayed diagnosis along with an uncertain natural history of posterolateral instability makes the treatment of these injuries a challenge.
LCL and posterolateral ligaments, as discussed above, rarely occur in isolation. Therefore, other injuries must also be considered in the treatment plan of a 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 feasible only in the first few weeks following the knee injury.
The knee with chronic posterolateral instability will often require 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.
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Figure 3-15. A: An oblique view of the proximal tibiofibular joint shows an avulsion fracture of the head of the fibula (arrowhead) due to traction by the lateral collateral ligament and/or the biceps femoris. B: Subluxation of the proximal tibiofibular joint, demonstrated in an oblique view. (Reproduced, with permission, from Anderson J: An Atlas of Radiography for Sports Injuries. McGraw-Hill, 2000. ) |
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The rehabilitation of the knee after posterolateral reconstructions or repairs is largely guided by associated injuries to the ACL or posterior cruciate ligament (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.
Complications
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.
Prognosis & Return to Play
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 do well when an isometric lateral reconstruction is achieved.
Albright J et al: Posterolateral knee instability and the reverse pivot shift. Presented at AOSSM, June 2000, Sun Valley, ID.
Buzzi R et al: Lateral collateral ligament reconstruction using a semitendinosus graft. Knee Surg Sports Traumatol Arthrosc 2004;12(1):36.
Lee MC et al: Posterolateral reconstruction using split Achilles tendon allograft. Arthroscopy 2003;19(9):1043.
Pasque C et al: The role of the popliteofibular ligament and the tendon of popliteus in providing stability in the human knee. J Bone Joint Surg B 2003;85(2):292.
Pavlovich RI, Nafarrate EB: Trivalent reconstruction for posterolateral and lateral knee instability. Arthroscopy 2002;18(1):E1.
Sugita T, Amis AA: Anatomic and biomechanical study of the lateral collateral and popliteofibular ligaments. Am J Sports Med 2001;29(4):466.
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Anterior Collateral Ligament Injuries
Essentials of Diagnosis
Prevention
Many centers are searching for improved methods and protocols to prevent ACL injury. Much of the current research centers around female athletes due to their increased incidence of ACL tears compared to their male counterparts. Strengthening, proprioceptive training, and altering the mechanics of running, jumping, and cutting are all being investigated as methods to prevent ACL injury. Unfortunately, there is no widely accepted method for prevention of ACL injury at this time.
Clinical Findings
The main clinical finding indicative of an acute or chronic ACL tear is a history of a knee injury associated with significant swelling and pain. In most patients this is often followed by symptoms of instability upon returning to athletic activities.
The mechanism of injury should be elicited in any evaluation of a knee injury. This can guide the examination to additional structures that may also be injured. ACL injury can occur from a variety of mechanisms, however, a few predominate. The most common mechanism of noncontact ACL injury 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 is not ACL specific, however. Upon return to competition the patient will often notice instability of the knee or describe the knee “giving out.” Substantial knee swelling secondary to a hemarthrosis typically occurs within the first 4–12 hours following the injury.
With the history obtained above and a proper physical examination, it should be possible to diagnose an ACL tear 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 assessing anterior laxity of the knee. It is performed with the knee in 20–30° of flexion as an anterior force is applied to the tibia with one hand while the other hand stabilizes the distal femur (Figure 3-16). The degree of anterior translation as well as the presence and character of an end point are 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, and grade 3 laxity is more than 10 mm of translation as compared to the injured contralateral knee.
The anterior drawer test is also used to evaluate anterior tibial translation. This is performed with the knee in 90° of flexion as an anterior force is applied to the tibia (Figure 3-17). This test is less sensitive than the Lachman test. In the acute setting of an ACL tear there is often a window in which an accurate examination can be performed before extensive knee swelling and guarding inhibit examination. Aspiration of a hemarthrosis can help to decrease pain and improve the quality of the examination in the acute setting as well.
Plain radiographs of the knee should be obtained to rule out fractures. The Segond fracture (Figure 3-18), as discussed above, 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
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method to evaluate 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.
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Figure 3-16. Lachman test. |
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Figure 3-17. A positive anterior drawer test signifying a tear of the anterior cruciate ligament. (Reproduced, with permission, from Insall JN: Surgery of the Knee. New York: Churchill Livingstone, 1984. ) |
The pivot shift test is performed to evaluate 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 (Figure 3-19). The reduction of the subluxation should occur at approximately 30° of flexion. MCL injury and some meniscal tears may produce a false-negative result.
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.
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Figure 3-18. Segond fracture (also known as the lateral capsular sign) is an avulsion at the attachment of the inferior meniscal ligament and is associated with anterior cruciate ligament rupture. (Reproduced, with permission, from Anderson J: An Atlas of Imaging in Sports Medicine. McGraw-Hill, 1999. |
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), utilizes a series of standard forces to measure anterior translation of the tibia with the knee in 20–30° of flexion similar to the Lachman test.
Treatment
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 have been restored, a gradual return to activities can be attempted to determine the functional level that can be attained without instability.
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Figure 3-19. Pivot shift test. |
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Conservative management with rehabilitation only after an ACL injury generally yields poor results in patients that return to competitive activities. The range of clinically significant episodes of instability resulting in pain, swelling, and disability ranges from 56% to 89% in various studies following a series of conservatively managed ACL tears. These episodes of instability are thought to place the menisci and articular cartilage of the knee at risk for further injury. Fewer than 20% of athletes are able to return to strenuous competition with conservative management of ACL tears.
The decision to surgically reconstruct an ACL tear is individualized based on the patient's desired level of continued competition, age, accompanying degenerative changes, and objective and subjective knee instability. For example, a young, active patient with both objective and subjective knee instability and with a continued desire to compete in sports involving cutting and jumping is an ideal candidate for surgical reconstruction. On the other hand, an older patient with some degenerative arthritis of the knee, minimal desire for continued competitive athletics, and no subjective instability would be much more suited to physical therapy and conservative care.
Early in the history of ACL reconstruction, it was noted that primary repairs of the ligament did not produce a good clinical result. These attempts gave way to various methods of ligament reconstruction using a variety of graft materials. Everything from synthetics to autograft and allograft tissues have been used for reconstruction of the ACL. Over time, bone–patellar tendon–bone and semitendinosis/gracilis hamstring autografts, and bone–patellar tendon–bone allograft constructs have proven to be the most commonly used grafts. All of these constructs have worked well both in the laboratory and clinically 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 placement 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.
Once the graft is in place, proper tension and fixation of the graft must occur to complete a successful ACL reconstruction. Establishing proper tension in the graft is important to the function of the graft clinically. A lax ACL graft may not restore clinical stability to the knee and an overtightened graft may cause the graft to fail 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.
Complications
Although ACL reconstruction usually results in a successful outcome, several potential complications can occur. One of the most common is a loss of knee motion. Efforts to minimize this include obtaining and maintaining full knee extension immediately following surgery. Knee flexion exercises are begun as soon as possible postoperatively and a goal of 90° at 1 week is set. Additionally, patellar mobilization is performed in an attempt to minimize patellofemoral scarring. Another common complication 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.
Prognosis & Return to Play
The goal of any rehabilitation protocol for an ACL reconstruction is to return the patient to the full desired level
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of activity in as short an amount of time as possible while avoiding any complications or setbacks. Because of improved surgical techniques and accelerated rehabilitation protocols, most studies have shown 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 successfully returning 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 include full range of motion, KT-1000 testing within 2–3 mm of the uninjured knee, ≥85% quadriceps strength and full hamstring strength, and functional testing within 85% of the contralateral leg.
An KN: Muscle force and its role in joint dynamic stability. Clin Orthop Related Res 2002;403 suppl:S37.
Bales CP et al: Anterior cruciate ligament injuries in children with open physes: evolving strategies of treatment. Am J Sports Med 2004;32(8):1978.
Beynnon BD et al: The science of anterior cruciate ligament rehabilitation. Clin Orthop Related Res 2002;402:9.
Cascio BM et al: Return to play after anterior cruciate ligament reconstruction. Clin Sports Med 2004;23(3):395.
Dunn WR et al: The effect of anterior cruciate ligament reconstruction on the risk of knee reinjury. Am J Sports Med 2004;32(8):1906.
