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Patellar Tendinopathy (Jumper’s Knee)
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Rapid repetitive acceleration, deceleration, jumping, and landing result in microtears of the extensor tendon matrix at three distinct locations: (1) the quadriceps tendon as it inserts into the patella, (2) the patellar tendon at the inferior aspect of the patella, and (3) the patellar tendon as it inserts into the tibial tubercle.46
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The most common location for injury is the patellar tendon at the insertion of the inferior patella, termed “jumper’s knee” or patellar tendinopathy.47 Two-thirds of patients have been found to have structural tendon changes.48 This condition can be disabling, with one-third of athletes unable to return to sports within 6 months and one-half of patients refraining from their sport due to the condition at 15 years of age.49,50 Colosimo and Bassett51 classify jumper’s knee into four stages (Table 20–3).
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During examination, the knee should be held at full extension. If the quadriceps tendon is involved, tenderness will be present over the insertion of the quadriceps tendon or the upper pole of the patella. Patients with patellar tendinopathy will have tenderness at the lower pole of the patella and the proximal portion of the patellar tendon.46
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Plain radiographs are usually normal. Occasionally, the patella will have an elongated or fragmented tip. Ultrasonography will reveal an enlarged and hypoechoic tendon and is used to confirm the diagnosis.51 MRI will also be diagnostic.
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Treatment of jumper’s knee includes avoiding the inciting activity and resting the affected extremity. The extent of treatment depends on the stage. Stages I and II are treated with adequate warm-up and ice packs or ice massage after the activity. Anti-inflammatory medications are administered for 10 to 14 days followed by physiotherapy. Eccentric training and shock wave therapy have proven to produce good results and should be used prior to surgical intervention.52–55 Elastic knee support is recommended. Patients with stage III disease should undergo a prolonged period of rest, in addition to ice and anti-inflammatory medications. If this is not curative, the patient should consider either giving up sports, or having surgery to excise abnormal tissue. Surgery is required for patients with stage IV disease (rupture). Arthroscopic treatment of this condition in those that do not respond to conservative therapy produces good results.56
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Steroid injection is controversial. Some authors support its use, whereas others feel that it could lead to further damage and eventual rupture as it allows the athlete to continue to overload the weak tendon.51,57 Researchers are also evaluating the effectiveness of platelet-rich plasma injections and focused extracorporeal shock wave therapy, though this therapy is too new to recommend routinely.58,59
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Extensor Mechanism Disruption
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The extensor mechanism of the knee may be disrupted at four locations: (1) quadriceps tendon, (2) patella, (3) patellar tendon, and (4) tibial tubercle (Fig. 20–28). Patella and tibial tuberosity fractures are covered in the section on fractures. For this discussion, we will focus on quadriceps and patellar tendon rupture.
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The initial examiner misdiagnoses these injuries in 38% of patients. This fact is important because when treatment is delayed, functional results are poor.60 The clinical picture of an extensor mechanism disruption typically includes a history of a sudden buckling of the knee with extreme pain. After the acute injury, the pain is reduced.
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Rupture of the quadriceps tendon is often seen in patients older than 40 years. The most common site of rupture is just proximal to the patellar insertion, through an area of degenerated tendon. Patellar tendon ruptures are less common than quadriceps tendon ruptures and are typically seen in those younger than 40 years. Most patellar tendon ruptures occur at the site of insertion into the patella. Steroid injections are thought to predispose to rupture. Other factors predisposing to tendon rupture include tendon calcifications, arthritis, collagen disorders, fatty tendon degeneration, and metabolic disorders.
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The injury may be either direct or indirect. The direct mechanism is less common and is the result of a violent impact against a taut quadriceps tendon. The more common indirect mechanism results from forced flexion when the quadriceps is contracted. This mechanism is commonly seen in patients who stumble while descending a staircase or stepping down from a curb.61,62
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On examination, the position of the patella should be assessed. Inferior displacement of the patella with proximal ecchymosis and swelling indicates a quadriceps rupture. Superior displacement of the patella along with inferior pole tenderness and swelling indicates a patellar tendon rupture (Fig. 20–29).63 In both instances, the patient may have intact, “active” extension but it will be very weak when compared with the uninjured extremity (Video 20–2). A quadriceps tendon rupture results in a suprapatellar gap just superior to the patella with swelling to the tissues above (Fig. 20–30A).64 The most significant finding on clinical examination with extensor mechanism rupture is that the patient has loss of active extension of the knee or inability to maintain the passively extended knee against gravity. With partial ruptures, the patient may have active extension as previously indicated; however, it will be markedly weakened.
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The AP and lateral knee radiographs are often highly suggestive of these injuries. In the normal AP knee radiograph, the inferior aspect of the patella should lie within 2 cm of the distal femoral condyles. On the lateral view at 90-degrees flexion, the patella should remain inferior to a line drawn along the anterior aspect of the femoral shaft. Inferior patellar displacement (patella baja) or a superior pole avulsion fragment suggests a quadriceps tendon rupture (Fig. 20–30B and 20–30C).65 Superior displacement (patella alta) is diagnostic of a patellar tendon rupture (Fig. 20–31). An inferior bony avulsion fragment may be present (Fig. 20–32). Comparison views may be helpful in diagnosing subtle patellar displacements.
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Because treatment is altered depending on whether the injury is partial or complete, MRI or ultrasound is used to distinguish between cases that remain unclear after the initial assessment.
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The initial treatment of partial and complete quadriceps and patellar tendon injuries is the same.55 Ice and a compression dressing are applied to reduce swelling. The knee is held in extension with a knee immobilizer (Appendix A–16). In complete or severe injuries, the patient should not bear weight initially.
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The definitive treatment of these injuries is different if the injury is partial or complete. A partial quadriceps or patellar tendon rupture requires early referral for the placement of a long-leg cylinder cast with the knee held in extension for 6 weeks. A complete quadriceps or patellar tendon tear is best treated with early surgical repair.64 Ideally, surgery is performed within 2 weeks of the injury. When performed after 6 weeks, results are inferior.66
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Muscle Strain and Tendonitis
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The gracilis, the sartorius, and the semitendinosus insert on the medial tibia via the pes anserinus. Patients with tendonitis of the pes anserinus present with pain and tenderness 5 to 6 cm below the medial joint line. Other symptoms include pain upon standing from a sitting position, pain at night, and “giving way” of the knee.67 It is most common in runners. Ultrasound will show an increase in the size of the tendon with heterogeneous echogenicity.68 Differentiating this condition from anserine bursitis is difficult clinically, but the conditions are treated the same. Tendonitis is less common and the response to treatment is less dramatic.69
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The semimembranosus inserts both medially and posteriorly along the knee. Semimembranosus tendonitis causes pain in the posteromedial aspect of the knee, immediately below the joint line.69 The pain is worse after activity. This injury is often confused with a medial meniscus injury.
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The biceps tendon inserts on the fibular head and the LCL. Sudden contraction against resistance as in running or jumping may strain or rupture the tendon and muscle. Pain and tenderness is present over the posterolateral portion of the knee.
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The treatment of these injuries requires rest to allow healing and prevent further injury. Moderate strains consist of partial fiber tears with pain and bleeding. These injuries require 3 to 4 weeks of rest along with analgesics and ice. Heat is applied 48 hours after an acute injury. Complete ruptures are rare injuries that are best treated surgically.70
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Iliotibial Band Syndrome
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The iliotibial band originates from the fascia of the gluteus muscles and tensor fascia lata. It passes along the lateral portion of the thigh and inserts into a tubercle on the lateral tibial condyle. With the knee in extension, the iliotibial band lies anterior to the lateral femoral epicondyle. With flexion, the band slides posteriorly over the epicondyle (Fig. 20–33). Repetitive flexion and extension, as occurs with running or cycling, results in irritation of the iliotibial band and its bursa as it slides over the epicondyle.71,72
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The patient presents with pain on the lateral side of the knee during activity that may radiate proximally or distally. Climbing stairs or walking up an incline will exacerbate the pain. On examination, there will be a focal area of tenderness over the lateral femoral epicondyle approximately 3 cm proximal to the joint. Full range of motion is typical, and the pain will be exacerbated with weight bearing on the flexed knee. Nobel’s compression test will reproduce pain. To perform this test, the leg of the supine patient is elevated above the examination table. The examiner holds the ankle with one hand, while the thumb of the other hand compresses the lateral epicondyle of the femur. Active flexion and extension reproduces the pain.73
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The recommended treatment includes a reduction in activity with the avoidance of hills or banked tracks. A lateral wedged orthotic, ice, anti-inflammatory medications, iliotibial band stretching, and local steroid injections are also useful.74,75 Surgery is indicated in refractory cases.71 This includes splitting the posterior 2 cm of the iliotibial band transversely at the area of the lateral condyle so that this portion of the band is not taut.
