Internal Derangement of the Knee: Tendon Injuries


The Extensor Apparatus

The extensor apparatus consists of the quadriceps tendon, the patella, the patellar tendon, the infrapatellar fat pad, and the medial and lateral patellar retinacula.

Quadriceps Tendon Rupture

Anatomy

The quadriceps tendon is the conglomeration of the distal tendons of the quadriceps muscle and usually has a striated appearance on sagittal MR images, with the anterior striation representing the contribution from the rectus femoris, the middle striations representing the vastus lateralis and medialis, and the deep striation representing the vastus intermedius muscles ( Fig. 28-1 ). The quadriceps tendon inserts on the anterior aspect of the superior pole of the patella.

FIGURE 28–1, Normal quadriceps and patellar tendons. Sagittal, T1-weighted MR image shows the normal striated appearance of the quadriceps tendon (large black arrow) . The patellar tendon (white arrow) is straight and thinner than the quadriceps tendon, and its superficial and deep surfaces are parallel to each other. It is uniformly of low signal intensity except for a small triangle of intermediate signal intensity (small black arrow) along its proximal deep surface.

Prevalence

The quadriceps tendon typically tears in the unconditioned “weekend” athlete; in patients with systemic diseases such as diabetes, chronic renal failure, or rheumatoid arthritis; or in those on chronic corticosteroid therapy. It is more common in people more than 40 years of age than in teenagers or young adults.

Biomechanics

The cause of tears is eccentric contraction of the extensor mechanism, usually due to stumbling, as the flexing knee tries to extend against the weight of the stumbling person. The ruptured tendon usually has some underlying abnormality such as tendinosis or generalized weakening due to a systemic chronic medical condition.

Manifestations of the Disease

Radiography

A lateral radiograph is the most useful projection and demonstrates soft tissue swelling and effacement of the fat planes, loss of the normal shadow of the quadriceps tendon, and varying amounts of anterior tilt of the patella away from the femur ( Fig. 28-2 ).

FIGURE 28–2, Quadriceps tendon rupture. Lateral radiograph shows marked suprapatellar soft tissue swelling (asterisk) . The patella shows abnormal anterior tilt away from the femoral condyles. The unaffected patellar tendon (white arrow) is normal.

Magnetic Resonance Imaging

Acute rupture results in high–signal-intensity edema in and around the tear on T2-weighted images, and the proximal tendon edge may be retracted or “balled up.” Sagittal and coronal planes are useful to assess tendon discontinuity and degree of tendon retraction ( Fig. 28-3 ).

FIGURE 28–3, Quadriceps tendon rupture. Sagittal, fat-suppressed, T2-weighted MR image shows complete discontinuity of the distal aspect of the quadriceps tendon with edema within the tendon gap (arrow) . The proximal and distal torn ends of the tendon are heterogeneous and thickened, indicating underlying tendinosis. Edema evident by high signal intensity is present around the torn tendon edges.

Ultrasonography

Longitudinal scanning is useful to assess tendon discontinuity and degree of retraction. In cases in which the torn edges are apposed, longitudinal scanning with the knee flexed can distinguish a partial tear from a nonretracted rupture ( Fig. 28-4 ).

FIGURE 28–4, Quadriceps rupture. A , Longitudinal sonogram with knee in extension shows torn tendon edges (T) closely apposed to each other. There is a heterogeneously hypoechoic gap involving the anterior aspect of the tendon (arrow) . B , Longitudinal view of the same patient with the knee in flexion shows complete rupture and distraction of the tendon edges (T) with only a thin strand of tissue remaining (arrow) . The patella (P) is seen inferior to the tendon on both images.

Synopsis of Treatment Options

Partial tears and some nonretracted ruptures may be managed conservatively. Ruptures are usually surgically repaired.

Patellar Tendinosis and Tear

Tendinosis refers to chronic degeneration of the tendon.