Huston LJ et al: Anterior cruciate ligament injuries in the female athlete. Potential risk factors. Clin Orthop Related Res 2000;372:50.
McDevitt ER et al: Functional bracing after anterior cruciate ligament reconstruction: a prospective, randomized, multicenter study. Am J Sports Med 2004;32(8):1887.
Spindler KP et al: Anterior cruciate ligament reconstruction autograft choice: bone-tendon-bone versus hamstring: does it really matter? A systematic review. Am J Sports Med 2004;32(8):1986.
Posterior Cruciate Ligament Injuries
Essentials of Diagnosis
Prevention
The energy required to tear the PCL is significant. Beyond maintaining good strength in the musculature around the knee, there is no effective prevention beyond limitations in activity. A direct blow to the knee is the most common sports mechanism for PCL injury and therefore contact sports show the highest incidence.
Clinical Findings
PCL injury is associated with a significant injury to the knee. This is generally seen after a direct blow to the knee or an injury from an impact with the dashboard in a motor vehicle accident. PCL injury is associated with a large hemarthrosis and knee pain.
When evaluating a patient for a PCL injury it is important to determine 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 will 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 will often complain of feelings of instability and giving way. A few characteristic mechanisms of PCL injury differ significantly from the mechanism of ACL injuries. As above, one of the most common mechanisms of PCL injury is the “dashboard” injury during which the anterior tibia sustains a posteriorly directed force from the dashboard with the knee in 90° of flexion. Sports injuries to the PCL come from an outside force or blow in contrast to the typical deceleration twisting mechanism of an ACL injury. The most common methods of incurring a sports-related PCL injury are a direct blow to the anterior tibia or a fall onto the flexed knee with the foot in plantar flexion. The most common mechanism of incurring an 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.
A thorough knee examination should accompany the evaluation of any significant knee injury. Specific cues to injury of 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 a PCL
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injury is challenging due to 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 (Figure 3-20). The knee is flexed to 90° 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 end point are 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 with which to examine the PCL is the posterior sag or Godfrey test (Figure 3-21). This test involves flexing the knee and hip and noting the posterior pull of gravity creating a posterior “sag” of the tibia on the femur. An adjunct to this test involves noting a reduction of this subluxation with active quadriceps contraction.
The reverse pivot shift is the analog 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° of flexion and a palpable reduction of the posterolateral tibial plateau is noted between 20° and 30° 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 has been reported to occur in up to 60% of PCL injuries.
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 (Figure 3-22). In the chronic setting of PCL injury, radiographs are useful to assess for patellofemoral and medial compartment degenerative changes that can occur over time.
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Figure 3-20. Posterior drawer test. |
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Figure 3-21. Godfrey sign. (Reproduced, with permission, from Dutton M: Orthopaedic Examination, Evaluation, & Intervention. McGraw-Hill, 2004. ) |
Although plain films are necessary and useful in evaluating these injuries, MRI has become the diagnostic study of choice for the knee with a presumed PCL injury. It is reported to be 96–100% sensitive at diagnosing PCL tears. Equally or more important, MRI is extremely valuable in its ability to detect associated injuries. This is particularly important in diagnosing posterolateral corner injuries as these can often be missed on the initial clinical examination. In multiligamentous knee injuries, MRI can also be of use in assessing the ACL, as 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 is generally evaluated with radiographs. If these are normal, some surgeons will proceed with a bone scan to evaluate for increased uptake in these areas. If these areas are under increased stress on the bone scan before signs of advanced
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arthritis occur, this subset of patients may benefit from a PCL reconstruction to decrease the stresses seen by these two compartments.
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Figure 3-22. Abnormal tibiofemoral alignment. A lateral view shows posterior displacement of the tibia, indicative of posterior cruciate ligament deficiency. Also note changes of chondromalacia patellae. (Reproduced, with permission, from Anderson J: An Atlas of Imaging in Sports Medicine. McGraw-Hill, 1999. ) |
Treatment
There is considerable controversy regarding treatment of isolated PCL injuries. Multiple factors, including the patient's age, activity level, expectations, and associated injuries, must be evaluated in deciding how to treat a complete PCL rupture. The literature on operative versus nonoperative treatment of these injuries can be difficult to interpret, and there are no long-term follow-up studies of randomized patient groups.
Rehabilitation of the PCL injured knee is often largely dependent on the associated injuries sustained by the knee. This is particularly true with the commonly associated posterolateral corner injury. Therefore, we will focus on the rehabilitation of the isolated PCL injured knee. Regaining motion and regaining strength are the two key objectives of a rehabilitation program. Obtaining full quadriceps strength is essential for achieving the optimal result with conservative 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, the knee is usually 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 do quite well with conservative 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 stress on the patellofemoral and medial compartments of the knee. In patients with PCL injuries followed with serial radiographs, 60% displayed some degenerative changes of the medial compartment.
PCL injuries requiring surgical management include avulsion fractures, isolated acute PCL injuries, multiligament injuries, and chronic PCL insufficiency. Avulsion fractures of the PCL are rare. If nondisplaced, these injuries are treated conservatively. If significantly displaced, these fractures are generally treated with open reduction and internal fixation.
Isolated PCL injuries are usually treated with conservative care by the majority of surgeons at this time. However, nonoperative care of these injuries is not without its own consequences. Although subjectively these patients do relatively well over the short term, many continue to have objective instability and display degenerative arthritic changes over time. A follow-up of patients with PCL-deficient knees at an average of 15 years after injury found 89% had persistent pain and 50% had chronic effusions. All patients in this group showed degenerative changes when followed for 25 years. Therefore, given the risks of continued instability and 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 methods of reconstruction usually involve routing
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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 primary ones 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 still 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 makes the argument for ligament reconstruction more compelling in this patient population. Many of the studies involving PCL reconstruction for these complex knee injuries have involved attempts at primary repair. Although subjective results were generally good, residual pathologic objective laxity was very common following repairs. More recently ligament reconstructions with allografts and autografts have become the dominant method of PCL reconstruction in this challenging patient population.
Complications
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.
Prognosis & Return to Play
Even with conservative management of a PCL injury, the prognosis for a functional recovery and return to competition is very good. PCL laxity can be significantly compensated for by a strong quadriceps muscle and extensor mechanism. Athletes should spend a minimum of 3 months in rehabilitation before attempting a return to competition. However, a subset of patients experiences significant instability with a grade III PCL injury and cannot return to play. This group may benefit from PCL reconstruction.
On the other hand, 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 are essential for optimal recovery, a significant percentage of patients will not be able to return to full competition.
Christel P: Basic principles for surgical reconstruction of the PCL in chronic posterior knee instability. Knee Surg Sports Traumatol Arthrosc 2003;11(5):289.
Giannoulias CS, Freedman KB: Knee dislocations: management of the multiligament-injured knee. Am J Orthop 2004;33(11): 553.
Giffin JR et al: Single-versus double-bundle PCL reconstruction: a biomechanical analysis. J Knee Surg 2002;15(2):114.
Li G et al: Biomechanical consequences of PCL deficiency in the knee under simulated muscle loads—-an in vitro experimental study. J Orthop Res 2002;20(4):887.
Shelbourne KD, Carr DR: Combined anterior and posterior cruciate and medial collateral ligament injury: nonsurgical and delayed surgical treatment. Instruct Course Lect 2003;52:413.
Twaddle BC et al: Knee dislocations: where are the lesions? A prospective evaluation of surgical findings in 63 cases. J Orthop Trauma 2003;17(3):198.
Wind WM Jr et al: Evaluation and treatment of posterior cruciate ligament injuries: revisited. Am J Sports Med 2004;32(7): 1765.
Knee Pain
Anatomy
Patellofemoral
The human knee is one of the most complex mechanical systems in the body. It is designed to accept and redirect very high loads with magnitudes that can be many times body weight. Some of the highest compressive and tensile loads are transmitted by the patellofemoral joint. Understanding the functional anatomy of the patellofemoral joint allows musculoskeletal specialists to better identify injuries and direct appropriate treatments. Despite its seemingly simple construction, the patellofemoral joint is one of the more complex anatomic regions of the knee. It is composed of multiple fascial layers, ligamentous attachments, bursae, and bony landmarks.