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The fabella is a sesamoid bone embedded in the tendon of the gastrocnemius muscle that articulates with the posterior portion of the lateral femoral condyle (Fig. 20–34). It serves as the site of attachment for fibers of the popliteus, arcuate complex, and the fibular–fabellar ligament. The fabella is present in 11% to 13% of normal knees and is bilateral in 50% of these patients.
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The fabella syndrome occurs when the fabella undergoes a degenerative or inflammatory process secondary to irritation. The condition is most common in adolescence, but also occurs in adults. The clinical picture typically includes intermittent posterolateral knee pain exacerbated with extension.76 Tenderness to palpation is localized over the fabella and is exacerbated with compression against the condylar surface.67
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Radiographs may not reveal evidence of a fabella if it has not ossified. The differential diagnosis should include injury to the posterior horn of the lateral meniscus, tendonitis of the lateral head of the gastrocnemius, biceps femoris, or popliteus. The recommended treatment includes rest, analgesics, local anesthetic–steroid injection, and referral as surgical resection may be necessary when pain persists for more than 6 months.77
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The normal function of a bursa is to permit friction-free movement between two structures. Because of the number of muscles and ligaments that come into contact with bony structures, the knee has many bursae, several of which can become injured or inflamed (Fig. 20–35).
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Several knee bursae communicate with the joint space. The suprapatellar and popliteal bursae always communicate with the joint, whereas the semimembranosus does only some of the time. This communication is important for understanding Baker’s cysts, as well as evaluating for intra-articular involvement of foreign bodies or lacerations (Fig. 20–36). The suprapatellar bursa extends a full three finger breadths above the patella and a laceration in this location that involves the bursa may result in septic arthritis.
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Acute trauma or chronic occupational stresses cause bursitis around the knee. Other less common etiologies include infection or metabolic disorders such as gout or chronic arthritis. Clinically important bursae and their related conditions are discussed later. The treatment of bursitis surrounding the knee is similar and is discussed at the end of this section.
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This bursa is located superficial to the patella and usually becomes inflamed 1 to 2 weeks after a direct traumatic injury, such as a fall on the knee. Direct repeated trauma may also cause this condition and this is why it is also referred to as “housemaid’s knee.”
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The clinical presentation typically is one of pain with erythema, swelling, and increased warmth of the skin overlying the bursa (Fig. 20–37A). With palpation, the examiner will be able to identify the superficial bursal sac.67 Crepitation of the walls of the bursa may be noted. Knee motion is painless up to the point of skin tension, at which time pain is noted. Repeated trauma results in less pronounced symptoms and a palpably thickened bursal wall.
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Like olecranon bursitis of the elbow, many cases of prepatellar bursitis are infectious. If infection is a consideration, aspiration of the fluid for diagnostic testing and antibiotics are indicated as outlined for olecranon bursitis in Chapter 14. Typically, the WBC count is greater than 5000 WBC/mm3. Gram stain is positive in over half of the cases. Treatment of noninfectious prepatellar bursitis is discussed at the end of this section.
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Infrapatellar Bursitis
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The superficial infrapatellar bursa is located just beneath the skin and superficial to the tibial tubercle. Superficial infrapatellar bursitis is also referred to as clergyman’s knee because of its association with kneeling in a more erect position than would cause prepatellar bursitis. When inflamed, there will be swelling and tenderness inferior to the patella and over the tibial tubercle (Fig. 20–37B). In an adolescent, it may be difficult to differentiate this condition from Osgood–Schlatter disease.
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The deep infrapatellar bursa is located beneath the patellar tendon, separating it from the underlying fat pad and tibia. The clinical picture includes pain-free passive extension and flexion. Pain will be elicited with active complete flexion and extension and with palpation of the margins of the patellar tendon. It may be difficult to differentiate fat pad syndrome from this disorder, although complete passive extension is usually painful with a fat pad syndrome.
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The anserine bursa lies under the pes anserine tendon. This is a conjoined tendon composed of the sartorius, gracilis, and semitendinosus muscles. This condition is more common in middle-aged women and obese patients. Symptoms include knee pain, often nocturnal, particularly on walking up stairs or rising from a sitting position.78 Morning stiffness may last up to 1 hour. The findings on physical examination are marked tenderness over the pes anserine, which is 5 to 6 cm below the medial joint line. Often, coexisting osteoarthritis is present. An ultrasound may show an enlarged anserine bursa.79
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This entity, seen in the popliteal fossa behind the knee, is a benign outpouching of the semimembranosus bursa (Fig. 20–38). The incidence of Baker’s cysts is higher in patients with rheumatoid arthritis or osteoarthritis. A Baker’s cyst becomes enlarged when synovitis, arthritis, or any internal derangement of the knee results in the flow of excess synovial fluid into this bursa. At that point, the bursa expands posteriorly into the popliteal fossa.
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The clinical picture usually includes a history of intermittent swelling behind the knee. On examination, a tense and sometimes painful fluid-filled sac is palpated within the popliteal fossa. A change in pressure in a Baker’s cyst with extension and flexion of the knee (Foucher’s sign) suggests the diagnosis. Additional complaints include chronic pain or a giving way of the knee. A Baker’s cyst should never be aspirated or injected.
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Rupture of a Baker’s cyst presents with diffuse swelling in the leg as the synovial fluid dissects inferiorly. This entity may be clinically indistinguishable from a deep venous thrombosis. Nonruptured cysts must be differentiated from popliteal artery aneurysms, neoplasms, and true synovial hernias. The diagnosis can be confirmed by ultrasonography, CT, or MRI.80
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Lateral Knee Bursitis
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The popliteal bursa lies proximal to the joint line between the LCL and the popliteus tendon. The patient with popliteal bursitis presents with lateral joint line tenderness and swelling.
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The fibular head is surrounded by a large bicipital bursa lying under the biceps femoris tendon, a bursa under the LCL, and a bursa under the lateral head of the origin of the gastrocnemius. Inflammation of these bursae creates a clinical picture that includes pain and tenderness around the fibular head, the LCL, or the biceps insertion. It may at times be difficult to differentiate bursitis from injuries to the LCL, the bicipital tendon, or the lateral meniscus.
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Treatment of Bursitis
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The treatment of acute traumatic or chronic occupational bursitis includes local heat, rest, and anti-inflammatory agents with protection from recurrent irritation. Patients with prepatellar and anserine bursitis respond well to the injection of a triamcinolone–bupivacaine mixture followed by a compression dressing. Ultrasonic treatment causes dramatic improvement in patients with anserine bursitis.
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In some studies, steroid injection reduced the size of the cyst and led to increased comfort; however, this is not recommended by the authors.81,82 Those cases resistant to treatment may require surgical excision of the bursa. The treatment of a Baker’s cyst must be directed at the etiology, and early referral is recommended for diagnostic tests and possible closure of the synovial defect.
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Traumatic Prepatellar Neuralgia
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This is a well-recognized, but uncommonly diagnosed syndrome following a direct blow to the front of the knee. The patient typically presents with a chief complaint of a persistent, dull ache deep to the patella that makes bending or climbing stairs difficult. Patients often complain of pain behind the knee on one or both sides. The disorder occurs secondary to contusion of the superficial prepatellar neurovascular bundle. Repeated trauma may cause secondary fibrosis of the neurovascular bundle.
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On examination, the patient will complain of focal tenderness over the middle of the lateral border of the patella with no discomfort over the remainder of the patella.83 Most patients respond to an injection of a lidocaine–steroid mixture. Unfortunately, the pain returns after a couple of weeks. Refractory cases require prepatellar neurectomy.83
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This syndrome is also known as Hoffa’s disease, infrapatellar fat pad syndrome, and synovial lipomatosis.69 The fat pad, located beneath the patellar tendon, may become hypertrophied and inflamed in athletes secondary to repetitive trauma to the knee. The end result is pain on forced extension, catching, and anterior knee discomfort when sitting for long periods.