Anatomy

The patellar tendon is the continuation of the quadriceps tendon and is composed mostly of the rectus femoris component, which passes over the anterior aspect of the patella and inserts on the tibial tubercle (see Fig. 28-1 ). The normal patellar tendon is less than 75% of the thickness of the quadriceps tendon and has parallel surfaces. It is histologically a tendon, not a ligament.

Prevalence and Epidemiology

Patellar tendinosis is seen in adults and may occur anywhere along the course of the tendon. The development of tendinosis is related to age and weight. Rupture most often occurs at the proximal aspect of the tendon, usually through an area weakened by tendinosis or previous surgery. Rupture of the tendon at its mid-portion is usually a result of a direct blow. Patellar tendon rupture is less common than quadriceps tendon rupture and tends to occur in younger adults, where it is more common in males than females. In older adults, the same systemic diseases that are risk factors for quadriceps tendon tear, namely diabetes, chronic renal failure, rheumatoid arthritis, and chronic corticosteroid therapy, are also risk factors for patellar tendon rupture.

Biomechanics

Chronic overuse leads to areas of degeneration. A forceful tensile load during quadriceps contraction may cause the tendon to partially tear or rupture.

Pathology

Histologically, tendon degeneration shows crimping and disorganization of collagen fibers and mucinous degeneration of collagen. Neovascularization due to angiofibroblastic proliferation may also be present.

Clinical Presentation

Patellar tendinosis is usually asymptomatic. A patient with an acutely ruptured patellar tendon will complain of infrapatellar pain and swelling and inability to actively extend the knee.

Manifestations of the Disease

Radiography

The severely thickened patellar tendon may be seen on lateral radiographs of the knee as widening of the patellar tendon outline, but most foci of tendinosis are radiographically occult. In the case of tendon rupture, there is ill-defined soft tissue swelling with resultant loss of the outline of the tendon. The patella may be retracted proximally by the unopposed pull of the quadriceps muscle ( Fig. 28-5 ).

FIGURE 28–5, Patellar tendon rupture. Lateral radiograph shows loss of the normal shadow of the proximal aspect of the patellar tendon with surrounding soft tissue edema (arrow) . The patella is high riding due to the unopposed pull of the quadriceps muscle.

Magnetic Resonance Imaging

The appearance of patellar tendinosis is variable. There may be focal areas of intermediate signal intensity on T1- and T2-weighted images without focal tendon thickening. The degenerated tendon may also appear “wrinkled” or buckled (see eFig. 28-1 ) or may be diffusely thickened ( Fig. 28-6 ). A patellar tendon that is as thick as the quadriceps tendon is abnormal. Focal high signal intensity on T2-weighted images may result from marked mucinous degeneration and interstitial cyst formation.

FIGURE 28–6, Patellar tendinosis. Sagittal, proton density–weighted MR image shows a markedly thickened patellar tendon (arrow) with heterogeneous internal signal both proximally and distally.

eFIGURE 28–1, Patellar tendinosis. Sagittal, proton density–weighted MR image shows rupture of the proximal aspect of the patellar tendon, which has balled up on itself (arrow) but with only minimal retraction. The tendon shows diffuse degeneration manifested by thickening and signal heterogeneity. There is similar tendinosis in the visualized portion of the distal quadriceps tendon.

Acute rupture appears as discontinuity of the tendon with high–signal-intensity edema and hemorrhage in the region of tear. The patella may be retracted proximally.

Ultrasonography

Tendinosis may appear as focal hypoechoic loss of the normal echogenic fibrillar appearance of the tendon and/or tendon thickening ( Fig. 28-7 ). Rupture appears as discontinuity of the tendon.

FIGURE 28–7, Patellar tendinosis. A , Longitudinal sonogram of a normal patellar tendon shows an echogenic fibrillar appearance with superficial and deep surfaces (white arrows) that are parallel to each other. B , Longitudinal sonogram of the patellar tendon shows marked thickening. The superficial and deep surfaces (white arrows) are not parallel, and the tendon has a heterogeneous echotexture. The patella (P) is seen superiorly, and the proximal tibia (T) is seen inferiorly.