Fascial
Anatomic descriptions are most easily understood by proceeding from the most superficial subcutaneous layer to the deep capsular layer (Figure 3-1). The subcutaneous layer is the most superficial and contains relatively little fat. The skin overlying the patella is highly mobile and allows for extensive and uninhibited range of motion. As this layer progresses medially and laterally, the number of small perpendicular fascial attachments increases. These fascial attachments contain the subcutaneous prepatellar bursa in its anterior location. A more inferior subcutaneous prepatellar tendon bursa can be found immediately anterior to the patellar tendon. The
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bursae are highly variable in both their anatomic and their clinical location. The next deepest layer, the superficial fascial or arciform layer, is an extension of the fascia lata and is named for is transverse or “arcing” orientation over the anterior knee. This superficial fascial layer covers the iliotibial band on the lateral side, the distal quadriceps muscle on the medial side, and the patellar tendon inferiorly, and ends at the level of the tibial tubercle. This layer does not contribute to the patellar tendon, but its fibers are cut and often repaired during the patellar tendon harvest used for ACL reconstruction.
The intermediate oblique layer exists as a fascial layer anterior to the patella and is composed of fibers from the anterior portion of the rectus femoris, vastus medialis, and vastus lateralis. This layer is thicker than the arciform layer, and its fibers blend into the deeper layers just medial and lateral to the patellar margins, however, it does not contribute fibers to the patellar tendon. The potential space that lies superficial to the intermediate layer but deep to the arciform layer contains the intermediate prepatellar bursa. The deep longitudinal layer is derived from the rectus femoris and is named for the direction of its fibers as they course across over the anterior patella and become contiguous with the patellar tendon prior to inserting on the tibial tubercle. These fibers are adherent to the patella and provide the deep margin for the deep prepatellar bursa (Figure 3-5). The next deepest layer has thick fibers that are transverse in their orientation and form the medial and lateral retinaculum. These fibers provide a major static restraint to the patellofemoral articulation. The medial retinacular layer runs from the medial surface of the patella and inserts on the medial femoral condyle. The lateral retinacular layer runs from the lateral surface of the patella passing deep to the iliotibial tract and inserts on its undersurface. The deepest layer includes the capsular attachments from the medial and lateral borders of the patella as they insert on the medial and lateral meniscus (Figure 3-8).
Muscular & Ligamentous
Although the hamstrings and quadriceps are the major muscle groups that contribute to knee motion, the quadriceps muscle group also plays a critical role in patellofemoral joint structure and stabilization (Figure 3-2). The primary role of the quadriceps is deceleration through eccentric contraction during normal ambulation (Figure 3-3). At the level of the mid-thigh, the group includes the rectus femoris, vastus medialis, vastus lateralis, and vastus intermedius muscles. At the knee joint, the vastus medialis gives rise to the vastus medialis obliquus and the vastus lateralis becomes the vastus lateralis obliquus. The rectus femoris originates on the anterior inferior iliac spine and its tendinous insertion begins on the anterior surface of the patella and continues over the anterior surface as it travels distally and becomes part of the patellar tendon. The vastus intermedius lies deep to the rectus femoris. It originates from the anterior surface of the proximal femur and has a broad fibrocartilaginous insertion on the superior pole of the patella. Its broad fibrocartilaginous insertion serves to distribute load equally across a large portion of the quadriceps tendon insertion. The articularis genus lies deep to the vastus intermedius. It originates on the distal femur and inserts on the superior capsule of the suprapatellar pouch. It serves to retract the suprapatellar pouch during knee motion and often contributes to the formation of the medial and suprapatellar plicae. The vastus medialis and vastus lateralis muscles originate from the anterior surface of the proximal femur just medial and just lateral to the vastus intermedius origin, respectively. They insert on the superior medial and superior lateral borders of the patella. The vastus medialis is usually large in size and has a more distal insertion, whereas the vastus lateralis has a long tendinous insertion on the superior lateral patella. The lateral side also receives contributions from the iliotibial tract. In addition, the vastus medialis obliquus serves an important role in medial stabilization of the patella as the knee approaches full extension.
Whereas the quadriceps musculature functions as an important dynamic patellar stabilizer, several medial ligamentous structures function as important static soft-tissue restraints to prevent lateral translation of the patella. The major medial soft tissue stabilizer, the medial patellofemoral ligament (MPFL), provides 53% of the total restraining force to lateral displacement of the patella. The patellomeniscal ligament provides 22% of the total restraining force, and the medial retinaculum ligament and medial patellotibial ligament provide lesser contributions (Figure 3-7).
Patellar Tendon
The patellar tendon has a complex organization that allows for transmission of high tensile loads from its origin on the inferior pole of the patella to its insertion on the tibial tubercle. Its fibers have a broad origin from the posterior and inferior surfaces of the patella and include anterior contributions from the rectus femoris as they progress distally to a broad insertion on the tibial tubercle. The patellar tendon is composed of densely packed collagen fibers that are primarily arranged parallel to the long axis of the tendon. Eighty-five percent of its dry weight is collagen, the majority of which is type I (90%). The tendon is surrounded by three layers: the outermost paratenon, an inner epitenon, and an innermost endotenon. The blood, nerve, and lymphatic
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supply to the tendon is via the endotenon, which serves to bind and bring nutrients to individual cells and collagen fibers.
Patella
The patella acts as a fulcrum and provides a mechanical advantage to the quadriceps during force transmission across the knee joint. The forces across this fulcrum are complex and include high degrees of compression and tension, with a minimal amount of friction. The patellar osseous and cartilaginous anatomy is equally complex and its design reflects its function (Figure 3-7). The anterior surface of the patella is convex and is composed of fibrous insertions from the rectus femoris and perforations for blood supply from the genicular vessels. The posterior articular surface contains thick cartilage that covers three facets. The lateral facet is the largest and extends from the superior pole to the inferior pole and articulates with the lateral femoral condyle. It is separated from the medial facet by a longitudinal central ridge that articulates with the femoral trochlear groove. The medial facet also extends from the superior to the inferior pole, but is approximately one-third smaller than the lateral facet and articulates with the medial femoral condyle. A smaller “odd” facet lies medial to the medial facet and articulates with the medial femoral condyle only during the extremes of knee flexion. The thick cartilage that covers these facets serves to increase patellofemoral congruity and dissipate compressive loads during the wide range of knee motion.
Peeler J et al: Structural parameters of the vastus medialis muscle. Clin Anat 2005;18(4):281.
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.
Anterior Knee Pain
Patients who present with anterior knee pain are common in the practice of general orthopedics and sports medicine. The most frequent causes of anterior knee pain in the athlete include overuse injuries, patellofemoral instability, and direct trauma. Although anterior knee pain can come from many of the structures described above, in the most general sense, the cause of pain can be organized into the following categories: anterior knee pain with articular breakdown, anterior knee pain without articular breakdown, and anterior knee pain related to patellofemoral instability. Pain that is derived from the patellofemoral joint with articular breakdown often includes patients with the diagnosis of articular cartilage softening, known as chondromalacia, or frank patellofemoral chondrosis/ arthrosis. Anterior knee pain without evidence of articular breakdown includes patients with the diagnosis of patellar tilt-compression or some other form of patellar malalignment that precedes cartilage injury, patellar tendinitis or “jumper's knee,” synovial plica, painful retinaculum, infrapatellar contracture syndrome, and, in children, Osgood–Schlatter disease. Anterior knee pain related to patellofemoral instability usually results from patellar tilt with or without patellar subluxation. The essentials of the diagnosis and treatment of the most common of these disorders will be described below.
Differential Diagnosis
The terms patellofemoral chondrosis or patellofemoral arthritis are reserved for describing the degenerative changes specifically observed in the patellofemoral articulation, whereas the term chondromalacia patellae is used to describe the breakdown of articular cartilage on the undersurface of the patella. Degenerative changes such as patellofemoral chondrosis or chondromalacia often cause the pain that arises from the patellofemoral joint. Because articular cartilage is not innervated, it is believed that the pain is derived from abnormal force transmission across degenerative articular cartilage to subchondral bone. Damage to the articular surface can range from localized articular softening to full-thickness lesions with exposed subchondral bone. The etiology of patellofemoral chondrosis is highly variable and includes damage to articular cartilage due to direct trauma, chondral injury following acute patellar dislocation, patellofemoral malalignment, and chronic subluxation.