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On examination, point tenderness is noted over the anteromedial or anterolateral joint line. The knee appears tender, puffy, and the fat pad bulges out on either side of the patellar tendon. Pain is reproduced when the slightly flexed knee is allowed to passively extend (bounce test).69 The physician must not confuse these symptoms with patellar tendinopathy or superficial or deep infrapatellar bursitis.
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Treatment of this condition consists of rest, ice, and nonsteroidal anti-inflammatory medications. Local anesthetic-steroid injection into the fat pad will also offer relief and aid in confirming the diagnosis. Heel lifts may reduce knee hyperextension and reduce pain. Operative resection is rarely necessary.
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The stability of the knee is dependent on its surrounding ligaments and muscles. The knee is most stable in extension, yet the predominance of everyday activities are performed in some degree of flexion. The knee is thus predisposed to injury. The ligaments surrounding the knee function to guide motion and protect the knee from nonphysiologic movement.
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These ligaments are innervated by myelin-free nerve fibers. It is characteristic of ligamentous injuries that a partial tear is typically more painful than a complete rupture.
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The following discussion will center around six common mechanisms resulting in ligamentous injuries: (1) valgus, (2) varus, (3) hyperextension, (4) rotational, (5) anterior, and (6) posterior stresses.55 It is important to determine if the knee was weight bearing or a rotational force was present at the time of injury, as these factors will increase the likelihood of an associated meniscal injury. In addition, the position of the knee (flexion or extension) at the time the force was applied will impact the structures involved.
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Because the force of injury is more commonly a combination of stresses, it is difficult to predict the ligamentous injury pattern from the mechanism of injury alone. The following discussion should serve as a general guide to the types of injuries that are frequently the result of a particular mechanism. This is a controversial area and the following tables include what are the predominant theories.
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The most common mechanism of injury resulting in ligamentous damage is a valgus (an abducting force that opens up the medial side) stress with an external rotary component on the flexed knee. This is a common football or skiing injury where the patient typically complains of being clipped from the blind side or of catching a ski tip in the snow. The MCL is the first structure injured, making this ligament the most commonly injured ligament in the knee.84 With increasing force, the ACL ruptures, followed by the medial meniscus or PCL. Injury to the MCL, ACL, and medial meniscus is referred to as the “unhappy triad” because of the common association of these structures following a valgus stress to the knee. Table 20–4 lists the sequence of events as an increasing valgus force is applied to the knee in flexion and extension.71,75
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Varus (an adducting force that opens the lateral side of the knee) stress is thought to be the second most common mechanism resulting in ligamentous knee injuries. A varus stress may or may not be accompanied by an internal rotary force. The LCL is the first to be injured when this mechanism occurs in isolation, but the ACL, and finally, the PCL, can also rupture when a combined varus and internal rotational force is applied.
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A hyperextension stress usually results in injury to the cruciate ligaments. The ACL ruptures first, followed by the posterior capsule and PCL. The cruciate ligaments may rupture at their midpoint or at their femoral attachment.85–87 An additional rotational stress may result in damage to the collateral ligaments.
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There are two types of rotational stresses: internal and external. Internal rotational stresses result in ACL injury, followed by an LCL injury, whereas external rotational stresses may cause ACL, LCL, PCL, or meniscal injuries depending on whether the knee was flexed, extended, or weight bearing at the time of injury.
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Anterior and posterior stresses of the tibia on the femur may result in injuries to the cruciate ligaments. An anterior stress will rupture the ACL followed by the MCL. A posterior stress results in a PCL injury.
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In addition to the mechanism of injury as described here, the emergency physician should inquire about other historical features. Pertinent questions in subacute and chronic cases include the location of the swelling and also what activities reliably induce swelling. The usual duration of symptoms as well as the response to rest should be assessed.
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The exact location of the pain after an injury and those factors that exacerbate the symptoms give important clues in the specific localization of a ligamentous injury. Partial ligament ruptures typically produce more pain than do complete tears.3 In one study, 76% of patients with a complete rupture of a ligament in the knee walked without assistance.3
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Several studies have indicated that during an injury an audible pop or snap is a reliable indicator of an anterior cruciate rupture.88,89 Some authors have stated that patients with this history have a 90% incidence of anterior cruciate rupture at surgery.90 Sixty-five percent of patients with a torn anterior cruciate, however, did not hear a pop or snap at the time of injury. Rupture of the anterior cruciate is usually followed by the rapid onset of a bloody effusion. In fact, the most common etiology for a traumatic hemarthrosis within 2 hours of injury is a rupture of the anterior cruciate.
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Axiom: A history that includes a pop or snap at the time of injury suggests a rupture of the ACL until proven otherwise, especially when associated with the rapid development of a knee effusion
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How Much Time Has Elapsed Since the Injury?
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The time between the injury and the examination is important in deciphering the physical findings. Immediately after an injury there will be no effusion or spasm and ligamentous injuries will be easily demonstrated. By the time the patient presents to the ED an hour later, these same injuries will be difficult to detect secondary to the surrounding muscular spasm.81 If spasm is present, ligamentous laxity may not be demonstrable. This patient must be reexamined after 24 hours when the spasm has been relieved.
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Is There a Joint Effusion?
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The acutely injured knee should be examined methodically, first noting any swelling. When seen early, up to 64% of patients have localized edema at the site corresponding to the acute ligamentous tear.3 Complete ligamentous ruptures or capsule disruption may exhibit no swelling, as the fluid extravasates through the torn capsule.
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An effusion seen within 2 hours of an injury is suggestive of torn tissues, whereas those presenting 12 to 24 hours postinjury are typically reactive synovial effusions. A tense and painful effusion that severely limits the range of motion can be relieved with aspiration in the ED.
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A hemarthrosis that develops within the first 12 hours after injury most commonly suggests an ACL tear. After athletic injuries, 67% of patients with an acute hemarthrosis and no fracture on radiographs were found to have a partial or complete tear to the ACL.91 Other injuries included osteochondral fractures (13%) and meniscal tears (16%). Fat globules found in the bloody aspirate suggest an osteochondral fracture.
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Is There Localized Tenderness?
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Next, the physician should gently palpate the knee in an attempt to localize tenderness. In one series, 76% of patients had their surgically confirmed injury localized initially on the basis of focal tenderness.3 Joint line tenderness suggests an injury to the capsule, ligaments, or menisci. At this point, the physician should perform a gentle examination to document the range of motion.
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Are There Any Abnormalities With Stress Testing?
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Ligamentous injuries should be classified on the basis of involved ligaments as well as the degree of involvement (Table 20–5). Grade I (mild) sprains imply a stretching of the fibers without a tear. Grade II (moderate) sprains imply a tear in the ligament fibers without a complete rupture. Grade III (complete) sprains indicate a complete rupture of the ligament.85
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The use and interpretation of various tests to examine the acutely injured knee is controversial.92 After an acute injury, these tests are difficult to perform for the examiner and patient. The following discussion is based on published data and personal experience.
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Stress testing for ligamentous injuries should be employed only after radiographs have ruled out the possibility of a fracture. It is important to document the feel of the joint at maximum stress (firm or “mushy”) along with the amount of joint opening. On stress testing, grade I and II injuries have a firm end point that does not exist for grade III injuries. Measuring the degree of joint opening on stress testing is an objective classification that requires examiner experience and a comparison to the opposite knee. Joints that open 0 to 5 mm suggests a mild (grade I) ligament tear, whereas 5 to 10 mm suggests a moderate (grade II) tear, and greater than 10 mm is consistent with a complete (grade III) tear.
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The valgus stress test is performed with the hip in slight extension to relax the hamstrings (Fig. 20–39). This can be accomplished by hanging the thigh and the leg over the side of the table with the knee in 30-degree flexion and the patient supine. The examiner places his or her thigh against the lateral side of the patient’s thigh to stabilize the femur. The examiner then places the fingers of one hand on the medial aspect of the joint line to feel for joint opening. The other hand grasps the foot and a gentle abduction stress, with external rotation of the foot, is applied. The slight external rotary stress tightens the medial capsular ligaments. It is essential that the stress examination of the injured extremity be compared with that of the uninjured extremity.