Jumper's Knee (Patellar Tendinitis)

Jumper's knee refers to a symptomatic focus of tendinosis and partial tearing that occurs in the proximal aspect of the patellar tendon.

Prevalence

“Jumper's knee” gets its name because it is seen in basketball players, volleyball players, and other athletes whose sport requires repetitive forceful extension of the knee. It usually occurs in teenagers and young adults.

Biomechanics

Jumper's knee is a chronic overuse injury of the proximal aspect of the patellar tendon, due to repetitive forceful extension of the knee. It occurs in the proximal aspect of the tendon because the stress in the tendon is greatest at the tendon's insertion on the inferior pole of the patella.

Pathology

There is mucoid degeneration of the collagen fibers and angiofibroblastic proliferation, with eventual partial tearing. The term tendinitis is a misnomer because there is no acute inflammation histologically.

Manifestations of the Disease

Magnetic Resonance Imaging

The normal patellar tendon exhibits uniformly low signal intensity on all pulse sequences, except at its proximal attachment, where there may be a V-shaped focus of high signal intensity on T1-weighted images along its deep surface (see Fig. 28-1 ). On sagittal and axial T2-weighted MRI of jumper's knee, there is focal swelling of the proximal aspect of the patellar tendon, most often affecting the central third of the tendon, with focal internal high signal intensity ( Fig. 28-8 ). There may also be edema in the adjacent fat pad and in the inferior pole of the patella.

FIGURE 28–8, Jumper's knee. A , Sagittal, proton density–weighted MR image shows fusiform swelling of the proximal aspect of the patellar tendon and internal high signal intensity (arrow) . B , Axial, fat-suppressed, T2-weighted MR image in the same patient shows the high–signal-intensity focus involving the deep aspect of the central third of the tendon.

Ultrasonography

The normal patellar tendon exhibits an echogenic coarse fibrillar pattern. In jumper's knee, the fibrillar appearance is hypoechoic and the tendon is thickened. Power or color Doppler imaging reveals hyperemia, reflecting the degenerative angiofibroblastic proliferation ( Fig. 28-9 ).

FIGURE 28–9, Jumper's knee. A , Longitudinal sonogram of a normal patellar tendon shows the normal fibrillar echogenic appearance of the tendon with parallel superficial and deep surfaces (black arrows) . The inferior pole of the patella is seen (white arrow) . B , Longitudinal ultrasound image of a different patient shows fusiform swelling of the proximal aspect of the patellar tendon ( black arrows ). The inferior pole of the patella is seen (white arrow) . C , Power Doppler image of the same patient as in B shows marked interstitial hyperemia representing angiofibroblastic proliferation.

Synopsis of Treatment Options

Initial treatment is conservative, consisting of rest, ice, and nonsteroidal anti-inflammatory medication. Percutaneous dry needling or sclerotherapy with sonographic guidance may also provide relief. Cases refractory to conservative treatment may be treated with resection of the tendinotic focus or shift of the patellar tendon attachment.

Osgood-Schlatter Disease, Sinding-Larsen-Johansson Syndrome, and Patellar Sleeve Avulsion

Prevalence and Epidemiology

These abnormalities affect adolescents, before the patella is completely ossified and before the tibial tubercle apophysis has fused. Girls may be affected at a slightly younger age than boys.

Osgood-Schlatter disease (OSD) affects the distal aspect of the patellar tendon, whereas Sinding-Larsen-Johansson syndrome (SLJS) and patellar sleeve avulsion (PSA) affect the proximal aspect of the tendon.