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Essentials of Diagnosis
—Anterior knee pain with activity, for example, with stairs, running, or squatting.
—History of trauma to the anterior knee or patellar dislocation.
—History of effusions or crepitus from the patellofemoral joint.
—Knee effusions and crepitus are common and can be nonspecific.
—Quadriceps wasting or weakness.
—Pain with patellofemoral compression during knee range of motion.
—Radiographs often read as normal except in end-stage arthrosis.
—Abnormal patellar tilt and subluxation are often present on Merchant view or CT.
—MRI can localize and quantify the extent of articular damage.
—Knee arthroscopy is the gold standard for evaluation and initial treatment.
—Useful for grading, localization, and planning treatment strategies.
Pathogenesis
During the initial history and examination it is important to ask questions about previous knee injuries, knee trauma, duration of symptoms, as well as exacerbating and remitting factors. Previous injury, surgery, and type of sport can be critical in narrowing the differential diagnosis. It is also important to distinguish symptoms of pain from those of instability. A careful history and physical examination should steer the physician to one of the three general categories listed in the differential diagnosis: anterior knee pain without evidence of articular breakdown, anterior knee pain with evidence of articular breakdown, and anterior knee pain resulting from patellofemoral instability. Plain radiographs should be obtained in all patients with possible patellofemoral pathology and should include an anteroposterior view, lateral view, tunnel view, and Merchant view. Other ancillary studies such as CT or MRI are indicated in certain cases as outlined below.
Prevention
Anterior knee pain in athletes is commonly related to overuse. The key to prevention is the identification and modification of factors that predispose the athlete to developing symptoms. Sport-specific training programs that include balanced quadriceps strengthening and patellar stabilization exercises are important elements for both the prevention of injury and long-term rehabilitation following previous injury.
Clinical Findings
Anterior symptoms related to patellofemoral chondrosis are typically described as deep and aching pain that worsens with activity or with sitting for prolonged periods with the knee in a flexed position. Symptoms are often vague and poorly localized beyond the anterior knee or patellofemoral joint. Patients with patellofemoral subluxation describe a feeling of instability localized to the anterior aspect of the knee. A history of previous patellar dislocation may be present, but more often, symptoms related to extensor mechanism imbalance are present in the history. Particular activities that increase patellofemoral contact pressures such as running, stair-climbing, and deep squats tend to exacerbate symptoms. Patients also describe intermittent knee effusions that often correlate with periods of increased activity. Popping and crepitus are common, but can be nonspecific findings present in many of the diagnoses listed above. In general, symptoms usually become worse with activity and improve with rest.
The correlation of clinical findings to articular changes is critical in both the diagnosis and treatment of anterior knee pain due to patellofemoral arthritis. Many patients may have symptoms of anterior knee pain without articular change, and previous studies have documented articular changes during arthroscopy in patients who did not have symptoms of pain. The physical examination and radiographic studies are important keys to narrowing the differential diagnosis prior to proceeding with various treatment options including knee arthroscopy.
All physical examinations should be performed with the athlete barefoot and wearing shorts to allow inspection and examination of the entire lower extremity. In general the athlete's attitude and cooperation with the examination may provide important clues for previous or future compliance with treatment and rehabilitation protocols. The examination should begin with an evaluation of the athlete's stance and gait, followed by careful examination of the hip, particularly in adolescents, as knee pain is often the result of hip pain until proven
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otherwise. Examination of the knee joint begins with inspection for overall femoral–tibial and patellofemoral alignment. Evaluation of the skin may point toward a diagnosis of reflex sympathetic dystrophy, particularly in patients with pain out of proportion to injury. Quadriceps, hamstring, and calf muscle size, definition, tone, strength, and flexibility should be assessed. Evaluation of active and passive knee range of motion focusing on knee joint stability and patellofemoral tracking throughout a full range of motion may aid in narrowing the differential diagnosis. Prone positioning is particularly helpful in evaluating quadriceps tightness and patellar tendon pathology. A careful ligamentous examination including the collaterals and cruciates should follow and may help identify other potential causes of knee pain or instability. Examination of the PCL is particularly important as chronic PCL tears have been associated with patellofemoral arthrosis. Tenderness to palpation may be present in a variety of locations and can help differentiate meniscal pathology (medial or posteromedial joint line tenderness) from the anterior retinacular pain often associated with patellofemoral pathology.
The physical examination of the athlete with ordinary patellofemoral chondrosis related to overuse is relatively nonspecific. Other causes of knee pain must be excluded by a careful history and complete physical examination. Crepitus and effusions are common, as is quadriceps wasting. Once the diagnosis of patellofemoral chondrosis or chondromalacia patellae is suspected, it is important to try and isolate the location of the articular pathology. This can be determined by applying patellofemoral compression while taking the knee through a full range of motion and documenting the point or points at which maximal pain occurs. The quadriceps angle (Q angle) should be documented with the knee in slight flexion and at 90° (Figure 3-6). An abnormal Q angle and patellar apprehension with attempts to move the patella laterally out of the trochlea may indicate chronic subluxation due to patellar malalignment or a tight lateral retinaculum. This will be discussed further in the section on patellar maltracking.
Articular degeneration within the patellofemoral joint can be classified into four types based on location and may identify potential causes and guide treatment strategies. Type I includes a distal mid-patellar lesion that is caused by chronic subluxation and/or patellar tilt. Type II lesions are subdivided into IIA and IIB: IIA lesions result from lateral patellar pressure syndrome and exhibit articular breakdown of the lateral patellar facet; IIB lesions, which include combinations of types I and IIA, also result from chronic subluxation and excessive patellar tilt. Type III lesions involve the medial patellar facet and can result from a variety of causes including a forceful reduction of acute patellar dislocation and deficient contact pressures secondary to chronic subluxation/patellar tilt, or can follow tibial tubercle transfers with posterior displacement of the tibial tubercle. Type IV lesions include IVA lesions, which involve the proximal patella, and IVB lesions, which involve the proximal patella plus at least 80% of the whole patella. Type IV lesions are typically the result of direct trauma to the anterior aspect of the flexed knee. In general, distal lesions are more painful early in the knee flexion arc, whereas proximal lesions are more painful during deep flexion.
Initial radiographic evaluation includes standard weight-bearing anteroposterior, lateral, and tunnel views, as well as an axial Merchant view. Although the anteroposterior and lateral views provide important clues regarding patellar alignment, particularly with regard to patellar alta and baja, the axial Merchant view may show subtle irregularities such as joint space narrowing in the lateral patellofemoral joint. It is often useful for diagnosis of patellar tilt, with and without frank patellar subluxation. The Merchant view is typically taken with the knee flexed 45° and the x-ray beam projected caudad at an angle of 30° from the plane of the femur (Figure 3-4). Radiographic evaluation is often normal, particularly in the early stages of patellofemoral chondrosis. CT scan is typically reserved for evaluation of patellar maltracking (Figure 3-9). It offers sequential axial images at any desired degree of knee flexion, and therefore allows the physician to determine the specific pattern of patellofemoral malalignment. In addition, in more advanced cases, CT allows visualization of subchondral and cystic irregularities that are often present in the lateral patellofemoral joint. MRI is perhaps the most useful imaging modality to quantify the extent and location of articular surface injury. Because it provides very clear images of chondral, osteochondral, and soft tissue lesions throughout the knee it is a useful tool in the diagnosis of patellofemoral chondrosis, but is often less helpful than plain radiographs and CT in evaluating patellofemoral malalignment.
Treatment
Treatment of anterior knee pain due to patellofemoral chondrosis or chondromalacia usually begins with nonoperative management. After rest, NSAIDs, and modification of activity have decreased the acute symptoms, a well-structured rehabilitation program is ordered. The program should focus on stretching of the extensor mechanism, iliotibial tract, retinaculum, and hamstrings. Strengthening of the quadriceps, which is also important, is usually directed toward the vastus medialis obliquus (VMO) as it is the major dynamic medial patellar stabilizer. The VMO is believed to be deficient
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relative to the larger vastus lateralis and thus is unable to resist lateral patellar subluxation. It is important to encourage short-arc quadriceps strengthening exercises and straight leg rises to minimize the patellofemoral joint reactive force. Additional modalities include elastic knee supports, patellar taping, orthotics, and reassurance. The majority of patients with anterior knee pain due to isolated patellofemoral chondrosis will improve with nonoperative modalities. Persistent pain, effusions, and crepitus in conjunction with patellar malalignment indicate worsening articular cartilage degeneration and alternative treatment strategies should be pursued.