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This test is a reliable indicator of injury to the MCL. In our experience and that of others, a torn anterior cruciate will result in a much greater degree of valgus instability. With extreme opening, the PCL may also be ruptured, and the knee should be treated as a reduced dislocation with potential for popliteal artery injuries.93,94
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The valgus stress test in extension is performed after the flexion examination using the same technique, but with the knee extended. The interpretation of this test is similar to the valgus stress test at 30-degree flexion, except that joint opening in extension suggests a greater degree of ligamentous injury. Remember, the knee joint is most stable in extension and the ACL is taut. Joint laxity while in extension is therefore indicative of an anterior cruciate and a posterior capsular rupture, in addition to an MCL tear. When one suspects posterolateral instability a careful valgus stress test in 0 and 30 degrees of knee flexion often will demonstrate the instability.95
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The varus stress test is applied with the knee in 30-degree flexion with the foot and the leg internally rotated (Fig. 20–40).96 The patient’s thigh must be more abducted than during the valgus stress test because the applied force will be toward the examination table. The examiner starts by locating the lateral joint line. The thumb of the hand is placed on the lateral joint line with the rest of the hand stabilizing the medial aspect of the joint. The other hand is placed on the patient’s foot and a varus stress is applied. Joint opening is indicative of a rupture of the LCL. Wide opening suggests possible injury to the structures of the posterolateral knee complex (arcuate ligament, popliteus muscle, lateral head of the gastrocnemius, and iliotibial band) and ACL. Injury to the posterolateral knee complex is rare, reported in more than 2% of all acute ligamentous knee injuries.97
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The varus stress test performed with the knee in extension with internal rotation of the leg can also be performed. Significant joint opening during this test is more likely to suggest injury to the LCL, posterolateral knee complex, or ACL, than the varus stress test in flexion. A particularly wide opening may indicate a posterior cruciate rupture.98
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The anterior drawer test assesses the integrity of the ACL. However, following an acute injury, this test is difficult to perform and lacks sensitivity. When performing the anterior drawer test, the patient must be in a supine, relaxed position. The hip should be in 45-degree flexion with the knee in 80- to 90-degree flexion, and the foot immobilized. The examiner should then place the hands on the upper tibia with the fingers in the popliteal fossa and ensure that the hamstring muscles are relaxed. At this point, laxity is assessed by attempting to push and pull the tibia in an anterior–posterior direction. It is important to perform the test on both the injured and uninjured knee. The anterior drawer test is positive in up to 77% of patients with an ACL rupture.99,100 Unfortunately, this number overestimates the sensitivity of this test in patients with acute knee injuries.
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The Lachman test is more sensitive for an acute ACL injury than the anterior drawer test.101 To perform the Lachman test, begin with the knee in full extension. Cup the distal femur in one hand and elevate it, allowing the knee to flex proximally (Fig. 20–41). Place the other hand on the proximal tibia at approximately the level of the tibial tuberosity and attempt to displace the tibia anteriorly on the femur. Anterior displacement as compared with the opposite side indicates a positive test. In one study, the Lachman test was positive in 99% of patients with rupture of the ACL.102 This test is more easily performed than the anterior drawer sign in the patient who has a markedly swollen knee. Palpable hamstring spasm when performing the Lachman maneuver or the anterior drawer has been shown to interfere with the interpretation of this test in the awake patient.103
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The pivot shift test has also been described for the diagnosis of ACL tears. To perform this test, the examiner internally rotates the leg with one hand, while the other hand rests laterally at approximately the level of the fibular head (Fig. 20–42). A mild valgus stress is applied with slight traction on the fully extended knee. The knee is gradually flexed. With a positive test, the lateral femoral–tibial articulation, which starts out subluxed, is felt to “pop” back to a reduced state at approximately 30-degree flexion.
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The posterior drawer test is performed in a similar manner to the anterior drawer test, except that a posterior force is applied to the anterior tibia (Fig. 20–43). A positive posterior drawer test indicates a rupture of the PCL. A negative test, however, does not exclude this injury. PCL injuries are more common than was once recognized.104 These injuries account for 1% to 20% of ligament injuries and occur most commonly after sports and motor vehicle collisions.104,105
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Is There Muscle Weakness?
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After a negative examination for ligamentous instability, the muscle strength of the involved extremity should be assessed and compared with the normal extremity. Loss of muscular strength may be seen after rupture of a musculotendinous unit.106
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Plain radiographs of the knee are usually necessary to rule out an associated fracture. A Segond fracture is a subtle avulsion fracture of the lateral tibial condyle that suggests a high likelihood of an ACL tear or menisci injury (Fig. 20–44). More recently, a “reverse Segond” fracture was also described that suggests a high likelihood of a PCL tear or menisci injury.107 A “reverse segond” fracture is a subtle avulsion fracture of the medial tibial condyle that represents an avulsion of the deep portion of the MCL (Fig. 20–45) These films should precede an in-depth physical examination. If the radiographs are normal, diagnostic manipulation and stress testing can be undertaken.
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It is likely that plain radiographs will be all that the emergency physician has at their disposal. The valgus stress test performed while taking a plain film is useful when uncertain of the degree of opening.108 However, it should be understood that with the advent of MRI, the delineation of soft-tissue injuries has been revolutionized. The accuracy in diagnosing ligamentous injuries based on confirmation by arthroscopic findings, may be as high as 99%.109–115
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The initial management of ligamentous injuries of the knee should include ice, elevation, and a Jones compression dressing extending from the midcalf to the midthigh (Appendix A–15). Alternately, a knee immobilizer (Appendix A–16) or long-leg posterior splint (Appendix A–17) may be used.
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Stable knee injuries refer to grade I or II injuries of a single ligament after an adequate examination can be performed. The treatment protocol for stable knee injuries is outlined in Table 20–6. The involvement of multiple ligaments or a single ligament with a grade III injury is considered unstable, requiring immobilization, nonweight bearing, and orthopedic referral.116
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Frequently, an accurate initial examination will be impossible secondary to swelling and muscular spasm. When significant joint instability exists on stress testing, operative treatment is indicated. In the presence of significant spasm and a negative initial examination, the injured extremity should be reexamined 24 hours later for confirmation of the previous findings and the patient should be kept nonweight bearing. Intravenous analgesics, intra-articular lidocaine, and even general anesthesia may be necessary to gain a reliable physical examination even after 1 to 2 days. Reexamination is indicated in a stable knee when any of the criteria listed in Table 20–7 are present.
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Nonoperative therapy for complete tears of the MCL with only mild-to-moderate joint instability is advocated.62,117 The treatment has been divided into three phases. In phase A, the leg is placed in an orthosis in approximately 30-degree flexion with partial weight bearing with crutches. Isometric quadriceps exercises and hip strengthening exercises are started in the second week. In phase B, which lasts for an additional 4 weeks, the orthosis is adjusted to allow 30 to 90 degrees of motion and isotonic as well as isokinetic exercises are performed.118 In phase C, which occurs 6 weeks after diagnosis, the orthosis is removed and exercises are continued with a mild running program. When significant joint instability exists on stress testing, operative treatment is indicated.
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It is important to rule out concomitant cruciate ligament ruptures or meniscus injury. When an MCL and ACL injury coexist, the majority of orthopedic surgeons treat the MCL injury first with conservative management, followed by delayed ACL reconstruction.
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Isolated LCL injuries are also treated nonoperatively. When there is associated genu varum or injury to the posterolateral ligamentous complex or the PCL, surgery is indicated.62
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Isolated ACL tears are common and can be treated with partial weight bearing with crutches. Immobilization is not needed unless there are other ligamentous injuries and joint instability. Strengthening exercises are started after range of motion has returned. These injuries are managed operatively or nonoperatively. The decision to reconstruct the ligament depends on the patient’s age, activity level, patient preferences, and the presence of additional injuries. Operative repair is performed via arthroscopy in most cases. The ACL is reconstructed using autografts from the middle third of the patella tendon or a semitendinosus or gracilis graft.33
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In contrast to ACL injuries, isolated PCL tears are uncommon. When they do occur, they are usually treated nonoperatively.105 Isolated acute PCL injuries should be managed by splinting the knee in extension until the pain subsides, then allowing early motion. It is essential that the rehabilitation of this ligament emphasizes quadriceps strengthening.