Biomechanics

OSD and SLJS are chronic overuse injuries, and PSA is an acute injury. All are seen in sports that involve forceful contraction of the extensor mechanism, as encountered in cutting maneuvers and jumping. There is controversy as to whether patella alta, patella infera, or tibial torsion predisposes to OSD by virtue of altered tensile stress on the patellar tendon/tibial tubercle apophyseal attachment.

Pathology

PSA is a tear of the proximal aspect of the patellar tendon from the inferior pole of the incompletely ossified patella, with an osteochondral avulsion fragment of the patella. SLJS proximally and OSD distally represent repetitive partial tearing of the tendon and small avulsions of the cartilaginous attachment of the patellar tendon to the lower pole of the patella and tibial tubercle apophysis, respectively. The small avulsed cartilage fragments may ossify, and the small tendon tears may eventually develop foci of heterotopic ossification.

Manifestations of the Disease

Radiography

Lateral radiographs in PSA may belie the underlying injury, because most of the avulsed fragment is typically radiolucent cartilage, with only a small piece of bony patella. Soft tissue swelling may be present and the patella may be high riding.

Both OSD and SLJS demonstrate heterotopic ossification within the patellar tendon, but normal variations in development of the ossification centers of the tibial tubercle apophysis and lower pole of the patella may look similar. The distinguishing feature of these conditions from normal variation is the presence of tendon thickening and soft tissue swelling and the clinical presence of pain and tenderness in the affected region. A distended deep infrapatellar bursa may be visible as a soft tissue density deep to the tendon in OSD ( Fig. 28-10 ).

FIGURE 28–10, Osgood-Schlatter disease. Lateral radiograph shows heterotopic ossification (black arrow) in the distal aspect of the patellar tendon. The tendon is thickened. Ill-defined soft tissue density (white arrow) in Hoffa fat pad represents a distended infrapatellar bursa.

Magnetic Resonance Imaging

Sagittal T2-weighted images will display the fracture through the inferior pole of the patella in PSA and reveal the true extent of the fracture through the bone and cartilage anlage. On sagittal MR images of OSD and SLJS, the distal and pro­ximal aspects, respectively, of the patellar tendon are enlarged, with low–signal-intensity foci of heterotopic ossification and possible enlargement or irregularity of the bony attachment site ( Figs. 28-11 and 28-12 ). In OSD there may also be distention of the deep infrapatellar bursa, manifest as fluid located between the anterior cortex of the tibia and the deep surface of the patellar tendon ( Fig. 28-13 ).

FIGURE 28–11, Osgood-Schlatter disease. Sagittal, proton density–weighted MR image shows thickening of the patellar tendon and focal heterotopic ossification (arrow) .

FIGURE 28–12, Sinding-Larsen-Johansson syndrome. A , Sagittal, T1-weighted MR image shows thickening of the proximal aspect of the patellar tendon (white arrow) , irregular ossification of the inferior pole of the patella (long black arrow) , and focal heterotopic ossification within the patellar tendon (short black arrow) . B, Sagittal, T2-weighted image shows patella baja and a focus of heterotopic ossification at the proximal aspect of the patellar tendon (arrow) . C, Sagittal T2-weighted image shows thickening of the proximal aspect of the patellar tendon with small focus of ossification.

FIGURE 28–13, Osgood-Schlatter disease. A, Sagittal, T2-weighted image shows thickening of the patellar tendon and fragmentation of the tibial tubercle (arrow) . B, Sagittal short tau inversion recovery image shows intraligamentous ossicle and increased signal and thickening (black arrow) in the distal patellar tendon and a distended infrapatellar bursa (white arrow) .

Ultrasonography

Longitudinal scanning of PSA demonstrates the echogenic fibrillar patellar tendon and attached piece of hypoechoic patellar cartilage separated from the rest of the patella. Longitudinal scanning in OSD and SLJS demonstrates the thickened tendon. The foci of internal heterotopic ossification will have echogenic surfaces with varying amounts of posterior acoustic shadowing ( Fig. 28-14 ). The distended deep infrapatellar bursa appears as a hypoechoic collection deep to the distal aspect of the tendon.