A variety of surgical treatment options for patello-femoral chondrosis exist. For the athlete these include procedures directed at anatomic realignment and in some cases articular cartilage regeneration. For severe end-stage patellofemoral arthrosis, joint resurfacing and patellectomy have sometimes been advocated.
Knee arthroscopy is an important part of both the diagnostic evaluation and the potential treatment. Although diagnostic arthroscopy with lavage and debridement has been controversial, it is helpful for staging lesions and for planning future surgical treatments. In general, arthroscopic lavage relieves pain and improves function in the short term by removing debris and inflammatory proteoglycans. Because the pathology is often not addressed by this procedure, symptoms usually return. In cases involving isolated lesions, diagnostic arthroscopy allows the lesion to be graded and provides exposure for other modalities.
The grading system defined by Outerbridge is most commonly used because of its simplicity and reproducibility. This system grades lesions based on lesion depth and must be combined with documentation of the location, shape, and size of the lesion. Grade I lesions include articular surfaces that are swollen, soft, and in some cases blistered. Grade II lesions are characterized by articular fissures and clefts with diameters <1 cm. Grade III lesions include deep fissures extending to subchondral bone with diameters >1 cm. Finally, grade IV lesions include those with exposed subchondral bone.
The use of lavage and debridement for treatment of traumatic lesions has yielded better results in patients without evidence of patellar instability than in patients with degenerative or atraumatic lesions. For patients with known patellar tilt and minimal articular involvement of primarily the lateral facet, lateral release at the time of arthroscopic evaluation has been advocated. To be effective, lateral release must be reserved for patients with objective evidence of patellar tilt and without severe articular breakdown. In general, arthroscopic lavage and debridement with or without lateral release are reserved for grade and I and II lesions, as long-term results are generally poor with grade III and IV lesions. In cases involving more advanced articular degeneration, arthroscopic chondroplasty has been advocated. The techniques of abrasion arthroplasty or microfracture chondroplasty include mechanical penetration of subchondral bone and subsequent delivery of marrow-derived mesenchymal stem cells to articular defects to induce a fibrocartilaginous healing response. Arthroscopic chondroplasty is typically reserved for patients younger than 30 years with relatively well-defined grade III lesions. It is not indicated for more advanced articular defects or damage.
Additional treatment strategies are directed toward restoration or regeneration of normal hyaline articular cartilage. These strategies include autologous chondrocyte implantation (ACI), osteochondral autograft transfer, mosaicplasty, and osteochondral allograft transplantation. Although an in-depth discussion of each of these procedures is beyond the scope of this chapter, some key points will be highlighted. ACI was developed for the treatment of significant, symptomatic, full-thickness chondral defects involving the femoral condyle. The procedure involves harvesting autologous chondrocytes, expanding the cells in culture, and reimplanting them under a periosteal flap after debridement of the articular lesion. Results have been variable, but long-term follow-up in a multicenter study has reported 79% good to excellent results. In general, ACI is indicated in younger (aged 20–50 years) active patients with isolated (2–4 cm 2) traumatic femoral condyle defects. Results in patients with trochlear or patellar defects are much less predictable. Contraindications include diffuse osteoarthritis, instability or abnormal tracking, and previous meniscectomy.
Osteochondral autograft transfer and mosaicplasty are appealing because they can use normal donor articular cartilage to replace deep lesions. Both techniques are dependent on surgical skill to match or recreate the topography of the surface being replaced. In addition, donor sites are limited and raise the potential of donor-site morbidity. Osteochondral allografts are typically reserved for larger (10 cm2 or greater) defects of the femoral condyles and are often used after previous treatments have failed. Fresh allografts allow greater chondrocyte survivability but carry an associated risk of an immunologic response and the potential for disease transmission. Additional considerations include a technically demanding procedure and the need for the surgeon and patient to be available on relatively short notice. Although fresh-frozen allografts confer decreased immunogenicity and allow for greater flexibility with regard to timing of the procedure, chondrocyte viability is a major concern that may affect long-term graft viability. Patellectomy and patellar resurfacing are reserved for patients with extensive articular damage to the patella, significant functional limitation related to pain, and
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failure of previous treatments. Results of both procedures are inconsistent. Major anatomic realignment procedures such as osteotomy, tibial tubercle transfer and elevation, and others will be discussed in the section on patella maltracking.
Prognosis
Ultimately the goal of a patellofemoral rehabilitation program is to return the patient to an acceptable level of preinjury performance or activity. To achieve this goal, rehabilitation should initially be directed toward decreasing inflammation, restoring range of motion, and regaining muscle strength, endurance, power, and flexibility while maintaining the athlete's overall cardiovascular fitness. In the final stages of rehabilitation, therapy should focus on regaining proprioceptive awareness, agility, and functional skills with sport-specific exercise and activity. The rehabilitation program must therefore be individualized and should consider the athlete's age, prior level of muscular and cardiovascular performance, familiarity with exercise equipment, and degree of motivation.
Return to Play
Regardless of the treatment strategy utilized, return to athletic activities is dependent on the restoration of normal motion, stability, and strength to the involved lower extremity. A four-phase rehabilitation protocol should be complete, and patients should be able to perform sport-specific rehabilitation activities without significant pain, functional limitation, or recurrence of knee effusions. Counseling regarding continued use of sport-specific exercises and avoidance of activities that increase patellofemoral contact pressures should also be emphasized.
Aderinto J, Cobb A: Lateral release for patellofemoral arthritis. Arthroscopy 2002;18:339.
Browne JE, Branch TP: Surgical alternatives for treatment of articular cartilage lesions. J Am Acad Orthop Surg 2000;8:180.
Cartilage Repair Registry Report: Genzyme Tissue Repair, Vol 4. Cambridge, MA, February 1998.
Christoforakis JJ, Strachan RK: Internal derangements of the knee associated with patellofemoral joint degeneration. Knee Surg Sports Traumatol Arthrosc 2005;13(7):581.
Minas T, Chiu R: Autologous chondrocyte implantation. Am J Knee Surg 2000;13:41.
Steadman JR et al: Outcomes of microfracture for traumatic chondral defects of the knee: average 11-year follow-up. Arthroscopy 2003;19:477.
Patellar maltracking falls under the general category of patellar instability and includes disorders such as patellar tilt, patellar subluxation, and patellar dislocation. In general, patellar maltracking most commonly presents in the form of abnormal patellar tilt with or without lateral subluxation. Although this can be caused by a variety of factors, it is most commonly multifactorial and includes elements of a tight lateral retinaculum, VMO atrophy, and preexisting malalignment such as genu valgum or hyperlaxity.
Essentials of Diagnosis
—Feeling of anterior knee instability or anterior knee pain.
—History of trauma to the anterior knee or previous patellar dislocation.
—History of previous knee surgery or lateral retinacular release.
—Extensor mechanism imbalance with VMO wasting or weakness.
—Apprehension or reverse apprehension with lateral or medial patellar displacement.
—Patellar hypermobility, patella alta, and abnormal Q angle are hallmarks.
—Abnormal patellar tilt and subluxation are often present on axial radiographs.
—CT may reveal subtle patellar tracking abnormalities.
—MRI is useful for evaluating soft tissue structures (ie, MPFL) as well as for articular cartilage damage.
Pathogenesis
A thorough history and a physical examination including timing of onset, duration of symptoms, mechanism of injury, and previous patellofemoral problems are critical in narrowing the differential diagnosis. In general, patients with lateral subluxation describe a feeling of anterior instability and pain in the patellofemoral joint. Occasionally, patients also note the presence of an effusion, crepitance, and catching in the anterior aspect of the knee. They also have a history of previous knee injury or prior knee surgery. In patients with lateral patellar compression syndrome or patellar tilt, the onset of symptoms is often insidious and can be associated with minor trauma. This condition is caused by a tight lateral retinaculum that causes increased contact pressures between the lateral patellar facet and the lateral femoral trochlea. Patients often complain of diffuse anterior knee pain that localizes to the lateral retinaculum during knee flexion.