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Surgical reconstruction is reserved for symptomatic chronic PCL injuries and acute combined injuries (ACL, MCL, or posterolateral complex).119 In patients where a PCL injury is accompanied by a bony avulsion, operative treatment is recommended.105
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A small percentage of sprains become more painful during the healing phase. As the pain becomes severe, flexion may be limited. After 3 to 4 weeks, the plain film will show calcification in the area of the injured ligament. This condition is commonly referred to as post-traumatic periarticular ossification or Pellegrini–Stieda disease. Pathologically, calcium is deposited in the hematoma surrounding the partially torn ligament. This calcified mass may be connected to the underlying bone by way of a pedicle. In the early stages of development, massage or manipulation may worsen the symptoms. The recommended treatment includes a compression dressing and multiple punctures to enhance resorption of the calcium.
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The medial meniscus is a “C”-shaped structure that is divided into an anterior and posterior horn. It is attached to the knee in three locations—on each end (intercondylar eminences) and at its midpoint (deep medial capsular ligament). The lateral meniscus also has an anterior and posterior horn. The lateral meniscus has more of an “O” shape and is attached medially to the intercondylar eminence (Fig. 20–46). The menisci move posteriorly with flexion and in an anterior direction with extension. Because of its single medial attachment, the lateral meniscus is more mobile than the medial meniscus.120
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Meniscal degenerative changes typically begin in the second decade of life and progress more rapidly under conditions of undue stress.121 Several factors increase the propensity for meniscal injuries, including a congenitally discoid meniscus, weakness of the surrounding musculature, and ligamentous laxity. Once an injury has occurred, healing is limited because the menisci are relatively avascular with a capillary supply limited to the peripheral one-fourth.
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One-half to two-thirds of meniscal tears are longitudinal, extending from the anterior to the posterior horn (Fig. 20–47A and 20–47B). These injuries are referred to as “bucket handle tears” and can result in migration of the torn meniscus into the interior of the knee joint (Fig. 20–47C). The fragment may become uplifted, resulting in locking of the knee joint (Fig. 20–47D). The medial meniscus is more commonly affected because of its more secure attachments. Transverse tears are uncommon and may be seen in both the medial and lateral menisci (Fig. 20–47E). Transverse tears or a spontaneous detachment is usually seen after a degenerative process with repeated exposure to minor stress.
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Meniscal injuries occur frequently in patients with sudden rotary or extension–flexion motions. In older patients with degenerative disease of the menisci, a simple twist or squatting motion may result in a tear. With knee flexion, the femur rotates internally on the fixed tibia, and displaces the medial meniscus toward the center of the joint. With a rapid forceful extension, the meniscus may be trapped centrally, resulting in peripheral segment stretching or tearing. With knee flexion, the lateral meniscus is also displaced centrally and a sudden forceful extension may result in a transverse tear at the junction of the anterior and middle thirds.
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The sensitivity of detecting a meniscal lesion by any one clinical test is low.120,121 The combined use of history and physical examination improves the ability of the experienced clinician to detect these injuries. The emergency physician should have a high index of suspicion for these injuries and refer patients to their primary physician or an orthopedist when questions arise.
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The menisci have no sensory nerve fibers, and the pain that results after these injuries is from irritation of the ligaments near the joint line. Several symptoms suggest the presence of a meniscal tear including (1) joint line pain, (2) joint effusion, (3) locking, and (4) giving way of the knee.
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Joint pain or tenderness on palpation of the joint line is seen in three-fourths of patients after a meniscal injury.108 Bragard sign (indicating medial meniscus injury) refers to point tenderness along the anterior medial joint line that is increased with internal rotation and extension of the tibia. With internal rotation and extension, the torn medial meniscus is forced against the palpating finger of the examiner. To confirm a meniscal tear, Steinmann’s sign may be useful (Fig. 20–48). This sign is considered positive for a meniscal tear when flexion of the knee displaces the point of maximal tenderness posteriorly. This test is useful to distinguish meniscal from ligamentous injuries because when the ligaments are the source of pain, the location of maximal tenderness will not change.
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A joint effusion immediately after an injury suggests a ligamentous injury or an osteochondral fracture. Effusions developing 6 to 12 hours after an injury typically follow minor ligamentous sprains or meniscal tears. An acute tear in a degenerated meniscus may produce no effusion.
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Knee locking may be of two types—true or pseudo. Pseudo locking is usually secondary to an effusion that causes pain and muscle spasm. True locking occurs spontaneously with some degree of flexion to the knee. A torn meniscus, loose body, rupture of the cruciate ligament, or an osteochondral fracture can all cause true locking. Childhood locking is rare; however, it may indicate a congenital discoid meniscus.92
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Only 30% of patients with meniscal injuries have true locking. Classically, the patient will complain of a sudden inability to fully extend the knee. Extension can be completed by rotating and passively extending the knee. True locking due to a meniscal tear is never complete, as some extension against a rubbery resistance will be present. In addition, meniscal injuries rarely lock in full extension. An inability to fully extend the knee after trauma is usually secondary to muscular splinting, a loose body, or an effusion.
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Giving way of the injured knee is a common complaint of patients with meniscal tears.122 It occurs when the knee cannot support weight on it irrespective of pain. When a patient reports that the knee gives way, the physician should ascertain the frequency, as well as any previous injuries to the knee. Other causes of this complaint include quadriceps weakness, patellar disorders, and ACL injuries.
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There are several clinical signs that suggest the presence of a meniscal tear or help to differentiate it from a ligamentous tear.
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Payr sign involves placing the patient in a cross-legged position and pushing down on the thigh (Fig. 20–49). When this causes posterior knee pain, it suggests a tear of the posterior horn of the medial meniscus.
Internal rotation of the flexed knee will result in pain in the anterolateral joint line in patients with a lesion of the lateral meniscus.
Anteromedial joint line pain with external rotation of the flexed knee is indicative of a medial meniscus tear.
Apley test is performed on a prone patient with the knee flexed (Fig. 20–50). The examiner gradually extends the leg while it is externally rotated. This maneuver is repeated first while providing distraction and then compression. If the pain is worse with compression the test is positive, indicating the possibility of a medial meniscus tear.
McMurray test is performed with the patient supine and the hip and knee flexed (Fig. 20–51). To check the medial meniscus, the examiner palpates the posteromedial joint line with one hand while the other hand grasps the foot. The leg is externally rotated to trap the medial meniscus and the knee is slowly extended. Conversely, the lateral meniscus is examined with the clinician palpating the posterolateral joint line while internally rotating the leg. A painful click, popping, or thud felt in early extension is considered abnormal. Unfortunately, McMurray test has been found to have a limited sensitivity in detecting meniscal lesions.123,124
Thessaly test is a newer test for the detection of meniscal tears that was originally described in 2005.125 The Thessaly test is performed with the patient standing on the affected leg only while the examiner holds their hands (Fig. 20–52). The patient flexes their knee to 5 degrees and then rotates their knee and body, internally and externally, three times, keeping the knee flexed. The test is repeated at 20 degrees of knee flexion. This maneuver causes a dynamic reproduction of load transmission in the knee joint that subjects the meniscus to an excessive load and often reproduces the pain they reported. This test is considered positive if the patient experiences medial or lateral joint line discomfort or has the sense of locking or catching. The sensitivity and specificity of detecting injuries of the medial meniscus was 66% and 96%, respectively, at 5 degrees of flexion, and 89% and 97%, respectively, at 20 degrees of flexion. For the lateral meniscus, the sensitivity and specificity at 5 degrees of flexion was 81% and 91%, respectively, and at 20 degrees of flexion, 92% and 96%. Overall, accuracy for detecting a meniscal injury at 20 degrees of flexion was 94% for the medical meniscus and 96% for the lateral meniscus.