FIGURE 28–14, Osgood-Schlatter disease. A , Longitudinal ultrasound image shows a normal-appearing midportion of the patellar tendon (small white arrows) . The distal aspect of the patellar tendon is thickened and hypoechoic (black arrows) with interstitial focal heterotopic ossification (large white arrow) . T, Tibia. B , Longitudinal ultrasound image of the contralateral normal knee shows a normal-appearing patellar tendon (white arrows) inserting on the tibia (T) .

Differential Diagnosis

Patellar sleeve avulsion should be easily distinguished from other causes of acute knee pain in the adolescent because it is an acute event. The knee gives way, and the patient cannot stand or actively extend the knee. The area is painful and swollen, and there may be a palpable defect at the site of avulsion.

Patients with OSD and SLJS have chronic pain and tenderness to palpation over the affected region. Other causes of chronic anterior knee pain in the adolescent are jumper's knee, chondromalacia patellae, patellar tracking abnormalities, irritation of a medial or infrapatellar plica, and abnormalities of the Hoffa fat pad. Patellar tendon/lateral femoral condyle friction syndrome may affect adolescents but is more common in adults.

Patellar Tendon/Lateral Femoral Condyle Friction Syndrome

Prevalence

This abnormality usually occurs in young adults but has a reported age range of 13 to 56 years. Most people affected do not participate in routine athletic activities.

Biomechanics

The biomechanics are not well understood, but may be related to an overuse injury in which the patellar tendon chronically rubs against the lateral femoral condyle or compresses the lateral aspect of the Hoffa fat pad against the lateral condyle. It is likely related to patellar maltracking or malalignment, because most patients with this abnormality have associated patella alta or lateral subluxation of the patella.

Manifestations of the Disease

Magnetic Resonance Imaging

T2-weighted images demonstrate focal edema in the lateral aspect of the Hoffa fat pad, with an occasional focal fluid collection in this region. Marrow edema may be present in the lateral aspect of the patella, the cartilage of the lateral patellar facet may be thinned, and there may be tears in the proximal aspect of the patellar tendon.

Infrapatellar Fat Pad Impingement (Hoffa Disease)

Anatomy

The infrapatellar fat pad (also called the Hoffa fat pad) is a pyramidal fibrofatty structure located between the patella and femoral condyles superiorly and the tibia inferiorly. Its base is along the deep surface of the patellar tendon, and its apex points toward the intercondylar notch. The synovium of the anterior aspect of the knee joint is reflected over its deep surface, and thus the fat pad is intracapsular but extrasynovial. Synovial-lined vertical and horizontal clefts may be present within it.

The fat pad is not freely mobile but is attached to the inferior pole of the patella and the roof of the intercondylar notch by the ligamentum mucosum (also called the infrapatellar plica). It has attachments to the anterior horns of the menisci and to the periosteum of the tibia. The deep infrapatellar bursa is located at the inferior edge of the fat pad.

The blood supply of the fat pad comes from two vertically oriented and peripherally located vessels, which are branches of the superior and inferior genicular arteries with horizontal anastomotic branches. It is well innervated by branches of the femoral, common peroneal, and saphenous nerves.

Biomechanics

A single traumatic episode or repetitive overuse due to hyperextension and rotational forces leads to hemorrhage and inflammation of the fat pad, which in turn cause swelling of the fat pad. The enlarged fat pad then gets impinged between the tibia and femur, further exacerbating the inflammation and enlargement.

Pathology

Acutely, there is inflammation and hemorrhage of the fat pad. This gives way to an influx of macrophages and the deposition of fibrin and hemosiderin. Chronically, there is fibroblast proliferation, leading to fibrosis of the fat pad, which may undergo fibrocartilaginous metaplasia, and the fibrocartilaginous tissue may eventually ossify.

Manifestations of the Disease

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