John H. Wilckens
Simon C. Mears
Ronald P. Byank
Knee, leg, or ankle pain represents one of the most common reasons patients visit their physicians. Pain can be the result of injury, overuse, or a degenerative, inflammatory, or neoplastic process. Because the knee, lower leg, and ankle are weight-bearing structures, pain located in these anatomic structures greatly affects ambulation, activities of daily living, recreation, and employment. This chapter provides an overview of the anatomy of the knee, lower leg, and ankle and presents a commonsense approach to the diagnosis and treatment of pain in these areas.
The Knee
Anatomy
The knee, which is the largest joint in the body, moves along three axes. The principal anatomic components (Fig. 72.1) and their functions are as follows:
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onto the calcaneus as the Achilles tendon. The quadriceps (rectus femoris, vastus medialis, vastus lateralis, and vastus intermedius) forms the extensor mechanism of the knee that inserts onto the patella via the quadriceps tendon and to the tibial tubercle from the patella via the patellar tendon. The patella by its position improves the mechanical advantage of the quadriceps. The patella is stabilized additionally by the medial and lateral retinaculum and the medial patellofemoral ligament (MPFL).
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FIGURE 72.1. A: Important structures of the knee. B: Five bursae of the knee: suprapatellar, prepatellar, superficial patellar tendon, retropatellar tendon, and pes anserinus. |
General Evaluation
A thorough history is essential to evaluation of knee pain. The history should include any episodes of trauma (acute, remote, or chronic), repetitive stress, or overuse; exacerbating factors; location of pain and its radiation; presence of swelling; and mechanical symptoms, such as catching, locking, and giving way.
A systematic, basic knee examination is presented here. Emphasis should be placed on the need to examine the affected knee and to compare it with the contralateral knee.
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Varying amounts of chronic effusion represent the synovial membrane's response to inflammation, which may be mechanical or biologic. A large effusion will allow one to ballot or “bob” the patella. Large effusions can result in pain and stimulation of mechanoreceptors in the joint, causing quadriceps mechanism inhibition and weakness. Swelling about the knee can be extra-articular and extensive. Bursae, particularly the prepatellar bursa, can become quite large and mimic an effusion; the discriminating point is that in an effusion the patella can be palpated and balloted, whereas it usually cannot in prepatellar bursitis. With severe injuries to the knee that involve tearing of the capsule, the hemarthrosis may leak out into the surrounding tissues, making the effusion less dramatic, but usually ecchymosis is visible at the area of capsular injury.
Meniscal Injuries
Definition and Mechanism of Injury
Menisci (see above) frequently are injured, usually as a result of a twisting motion of the knee on a fixed or planted foot. Meniscal tears can occur when an individual
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performs a deep squat followed by a forceful extension to a standing position. In young patients (<30 years old), meniscal injuries usually occur in concert with an injury to a ligament. A meniscus tear can occur in a knee with normal ligaments, but the tear usually occurs through a degenerated portion of the meniscus. Because the menisci are secondary stabilizers, they are at increased risk for tearing with subsequent giving-way episodes in knees in which the ACLs are defective. Degenerative tears can occur with relatively minor trauma. Such patients usually have a prodrome of joint-line tenderness before the meniscus tear.
Signs and Symptoms
Patients with meniscal tears usually present with localized joint-line tenderness and swelling and a history of a specific twisting injury, which may be incidental in the case of a degenerated meniscus. Pain and swelling are worse with weight-bearing and impact-loading activity and may improve with rest. Patients have difficulty with twisting activities and squatting. If the tear displaces, the patient may complain of the knee catching or giving way. If a large tear displaces, it can lock the knee, block full extension, and cause difficulty with walking.
On examination, patients usually have localized joint-line tenderness and, if the tear is symptomatic, an effusion. The McMurray test is a sensitive, but not specific, test for meniscal pathology (1). The test consists of fully flexing the knee of a supine patient, internally rotating the tibia and providing a varus force to pinch the medial meniscus, and then extending the knee. The procedure is repeated with a valgus force to pinch the lateral meniscus. A painful clunk during either part of the test is very suggestive of a displaceable meniscus tear. Some normal mobile menisci may elicit a clear clunk without pain; this finding should be similar in the contralateral knee. Pain alone with the McMurray test is suggestive of a meniscus tear.