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Plain films should be obtained, but are usually negative. MRI is useful in detecting meniscal injuries, but is expensive and cannot readily be obtained from the ED. In addition, many authors feel that the accuracy of the clinical evaluation is comparable with MRI and that this imaging modality should be sparingly used in cases when the diagnosis remains unclear.120,126
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The accuracy of MRI was initially reported between 80% and 90% for meniscal injuries, but with improved technology and experience reading these films accuracy has improved to 90% to 95%.84,120,127 However, relying blindly on MRI to determine surgical intervention would result in inappropriate treatment. In one study using MRI in asymptomatic patients, 13% of patients younger than 45 years and 36% of patients older than 45 years were diagnosed with a meniscal tear.128 In elderly patients, meniscal tears are found in 65% of asymptomatic patients.129
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Arthroscopy is considered the gold standard for making the diagnosis and is also valuable because it can provide definitive treatment. The accuracy of arthroscopy is as high as 98%, depending on the skill and the experience of the arthroscopist.121,130
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Meniscal injuries frequently accompany ligamentous knee injuries and particularly injuries to the MCL and ACL. One-third of all meniscal tears are associated with an ACL injury. Meniscal injuries are also frequently associated with tibial plateau fractures, occurring in up to 47% of patients.120
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Patients presenting with an acute meniscal tear without ligamentous injuries should have a bulky compression dressing (Appendix A–15), knee immobilizer (Appendix A–16), or a long-leg posterior splint applied (Appendix A–17). Twenty-four hours after the initial injury and treatment, the patient should be reexamined to exclude an occult ligamentous injury.131 Those patients with meniscal tears without associated ligamentous injuries should be kept nonweight bearing if the pain is severe. It is important that immobilization does not persist for more than 2 to 4 days and that quadriceps-strengthening exercises are begun as early as possible. Referral to a primary provider is appropriate for minor injuries, whereas orthopedic referral is needed whenever a significant effusion or instability of the joint is present. In patients with chronic symptoms, orthopedic referral should be provided whenever the patient reports locking, giving way, or catching.130
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Nonoperative management is more likely to succeed in patients who are able to bear weight, who have developed swelling 24 to 48 hours after injury, who have minimal swelling, and who possess a full range of motion. Peripheral meniscal injuries also do better with nonoperative management because of improved vascularity to the peripheral portion of the meniscus. Limited improvement in symptoms after 3 weeks of conservative therapy suggests that surgery will likely be required.
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The indications for arthroscopy include (1) persistent symptoms that affect daily activities, (2) positive physical findings of meniscal injury, (3) failure to respond to conservative management, and (4) absence of other causes of knee pain.120 Depending on the size, direction, and location of the tear, the surgeon may repair, remove, or leave the lesion to heal on its own.101,120,132
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Meniscal repair is preferable to maintain its important role in shock absorption within the knee. Meniscal tears that can be repaired have the following characteristics in common: (1) a tear is located no more than 3 mm from the meniscocapsular junction, (2) minimal damage has occurred to the body of the meniscus, (3) a tear that can be displaced with probing, and (4) a complete vertical longitudinal tear greater than 10 mm.120,133,134 When repair is not feasible, partial meniscectomy is advocated.135,136 In some instances, the meniscal lesion will heal spontaneously. Stable vertical longitudinal tears heal spontaneously without treatment in 65% of cases.120
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A locked knee secondary to a meniscal tear should be reduced within 24 hours after the injury. The knee can be reduced by positioning the patient with the extremity hanging off the edge of the table and the knee in 90-degree flexion.137 Gravity will distract the tibia from the femur. Intra-articular injection of 5 to 10 mL of local anesthetic will aid in unlocking the knee by reducing pain. The knee may unlock on its own after a period of rest (30 minutes) in this position. If it does not, mild rotation of the tibia with careful traction along the axis of the leg will usually result in reduction. If unsuccessful after a gentle attempt, a posterior splint should be applied. Manipulation of the acutely locked knee may further damage the involved meniscus, and therefore, consultation before further attempts at reduction is strongly recommended.
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Osteochondritis Dissecans
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Osteochondritis dissecans, a condition of focal subchondral bone necrosis leading to articular cartilage disruption and displacement of a bony fragment into the joint space, is common in the knee joint, accounting for 75% of all cases. It occurs most frequently in the medial femoral condyle, but the lateral femoral condyle and patella are also affected. The remaining 25% of cases of osteochondritis dissecans occur in the elbow and ankle.
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There are several proposed theories as to the etiology of osteochondritis dissecans, including localized ischemia and repetitive trauma. The surface of the joint becomes irregular, predisposing toward the development of osteoarthritis. In some instances, a sequestrum of bone or cartilage may become free in the joint and locking occurs.
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Clinical Presentation
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Frequently, this diagnosis is made in an asymptomatic patient on the basis of radiographic findings alone. Symptoms can include a persistent ache at rest, which is exacerbated with exercise. Some patients complain of a stiff sensation that is relieved by kicking. Recurrent knee effusions may be associated with this disorder. Percussion of the patella with the knee in flexion typically exacerbates the pain.
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The plain film will be negative in early cases. Later, a cavity surrounded by dense bone may be seen (Figs. 20–53 and 20–54).138
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Lesions are radiographically occult in up to 57% patients with chronic knee pain.139 Radionuclide bone scans, CT, and MRI are much more sensitive than plain films in identifying these lesions. MRI is of particular value in determining the need for operative intervention.140
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The treatment of this condition is different in adults versus children. Children tend to heal well with conservative treatment, whereas adults frequently require surgery. Immobilization in a cast with nonweight bearing for 6 to 12 months frequently results in resolution of a newly acquired lesion in a child. Surgery is recommended in adults to prevent the development of premature degenerative arthritis. When a loose body is present in the joint space, surgical removal is indicated in both children and adults. Controversy exists as to the best surgical method to employ.141–143 Arthroscopic surgery has yielded excellent results in this condition.144–146
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These injuries typically present with persistent pain after an injury without radiographic abnormalities. Chondral fractures involve only cartilage, whereas osteochondral fractures involve the cartilage as well as the subchondral bone. The most common mechanism is a direct impact over the involved area.
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These injuries should be suspected if the patient’s complaints are significant in the absence of physical findings. Acutely localized tenderness, joint locking, and hemarthrosis are frequently associated with this injury. These injuries are often confused with a meniscal tear although arthroscopy will definitely exclude this problem.
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Arthroscopy is indicated in almost all cases. Degenerative arthritis with chronic pain, locking, and effusions develops if these injuries are left untreated.
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Patellofemoral Dysfunction (Chondromalacia Patellae)
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Osteoarthritis of the knee is covered in Chapter 3. Because the patellofemoral joint is unique, it will be covered separately. Patellofemoral arthritis is the result of erosion and degeneration of the patellar cartilage. Risk factors for patellofemoral arthritis are listed in Table 20–8.147 The terms chondromalacia patellae and patellar malalignment syndrome are used to describe premature patellar cartilage erosion occurring commonly in young adults, particularly women, due to patellar malalignment.
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The patella acts to improve the function of the quadriceps mechanism and decreases the forces applied to the patellar tendon. The angle at which this force acts is believed to alter the patellofemoral mechanics and predispose to injury. When the angle is normal, pressure is distributed evenly across the patella. When the angle is increased, however, the lateral facet of the patella assumes a greater load, and is injured.147
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Patellar malalignment is determined clinically by measuring the Q angle (Fig. 20–55). Two lines intersecting through the center of the patella form this angle. The first line is drawn from the middle of the femur through the center of the patella. The second line is drawn from the center of the patella through the tibial tubercle. The normal Q angle is 15 degrees, whereas measurements greater than 20 degrees are considered abnormal.
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Clinical Presentation
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When due to patellar malalignment, symptoms begin in the adolescent age group or the young adult. The patient will complain of a deep aching in the knees without a history of recent trauma.148,149 Strenuous athletic activities or prolonged sitting may exacerbate the pain hours later. Eventually, as the disorder progresses, slight exertion, as with climbing steps, will exacerbate the pain. The pain is usually localized to the anterior or medial portion of the knee. Acute trauma to the knee as during a fall may result in retropatellar pain and, in some instances, the development of chondromalacia patellae over a period of several weeks.
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During the physical examination, the knee should be in slight flexion, thus drawing the patella into the femoral groove. Palpation and compression in this position will avoid synovial entrapment. Firm compression of the patella into the medial femoral groove will elicit pain, which is virtually pathognomonic. Anterior knee pain is present when the knee is maximally flexed. In addition, palpation of the undersurface of the medially displaced patella will typically yield tenderness and crepitus (Fig. 20–56). Knee extension against resistance is also painful through the terminal 30 to 40 degrees.