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Clinical Findings
With patellar maltracking, the patella articulates abnormally with the femoral trochlea so that it subluxes either laterally or medially. Lateral subluxation is the more common form of malalignment and is usually the result of overall malalignment of the involved lower extremity including genu valgum or generalized hyperlaxity. In patients with this form of malalignment, the patella is usually stabilized by the femoral trochlea during knee flexion but shifts laterally from the trochlear groove as the knee approaches full extension. Patients usually complain of the knee “giving way” during these episodes, although they rarely suffer a frank patellar dislocation. The less common form of patellar instability is medial subluxation. This is usually the result of an iatrogenic injury following a lateral release that is too extensive or poorly indicated. Both types of patellar subluxation can predispose patients to patellofemoral chondrosis. The subsequent arthritis that can develop as a result was discussed in the previous section. Patellar maltracking can also predispose athletes to acute patellar dislocation, although this injury is uncommon. Two mechanisms have been proposed: a more common indirect injury and a less common direct blow. Either mechanism can result in articular damage to either the lateral condyle of the femur or the medial patellar facet, or to both.
The basic elements of the general knee examination outlined above apply here as well. The examination should begin with an evaluation of the athlete's stance and gait. Various risk factors predispose athletes to patellar instability and must be evaluated during the initial physical examination. These factors include excessive femoral anteversion, genu valgum, patellar dysplasia, femoral dysplasia, patella alta, VMO atrophy, high Q angle, pes planus, and generalized hyperlaxity. Examination of the knee joint continues with inspection of overall femoral–tibial alignment and patellofemoral alignment. On initial inspection the Q angle should be measured and documented. This angle is measured from a line connecting the anterosuperior iliac spine and the mid-patella, and a line connecting the mid-patella and the tibial tubercle (Figure 3-10). The Q angle is commonly used as a measure of the valgus moment acting on the patellofemoral joint. In general, females have larger Q angles than males, and normal includes angles up to 20° for females and 15° for males. Q angles are increased by genu valgum, a laterally displaced tibial tubercle, increased femoral anteversion, and external tibial torsion. Although a Q angle does not necessarily predict anterior knee pain or patellar subluxation, it does potentially contribute to patellofemoral malalignment as the quadriceps contracts.
Gross dynamic evaluation of patellar tracking can be evaluated by passively extending the knee while the patient is sitting. In general the patella should follow a midline course throughout the full range of motion. In some cases, a “J sign” may be seen. This refers to the path that the patella travels (upside down J) in cases in which patellar maltracking is present and the patella is pulled laterally as the knee approaches full extension. A reverse J sign can be seen in cases of medial patellar subluxation in which the patella is pulled medially as the knee approaches full extension. If the J sign is seen during open chain knee extension, it can be indicative of VMO deficiency and may thus direct further treatment strategies.
The medial and lateral retinacular structures should also be carefully evaluated. Tenderness to palpation along the medial or lateral retinacular structures is common when these tissues are overloaded in patients with patellofemoral malalignment. Tenderness specifically over the medial epicondyle, known as Bassett's sign, may represent an injury to the MPFL in patients with a history of patellar dislocation. An additional test directed specifically at detecting a tight lateral retinaculum is the patellar tilt test. This test is performed with the knee relaxed and passively extended. The medial patellar facet is stabilized as attempts are made at lifting the lateral patellar facet. In normal patients, the lateral edge of the patella should lift approximately 15° beyond the horizontal plain. If this is not possible, a tight lateral retinaculum may be the cause of anterior knee pain and a subsequent lateral release may be indicated. The patellar apprehension test is particularly useful with regard to evaluating patellar instability (Figure 3-11). A positive test occurs when pain and guarding are elicited during lateral translation of the patella. This is highly suggestive of patellar hypermobility or instability.
The medial and lateral patellar glide tests assess for the integrity of the static retinacular restraints. The lateral patellar glide test includes evaluation of the medial joint capsule, medial retinaculum, and VMO. The patella is manually translated in the lateral direction and the distance is measured as the number of quarter widths that the patella is displaced beyond its neutral position in the trochlea. A value greater than three-quarters width indicates hypermobility, whereas a value less than one-quarter width with the medial patellar glide test indicates a tight lateral retinaculum. Although this test can provide useful information regarding the retinacular structures it is highly examiner dependent.
Although the majority of the examination is performed with the patient supine, it is also important to examine the knee with the patient prone. By stabilizing the pelvis and eliminating hip flexion, prone positioning allows accurate assessment of extensor mechanism flexibility. In addition, excessive femoral anteversion and tibial torsion can be easily assessed. Decreased internal
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rotation may be indicative of early hip osteoarthritis and pain that may be referred to the knee.
The initial radiographic evaluation of the patellofemoral joint should include standard weight-bearing anteroposterior and lateral views, as well as an axial view (Figure 3-12). The anteroposterior view is useful for evaluating gross subluxation, fracture, or deformity of the patella. A true anteroposterior view must be verified before any determinations about patellar subluxation are made. The lateral view allows several important assessments. First, it provides valuable information about trochlear depth and morphology. The center of the trochlea will be seen as the most posterior line, and the medial and lateral trochlear facets can also be visualized separately. Using these landmarks allows the measurement of the appropriate trochlear depth and the assessment of potential facet dysplasia. Additional information regarding patella alta or baja can be determined from the lateral radiograph by calculating the ratio of the patellar tendon length to the greatest diagonal length of the patella. Values for normal ratios are between 0.8 and 1.0, whereas values greater than 1.0 indicate patella alta and lower values indicate patella baja.
The axial radiograph provides additional valuable information about patellar tracking. The Laurin axial radiograph is obtained with the knee flexed to 20°, whereas the Merchant view is obtained with the knee flexed to 40°. Either one of these views is acceptable and will minimize radiation exposure. The axial radiograph is the most helpful in evaluating patellofemoral alignment and diagnosing patellar tilt or patellar subluxation. Two angles are measured using this radiograph, the Laurin lateral patellofemoral angle and the Merchant congruence angle. The Laurin lateral patellofemoral angle is measured between a line drawn across the femoral condyles and a line drawn along the lateral patellar facet. Normally, this angle opens laterally, however, in cases in which the angle is parallel or opens medially, patellar tilt is likely. The Merchant congruence angle is used to assess patellar subluxation. It is measured by bisecting the femoral sulcus angle and measuring the angle between this bisector and the line drawn from the lowest point in the sulcus to the median patellar ridge. Normal congruence is -6 ± 11° with the knee at 45° of flexion. The patella should be centered within the trochlea at this angle of knee flexion and abnormal congruence indicates the potential for patellar subluxation.
CT confers several advantages over axial radiographs in the evaluation of patellar maltracking. Although many of the same measurements can be made as on axial radiographs, axial CT images offer little distortion and no image overlap. In addition, CT images can be obtained at any angle of knee flexion. This is particularly useful in assessing patellar maltracking as the knee approaches terminal extension and the patella is no longer stabilized by the lateral femoral condyle (Figure 3-13). An additional advantage of CT versus axial radiographs is the ability to evaluate lateralization of the tibial tubercle. This is assessed by measuring the distance between the tibial tubercle and trochlear sulcus when two appropriate axial images are superimposed. A value greater than 9 mm has been shown to identify patients with abnormal patellofemoral alignment with 95% specificity and 85% sensitivity. Although MRI can be used to verify the osseus findings on plain radiographs and CT, it is most useful for visualization of soft tissues and evaluation of articular cartilage damage. MRI has also been found useful in the identification of findings associated with patellar dislocation. These include tearing of the MPFL from the femoral insertion, the less common avulsion of the MPFL from the medial patellar facet, joint effusion, increased signal intensity and injury to the VMO, and bone bruises in the lateral femoral condyle and medial patellar facet.
Treatment
As dynamic patellar instability is the most common cause of anterior knee pain resulting from patellar maltracking, nonoperative treatments provide the mainstay of therapy. After careful evaluation of quadriceps strength using isokinetic testing, an appropriate rehabilitation protocol can be developed. Again, the goal of any patellofemoral rehabilitation program is to return to an acceptable level of athletic performance by decreasing inflammation, restoring range of motion, and regaining muscle strength, endurance, power, and flexibility. Quadriceps strength, power, and endurance are most effectively improved with short-arc isotonic quadriceps extension exercises in the range of 0–30° of knee flexion where patellofemoral contact pressures are the lowest. Exercises should focus on restoring a balanced extensor mechanism with particular attention directed toward the VMO. The symptoms of patellofemoral instability can often be improved with patellar stabilization braces or patellar taping, both of which require patient compliance. Orthotics have also been shown to improve alignment of the lower extremity, particularly in patients who have valgus thrust that may contribute to patellar instability. Although most patients with patellar instability will improve with a well structured nonoperative treatment program, patients with persistent and disabling symptoms often require surgical treatment.
As is true for most patellofemoral disorders causing anterior knee pain, surgical treatment begins with a complete
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arthroscopic examination. The examination should then use the superomedial portal to focus on the patellofemoral joint throughout the full knee range of motion. Patellar tilt can be evaluated as the knee approaches extension. In addition, passive patellar tracking is assessed as the knee is taken through a full range of motion. Normal tracking is present when the lateral facet aligns with the trochlea at approximately 20–25° of knee flexion and the midpatellar ridge by 35–40° of flexion. Lateral overhang of the lateral patellar facet should be noted as the patella engages the trochlea. When used in combination with objective clinical or radiographic evidence of patellar subluxation, this can direct additional surgical realignment procedures.
Arthroscopic lateral release is indicated in patients with patellar tilt but without abnormal medial or lateral patellar glide. An adequate release includes the entire lateral retinaculum, vastus lateralis obliquus, and distal patellotibial band. Complete vastus lateralis release has been reported, but should be avoided to prevent retraction and atrophy with subsequent quadriceps imbalance. Lateral release should not be performed in patients without objective evidence of patellar tilt as iatrogenic medial subluxation can result. The most common complication following lateral release is hemarthrosis and delayed rehabilitation. This can be avoided by evaluation of the release with the tourniquet deflated prior to closure.
In patients who have failed nonoperative treatment and who have objective evidence of patellar subluxation, surgical treatment is often indicated. Multiple realignment procedures have been described, and the surgical procedure is determined by the type of patellar subluxation. Both proximal and distal realignment procedures exist. Proximal realignment procedures are directed at the dynamic elements of the extensor mechanism and include medial capsular imbrication, advancement of the vastus medialis, and advancement of the VMO. All procedures are aimed at centralizing the patella within the femoral sulcus and improving patellofemoral congruency through a full range of motion. For many patients with lateral subluxation due to patellofemoral malalignment, a distal realignment procedure such as an anteromedial tibial tubercle transfer usually produces satisfactory results. Medialization of the tibial tubercle typically corrects the abnormal Q angle, whereas moving the tubercle anteriorly unloads the patellofemoral joint and helps prevent the degenerative changes observed with direct medial tibial tubercle transfer. Arthroscopic evaluation should be used to verify alignment during these procedures to prevent over- or undercorrection.
The surgical treatment of patellar dislocations is controversial. Although surgical treatment is usually indicated only after patients have failed a comprehensive nonoperative treatment program, the chance of redislocation ranges anywhere from 15–44%. Recent studies have revealed markedly decreased rates of redislocation with surgical treatment in young athletic patients with acute patellar dislocation. The surgical procedure is aimed at open repair of the MPFL injury and may require additional realignment procedures. Again, arthroscopy is required both for the evaluation of patellofemoral tracking and for the evaluation of osteochondral lesions that are often associated with acute patellar dislocations. Chronic patellar dislocations are treated with the realignment procedures previously described.
Prognosis & Return to Play
Most patients with instability related to patellar tilt and/or patellar subluxation do well. Regardless of the treatment strategy utilized, return to athletic activities is dependent on the restoration of normal motion, stability, and strength to the involved lower extremity. Return to activity should be gradual. Therapy should be adjusted according to the procedure performed and allow adequate time for healing of skin, soft tissues, and bone. Ultimately, a four-phase rehabilitation protocol should be complete, and patients should be able to perform sport-specific rehabilitation activities without significant pain, functional limitation, or recurrence of symptoms.
Atkins DM et al: Characteristics of patients with primary acute lateral patellar dislocation and their recovery within the first 6 months of injury. Am J Sports Med 2000;28:472.
Katchburian MV et al: Measurement of patellar tracking: assessment and analysis of the literature. Clin Orthop Relat Res 2003;412:241.
Palmer SH et al: Surgical reconstruction of severe patellofemoral maltracking. Clin Orthop Relat Res 2004;419:144.
Historically, the term patellar tendinopathy referred to both quadriceps and patellar tendinitis. Patellar tendinitis, commonly referred to as “Jumper's knee,” is a common problem in the athletic population, and today refers to the tendinitis that affects the patellar tendon. Patellar tendinitis typically affects athletes who participate in sports that involve running and frequent jumping with eccentric loading of the patellar tendon. Although there is a predilection by sport, it can affect athletes of almost any age. The specific etiology of the tendinopathy varies depending on the particular activity and on the age of the athlete. Chronic tendon problems can result from a variety of causes including overuse injury, cumulative trauma, repetitive strain due to mechanical overload, and age-related degeneration and decreased vascular supply. The term tendinitis is a histopathologic diagnosis and implies the presence of inflammatory cells. The term tendinosis is used to describe the histopathologic alterations to cells that result from chronic tendinitis and tendon overload.
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Essentials of Diagnosis
—Athletes involved in sports that require quick accelerations and jumping, for example, running, track, tennis, volleyball, basketball, and soccer.
—Anterior knee pain localized to the inferior pole of the patella or the tibial tubercle.
—Pain before, during, and/or after activity depending on injury severity.
—Extensor mechanism tightness and/or weakness.
—Tenderness to palpation along the inferior pole of the patella or tibial tubercle.
—Pain symptoms reproduced with resisted knee extension.
—Plain radiographs are often normal, but useful for the evaluation of potential stress fractures or intratendinous calcifications.
—MRI is useful for the evaluation of the integrity of the tendon and surrounding structures.
—Ultrasound by an experienced ultrasonographer can be helpful for diagnosis.
Clinical Findings
The histories of patients with patellar tendinitis can be variable due to the wide range of etiologic factors that cause tendon problems. In younger athletes, the most common etiology includes repetitive and/or intense mechanical overload. Athletes should be specifically questioned regarding changes in duration, intensity, and method of training programs. The use of appropriate shoes and protective equipment should be explored. In older patients, age-related changes such as altered vascular supply predispose tendons to weaken and degenerate. In these cases, the degenerative tendinopathy appears to be prevalent at the bony origin or insertion rather than the midsubstance of the tendon.
Patients with patellar tendinitis typically complain of pain localized to the inferior pole of the patella along the origin of the patellar tendon. Patients can also complain of pain localized to the patellar tendon insertion on the tibial tubercle, although this is less common. During the early stages of the injury, pain typically occurs after activity. As the injury worsens and becomes more chronic, pain can occur during and prior to activity. Patients typically describe the pain as a dull ache located within the tendon. Periods of more intense pain localized to the tendinous origin can occur during activity as symptoms worsen. Patellar tendinitis can be classified into four stages based on symptoms. This classification can be helpful in guiding treatment and predicting outcome. Stage I includes pain after sports activities; stage II includes pain before and after, but not during sports activities; stage III includes patients with constant pain that prevents participation in sports activities; and stage IV includes complete tendon rupture.
Because of the superficial location of the entire patellar tendon, including its origin and insertion, the physical examination is relatively straightforward. As in all cases of anterior knee pain, a complete knee examination, as outlined in the sections above, should be performed. The pertinent examination findings in patients with patellar tendinitis include the following features. Patients typically have tenderness to palpation at the patellar tendon origin along the inferior pole of the patella. The undersurface, or joint surface, of the tendon is often involved and may require deep palpation to elicit symptoms. Occasionally, patients will have tenderness and swelling along the entire tendon indicating peritendinitis and/or tenosynovitis. Symptoms of pain can usually be reproduced with resisted knee extension and palpation of the tendon. Continuity of the quadriceps and patellar tendons should be evaluated to rule out partial or complete tendon ruptures. The straight leg raise with the knee in full extension allows tendon integrity and quadriceps strength to be determined. Finally, younger patients must be evaluated for apophysis traction injuries that affect the inferior pole of the patella (Sinding–Larsen–Johansson disease) or the tibial tubercle (Osgood–Schlatter disease) (Figures 3-14 and 3-15).