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The patellar inhibition test is performed with the knee extended. The examiner pushes the patella inferiorly into the femoral groove. The patient is then asked to contract the quadriceps muscle while the patella is held firmly against the femoral condyles (Fig. 20–57). Pain, tenderness, and crepitus are diagnostic of patellofemoral joint arthropathy.
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In addition to the Q angle, the examiner should note the course of the patella through flexion and extension of the knee. Normally with extension, the patella moves vertically with a slight medial shift as full extension is approached. A hypermobile or wandering patellae (patellar malalignment) with knee extension predispose to the development of chondromalacia patellae.
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Patellofemoral arthritis may be confused with several other causes of anterior knee pain including a torn medial meniscus, prepatellar bursitis, pes anserinus bursitis, fat pad syndrome, and osteochondritis dissecans.
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Radiographs are typically of little diagnostic value in a patient with this condition. Chronic changes including sclerosis or osteophyte development, however, may occasionally be seen.
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Conservative treatment includes rest, nonsteroidal anti-inflammatory medications, and isometric quadriceps strengthening exercises. Isometric quadriceps exercises are performed with the patient lying down and the lower extremity held horizontal to the ground. The patient is instructed to lift the leg with the knee in full extension and hold this position for 5 seconds. This is repeated for 3 sets of 20 daily. The same technique is used with the knee held in 30-degree flexion. It is of critical importance to stress to the patient that the straight-leg exercises with the knee held at 30-degree flexion are key to resolution of the symptoms.150
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Steroid use is not recommended as it may increase the rate of cartilage degradation. The avoidance of activities such as squatting, running, kneeling, and climbing of steps is strongly recommended during the initial management phase. Immobilization is contraindicated as it leads to quadriceps atrophy that may exaggerate patellar malalignment.
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Dislocations of the knee are considered orthopedic emergencies because an associated popliteal artery injury is present in one-third of these cases.151 The incidence of knee dislocation has been estimated to be less than 0.02%, but this figure underestimates the true incidence because it does not take into account dislocations that have spontaneously reduced.152 Therefore, the diagnosis can only be made if the examining physician retains a high index of suspicion.
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Dislocations are classified as anterior (40%), posterior (33%), lateral (18%), medial (4%), or rotary (uncommon) on the basis of the direction of the tibia in relation to the femur (Fig. 20–58). Combinations of these dislocations also occur. The most common combination is the posterolateral dislocation.153
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Bicruciate ligament injury without radiographic confirmation of dislocation is also considered a knee dislocation because these injuries are associated with the same high rate of associated neurovascular injury. In one series, more than half of the popliteal artery injuries occurred in patients with spontaneously reduced bicruciate ligament injuries.154
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Knee dislocations are due to high-energy (motor vehicle collision, fall from height) and low-energy (minor fall, athletic activity) trauma. Motor vehicle collisions account for two-thirds of cases.84,155 Low-energy mechanisms account for up to 20% of cases and are especially common in patients with a high body mass index after simple falls. Open dislocations are present in 16% of cases and are usually due to a high-energy mechanism.154
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Anterior dislocations typically result from hyperextension. Hyperextension results in a tear of the posterior capsule followed by a rupture of the anterior cruciate and a partial tear of the posterior cruciate. Posterior dislocations usually result from a direct force applied to the anterior tibia with the knee flexed slightly. There is posterior displacement of the tibia with rupture of the posterior capsule and cruciates. A violent adduction force on the tibia against the femur may result in a medial dislocation. Rotary posterolateral dislocations are seen when an anteromedial force acts on the anterior tibia, resulting in a posterior dislocation with rotation. A posteromedial dislocation is the result of anterolateral force acting on the anterior tibia.
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An accurate diagnosis of a knee dislocation is imperative and is based on a high index of suspicion. Spontaneous reduction prior to ED presentation is not uncommon and does not mean that the patient is not at risk for associated vascular injuries. A review of 63 knee dislocations noted that two-thirds were found in a reduced position at presentation.156
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Axiom: A grossly unstable knee after a traumatic injury should be considered a reduced dislocation.
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The initial assessment of a potentially dislocated knee is limited to inspection, palpation, and a distal neurovascular examination. Gross deformity may not be present due to significant adipose tissue or reduction prior to arrival in the ED (Fig. 20–59). There may or may not be an effusion because tears in the joint capsule will allow blood to dissect into the surrounding tissues.
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The distal neurovascular status must be assessed early and completely in all patients. Diminished or absent distal pulses, distal ischemia, an ankle-brachial index (ABI) less than 0.9, or an expanding or pulsatile hematoma are hard evidence of a vascular injury and necessitate surgical exploration.155 Nevertheless, a serious arterial injury may be present despite a warm foot or the presence of a distal pulse. Pulse examination is only 80% sensitive for detecting popliteal artery injury.151
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The ligamentous structures are examined, but this is difficult secondary to pain. A Lachman test and a posterior drawer test are used to assess the ACL and PCL, respectively. The collateral ligaments are stressed at 30-degree flexion.152 Hyperextension should be avoided because it places unnecessary traction on the peroneal nerve and popliteal artery.
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Peroneal nerve injury is assessed by noting hypoesthesia in the first web space or loss of dorsiflexion of the foot. If significant swelling is present in a tense leg, compartment syndrome should be suspected.157
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AP and lateral views demonstrate the knee dislocation (unless it has spontaneously reduced) and usually any associated fractures (Fig. 20–60).
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Arteriography has been considered the gold standard for diagnosing popliteal artery injuries, including the difficult-to-detect intimal injury. However, CT angiography is quickly surpassing arteriography because it is more readily available and has fewer complications when compared to traditional arteriography (Fig. 20–61).158,159
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CT is also playing a larger role in the evaluation of knee dislocations due to its higher sensitivity for fractures and associated proximal tibiofibular dislocations.159
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In patients without hard signs of vascular injury, duplex Doppler ultrasonography may be beneficial. The reported sensitivity is 95% with a specificity of 99%. Ultrasound can miss intimal tears, however, so the gold standard remains arteriography or CT angiography.
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Knee dislocations are associated with several significant injuries that are divided into three categories—vascular, ligamentous, and peripheral nerve injuries. In addition to the direct injuries that occur to the vessels and nerves following a knee dislocation, compartment syndrome may also occur due to significant soft-tissue swelling and hemorrhage. Concomitant fractures and other injuries are especially common when the dislocation is due to a high-energy mechanism.
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Anatomically, the popliteal artery is firmly anchored proximally by the adductor magnus muscle and distally by the gastrocnemius and soleus muscles. These attachments make the artery susceptible to injury and account for the 30% to 40% incidence of vascular injury after a knee dislocation. Vascular injury is more common after anterior and posterior dislocations, as well as following a high-energy mechanism.160 When injured, emergent repair is indicated because, if delayed more than 8 hours, up to 86% of patients will require an amputation.161
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Rupture of the ACL and PCL is present in all cases of knee dislocations with rare exception. The medial collateral is the next most common ligamentous injury occurring in 50% of cases, whereas the posterolateral complex is injured in 28%.154 The direction of the dislocation does not correlate with ligamentous injury. Muscle injury (gastrocnemii), meniscal damage, and chondral fractures may also be present.
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Nerve injury associated with knee dislocations is present in 16% to 40% of cases.152 The tibial and common peroneal nerves are not anchored as securely as the popliteal artery and, therefore, are injured less frequently. These injuries range from simple neurapraxia to complete disruption of the neural elements, which is rare. The mechanism of neural damage is usually a traction injury. Traction injuries to the peroneal and tibial nerves are frequently seen after anterior dislocations. The treatment of these injuries is controversial and left to the consultant.
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The emergency management of these injuries includes reduction, immobilization, assessment of vascular injuries, and emergent referral. Reduction should be performed with adequate analgesia and procedural sedation as outlined in Chapter 2.
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A posterior dislocation is reduced by having an assistant exert longitudinal traction while the proximal tibia is lifted anteriorly and reduced (Fig. 20–62). It should be noted that the distraction force should be gentle as excessive force may exacerbate arterial injury. An anterior dislocation is reduced in a similar manner, except the femur is lifted anteriorly into a reduced position (Video 20–3). Pressure over the popliteal space should be avoided. A posterolateral dislocation may be irreducible because the medial femoral condyle traps the medial capsule within the joint.153
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After reduction, the knee should be immobilized in a long-leg posterior splint (Appendix A–17) in 15-degree flexion to avoid tension on the popliteal artery.
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Expeditious treatment of a vascular injury is critical to a good outcome. In approximately 10% of cases, normal pulses are restored after reduction of the knee. If signs of ischemia are present, emergent operative exploration is indicated with or without an intraoperative angiogram.
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One study found that 4% of patients with a normal pulse examination who suffered a knee dislocation had a popliteal artery injury.162 If the pulses and perfusion are normal and there is no other evidence of vascular injury (i.e., expanding hematoma), the ABI is measured. The ABI is determined by dividing the systolic blood pressure (obtained by Doppler) of the affected leg by the same measurement in an unaffected upper extremity. The ABI has been found to be a helpful adjunct in detecting occult vascular injury when the rest of the vascular examination is normal. An ABI less than 0.9 is concerning in a patient with a knee dislocation and should warrant consultation and an arteriogram. However, ABIs will miss intimal flaps and false aneurysms as these injuries do not affect the flow of arterial blood.163 In patients with a normal vascular examination with an ABI measurement of greater than 0.9, diagnostic options include an arteriogram, CT angiography or admission for serial examinations (Fig. 20–63).154,162,164–166 Which option is chosen may depend on the hospital setting or the preference of the consultant.
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Once the possibility of vascular insufficiency has been resolved and the acute swelling has diminished, the patient will generally require operative ligamentous repair to achieve the best functional recovery possible.160,167–171 This procedure is generally performed 10 to 14 days following the injury, but should not be delayed more than 3 weeks because excessive scarring makes the procedure more complicated.152
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Knee dislocations are often complicated by the development of significant problems.
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Progressive distal ischemia may develop, resulting in amputation
Degenerative joint disease with arthritis
Persistent joint instability secondary to extensive ligamentous injuries
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Proximal Tibiofibular Dislocation
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Pain along the lateral aspect of the knee must be carefully evaluated as the anatomy and the biomechanics of this region are very complex. Proximal tibiofibular dislocation occurs after trauma, whereas subluxation may be chronic and atraumatic.172 This injury is often confused with a torn lateral meniscus. Proximal tibiofibular dislocations can be anterior, posterior, or superior (Fig. 20–64).173 Anterior dislocations are most common. Superior dislocations are always accompanied by superior displacement of the lateral malleolus.
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Subluxation of the proximal tibiofibular joint occurs when there is symptomatic hypermobility (Fig. 20–65).
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Anterior dislocations typically result from a fall where the leg is flexed and adducted. Posterior dislocations are usually secondary to direct trauma to the flexed knee. A secondary mechanism involves a violent twisting motion as seen in athletics. In addition, violent twisting may rupture the ligaments and result in dislocation.
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The location of the pain is generally along the lateral aspect of the knee. It radiates proximally into the region of the iliotibial band and medially into the patellofemoral joint. In cases of chronic subluxation, the patient will note a “clicking” or “popping” sensation in the front of the knee.173,174
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On examination, there will be a localized exacerbation of pain with inversion or eversion of the ankle. Inspection of the knee will reveal a prominent fibular head in an anterior lateral subluxation or dislocation. The pain will increase with palpation over the fibular head.174 With an anterior dislocation, the fibular head will be more prominent when the knee is flexed. In addition, dorsiflexion and eversion will exacerbate the pain. Superior dislocations present with proximal displacement of the lateral malleolus.
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If this injury is suspected, comparison views are recommended. AP and lateral views are usually adequate in defining this injury. If plain films are not diagnostic, a CT is the most accurate imaging modality to detect this injury.172
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It is important to recall that the peroneal nerve passes inferior to the fibular head and encircles the neck of the fibula. Posterior dislocations are associated frequently with peroneal nerve injuries. Superior dislocations are always associated with interosseous membrane damage.
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Acute dislocations should be reduced by direct manipulation with the knee in flexion. An audible click is often heard as the fibula snaps back into position. Posterior dislocations with interposed soft tissues require operative reduction. After reduction, the patient should be on crutches and nonweight bearing for 2 weeks followed by progressive weight bearing over the next 6 weeks.
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Treatment of chronic proximal tibiofibular subluxation involves modifying the patient’s activities and the use of a supportive strap along with lower leg strengthening exercises. For patients with chronic pain or instability, surgical correction is considered.
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Peroneal nerve injury occurs in 5% of these dislocations and may present as a complication during the recuperation period. Posterior dislocations have a tendency to remain unstable and to develop recurrent subluxation. Degenerative joint disease with arthritis may develop after any of these dislocations.
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Anatomically, the patella is an oval-shaped bone with two facets divided by a vertical ridge. The patella normally articulates in the groove between the femoral condyles. The vastus medialis, medial retinaculum, medial and lateral patellofemoral ligaments, and the patellotibial ligaments prevent dislocation of the patella.
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The most common location of patellar dislocations is lateral. Other dislocations that have been described include medial, superior, horizontal, and intercondylar (Fig. 20–66). Patellar dislocation with vertical axis rotation has also been described.175
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Patellar dislocations are typically seen in patients with chronic patellofemoral anatomic abnormalities. Dislocations and subluxations tend to be recurrent with redislocation rates ranging from 17% to 44%.176 Patellar subluxation is a common condition that usually occurs laterally and is associated with a tear of the retinaculum along the vastus medialis. Severe trauma is necessary for a dislocation to occur with a normal patellofemoral relationship. Patellar dislocations are associated with several conditions as shown in Table 20–9.
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Two mechanisms result in patellar dislocations. A powerful contraction of the quadriceps in combination with sudden flexion and external rotation of the tibia on the femur is the most common cause of a lateral patellar dislocation.175 Direct trauma to the patella with the knee in flexion may result in a dislocation, although this is uncommon. Horizontal dislocations are secondary to a direct blow on the superior pole of the patella followed by rotation.
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The patient will relate a history of feeling the knee “go out” and will note a deformity followed by swelling (Fig. 20–67). Frequently the patella will relocate prior to presentation. If the patella is still dislocated at presentation, deformity and hemarthrosis will be present and the knee will be flexed.
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If spontaneous reduction has occurred, there is generally tenderness along the undersurface of the patella and the patellar apprehension test is positive. To perform this test, the knee is flexed to 30 degrees and the patella is pushed laterally; if the sensation of impending redislocation occurs, the test is considered positive.
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AP and lateral views are usually adequate in assessing this injury (Fig. 20–68). Radiographs should be obtained to exclude a fracture. The presence of a fat–fluid level is indicative of a bony or osteochondral fracture. Note that an abnormal patellofemoral angle is not a reliable radiologic sign of patellar instability in acute dislocation.177
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The most common associated injury is an intra-articular loose body or osteochondral fracture of the medial facet of the patella or the lateral femoral condyle. Osteochondral injuries are present in 40% of cases.84 These injuries are often difficult to see on plain radiographs.
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To reduce a lateral patella dislocation, flex the hip initially. Then, while extending the knee, apply a gentle pressure over the patella in a medial direction (Video 20–4). Intra-articular and horizontal dislocations are sometimes reduced by closed manipulation, although most require open reduction. Superior dislocations and lateral dislocations with vertical axis rotation usually require operative reduction.
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After reduction, radiographs documenting the position of the patella should be obtained. The leg should be placed in a knee immobilizer (Appendix A–16) in full extension for 3 to 7 weeks. Ice is also recommended for the first 24 hours. Referral to an orthopedic surgeon is recommended. Some orthopedic surgeons believe that all first-time dislocations should be surgically repaired initially, whereas others elect for a more conservative approach. Recurrent patellar dislocations should be treated surgically; however, we do not advocate surgical treatment for first-time injuries.178,179 Dislocations associated with an osteochondral fracture are best treated surgically.180,181
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Patellar subluxation is managed conservatively; isometric exercises are initially undertaken to strengthen the quadriceps. Stretching exercises for the hamstrings are also advocated. In cases where tenderness is severe and one notices substantial laxity, the use of a patellar restraining brace is used. Operative therapy is reserved for patients who have failed conservative treatment after 6 to 12 months.
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Patellar dislocations are subject to degenerative arthritis and recurrent dislocation and subluxation.