Routine radiographs are obtained during the initial evaluation. At a minimum, these should include anteroposterior and lateral views to identify stress or avulsion fractures and calcifications within the patellar tendon. CT scans are generally not indicated if the diagnosis of tendinopathy is reasonably certain. MRI can be helpful in evaluating the tendon itself, as well as the surrounding soft-tissue structures. Although it is common to see increased signal at the inferior pole of the patella and within the substance of the tendon, MRI does not always correlate with the degree of clinical symptoms. Because of its superficial location, the tendon can also be imaged with ultrasound. Experienced musculoskeletal ultraso-nographers are able to evaluate for tendon enlargement, degenerative lesions, as well as partial and complete tears.
Treatment
The treatment of patellar tendinitis depends on the stage of presentation. Stages I and II can usually be successfully
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treated with nonoperative modalities. These include modification of activity, ice, and a short course of NSAIDs. Although NSAIDs can provide symptomatic relief, there are no data to support the contention that these medications alter the natural history of patellar tendinopathy. Antiinflammatory medications should be used with caution in older patients and should not be used in patients with known stomach or gastrointestinal problems. Local injection of corticosteroids is not indicated because of the possibility of steroid atrophy and the associated risk of tendon rupture. Patients should be encouraged to avoid eccentric loading, quick accelerations, and jumping. A comprehensive quadriceps stretching and strengthening program often allows gradual return to athletic activity; however, this can take as little as a few weeks to as long as several months. The initial treatment of stage III injuries follows the same course as that outlined for stages I and II.
In persistent cases that fail nonoperative treatment, surgery may be indicated. The surgical treatment of patellar tendinopathy includes arthroscopic or open debridement of the degenerative tendon usually at the inferior pole of the patella. Surgery is often performed through a tendon splitting approach with the goal of removing the affected tissue. In some cases, curettage of the inferior pole of the patella has been advocated to stimulate an inflammatory and subsequent healing response. Additional surgical approaches have included partial tendon excision, wide excision with reattachment of the remaining tendon, and multiple longitudinal tenotomies. All of these procedures carry the risk of postoperative patellar tendon rupture. A stage IV injury requires operative repair. Primary repair in a timely fashion usually allows patients to regain quadriceps strength and full knee range of motion, and to return to previous levels of activity.
Prognosis & Return to Play
Regardless of the treatment strategy, proper rehabilitation is critical in allowing athletes to return to sport and prevent reinjury. After appropriate rest and modification of activity, rehabilitation is directed at improving quadriceps tightness. A four-stage rehabilitation program includes static stretching of the hamstrings, static stretching of the quadriceps, eccentric strengthening exercises, and ice packs after additional stretching. Sport-specific exercises are gradually introduced and quadriceps strength and elasticity improve. Ultimately, athletes are allowed to return to sport when they have full range of motion, when isokinetic quadriceps strength is equal to at least 90% of the normal side, and when they no longer have tenderness or pain with activity.
Panni AS et al: Patellar tendinopathy in athletes: outcome of operative and nonoperative management. Am J Sports Med 2000;28:392.
Peers KH et al: Cross-sectional outcome analysis of athletes with chronic patellar tendinopathy treated surgically and by extracorporeal shock wave therapy. Clin J Sport Med 2003;13:79.
Warden SJ, Brukner P: Patellar tendinopathy. Clin J Sport Med 2003;22(4):743.
Lateral Knee Pain
Differential Diagnosis
Iliotibial Band Syndrome
Iliotibial band syndrome is the most common cause of lateral knee pain in distance runners. It is not restricted to runners, however, and has been known to affect other athletes involved in knee flexion activities including cycling, soccer, tennis, football, and skiing. It is caused by a combination of intrinsic and extrinsic factors. Intrinsic factors are related to an athlete's anatomic alignment, whereas extrinsic factors include training techniques and sport-specific activities.
Essentials of Diagnosis
—Athletes involved in sports that require running down hills.
—Aching lateral knee pain just proximal to the joint line.
—Symptoms are present during running, but usually are absent before and after.
—Point tenderness in the area overlying thelateral epicondyle.
—Positive Ober's test indicating iliotibial band tightness.
—Plain radiographs are often normal, but are useful in evaluating other potential conditions.
—CT and MRI are also not helpful in the diagnosis but may be helpful in evaluating other pathology.
P.98
Pathogenesis
Iliotibial band syndrome is common in runners and other athletes who use running as a training tool. Specific questions about timing of onset, duration, and changes in length or intensity of the athlete's training program should be entertained. The syndrome is typically brought on by downhill running. Running downhill significantly reduces knee flexion at foot strike and in-creases friction between the iliotibial band and the lateral epicondyle of the femur. Friction is typically highest at 30° of knee flexion.
Clinical Findings
Patients are usually asymptomatic both before and after activity. Symptoms usually begin shortly after the onset of running and continue throughout activity. They usually resolve with rest, but return when activity is resumed. Symptoms usually correlate with the intensity and length of training.
As has been mentioned previously, a comprehensive knee examination should be performed to evaluate for potential confounding injuries. A careful physical examination provides clues that are important for making the diagnosis of iliotibial band syndrome. It is important to evaluate for the presence of potential intrinsic anatomic factors that may predispose the athlete toward developing iliotibial band syndrome, such as genu varum, tibia vara, heel varus, forefoot supination, and compensatory foot pronation. Pertinent findings on physical examination include tenderness to palpation located 2–3 cm proximal to the lateral joint line in the area of the later epicondyle of the femur. Patients will also exhibit a tight iliotibial band with the Ober test. This test is performed by having the patient lie in a lateral position on the examining table with the involved knee up. The unaffected hip and knee are flexed. The involved knee is then flexed to 90° and the ipsilateral hip is abducted and hyperextended. A tight iliotibial band will prevent the involved extremity from dropping below horizontal. A provocative test, called the Noble test, allows confirmation of the diagnosis. This test is performed with the patient lying supine and with the involved knee flexed. Pressure is applied to the lateral epicondyle and the knee is extended. This test is positive when pain is reproduced when the knee is at 30–40° of flexion. Finally, functional tests, such as asking the patient to hop on the involved extremity with the knee flexed, may reproduce lateral knee pain and confirm the diagnosis.
Plain radiographs, CT, and MRI are usually normal in patients with iliotibial band syndrome. They can be helpful in ruling out other potential causes of lateral knee pain that are included in the differential diagnosis.
Treatment
Nonoperative therapy is the mainstay of treatment. Treatment is usually aimed at modification of intrinsic abnormalities and elimination of extrinsic factors. During the initial stages of treatment, the inflammatory process should be controlled with rest, ice, NSAIDs, and ultrasound or phonophoresis. Once the acute symptoms have improved, therapy can be initiated. The entire involved lower extremity should be addressed. In addition to stretching the iliotibial band, tensor fascia lata, and hip external rotators, hip abductor tightness and weakness must be improved. Modification of extrinsic factors involves altering the athlete's training program. For runners, this includes avoidance of hills, changing the duration and intensity of training, and running on the opposite side of the road or reversing the direction on a curved track. Cyclists can alter their seat height or the position of their foot within clipless pedals. In patients who have excessive foot pronation, a rigid lateral heel wedge or custom orthotic may help modify intrinsic factors.
Although surgical treatments have been described, they are not a mainstay of treatment. They include procedures that remove a small portion of the iliotibial band that is located directly over the lateral epicondyle when the knee is flexed to 30°. Success has been reported in athletes who have failed nonoperative treatments and continue to have significant symptoms.
Prognosis & Return to Play
Ultimately, a four-phase rehabilitation protocol should be complete, and patients should be able to perform sport-specific rehabilitation activities without significant pain, functional limitation, or recurrence of symptoms. When this program is complete, patients may return to play.
Farrell KC et al: Force and repetition in cycling: possible implications for iliotibial band friction syndrome. The Knee 2003;10(1):103.
Frederickson M, Wolf C: Iliotibial band syndrome in runners: innovations in treatment. Sports Med 2005;35(6):451.
Kirk LK et al: Iliotibial band friction syndrome. Orthopedics 2000;23(11):1209.