Treatment and Prognosis
The overall condition of the knee will dictate the urgency of referral to an orthopedic surgeon. Most symptomatic meniscus tears can be treated with activity modification; rest, ice, compression, and elevation (RICE protocol); and a short course of a nonsteroidal anti-inflammatory medication (NSAID), followed by a referral to an orthopedic surgeon if needed. If the patient's knee is locked (unable to obtain full extension) or the meniscus tear is associated with ligament instability, a more urgent referral to an orthopedic surgeon should be made.
Because meniscus tears usually occur with an injury, radiographs are indicated to rule out a fracture. Radiographs also can provide important information about alignment and degenerative changes. The most useful views are a standing posteroanterior view with the knee flexed 30 degrees and a lateral and tangential view of the patella (Merchant or sunrise view). The need for magnetic resonance imaging (MRI) and who should order it remain controversial. MRI has more than 90% sensitivity and specificity for detecting meniscal abnormality and a strong argument can be made for having the primary care clinician order the MRI. The MRI should not replace a detailed history and thorough examination, but a timely MRI may expedite definitive diagnosis and early treatment. An orthopedic surgeon may order an MRI, not to make the diagnosis of meniscus tear but to rule out other nonoperative conditions such as spontaneous osteonecrosis of the femoral condyle. MRI is extremely sensitive and may detect asymptomatic tears or degenerative changes in the meniscus that may or may not be the pain generators in the knee. MRI findings must be interpreted in the light of physical findings.
Treatment usually consists of an operation on the meniscus via an arthroscopic approach. The central two thirds of the meniscus are avascular, and degenerative tears in this area usually are excised. Large, peripheral tears, particularly in young patients, usually are repaired. Because of the importance of the menisci to the knee, every effort should be made to preserve as much of the stable, healthy meniscus as possible.
Collateral and Cruciate Ligament Injuries
Definition and Mechanism of Injury
Injuries to the ligaments of the knee represent substantial pathology that, if not recognized, can result in instability and additional injury. The MCL is the primary restraint to valgus loading and a secondary restraint to rotational force. The most common mechanism of injury to the MCL is a direct impact on the lateral aspect of the knee, “booking open” the medial compartment. ACL injuries can occur from contact injuries but they occur more commonly from noncontact injuries, as when an individual pivots or changes direction quickly or lands off balance from a jump. PCL injuries usually result from a direct blow to the front of the proximal tibia, such as a dashboard injury in a motor vehicle accident. Isolated LCL injuries are rare (<1% of ligament injuries) because the contralateral leg provides protection against direct contact with the medial aspect of the knee (2). LCL injuries usually occur in concert with ACL and/or PCL injuries.
Signs and Symptoms
ACL injuries usually occur with an audible pop or snap, followed by immediate swelling and pain in the knee and the inability to return to competition. Depending on
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associated disease, patients may or may not be able to bear weight. They describe a giving-way sensation with any lateral or rotational movement. On examination, a patient has difficulty obtaining full extension and has a large, tense a hemarthrosis. Of all hemarthroses that occur after injury in healthy patients, 75% result from ACL injury (3,4).
Acutely, the knee is very painful and difficult to examine. The most diagnostic test is the Lachman test, a gentle, painless, but subtle evaluation. With the knee flexed 15 to 20 degrees, the femur is stabilized with the examiner's opposite hand (for a right-side ACL, the examiner uses the left hand). The tibia is pulled gently forward with the other hand. The observer looks for tibial translation anteriorly and the quality of the termination of motion (end point), that is, does the motion end firmly or softly? The findings are compared with those of the contralateral knee. Other tests with which to diagnose an ACL-deficient knee include the anterior drawer and pivot shift tests. For the anterior drawer test, the patient is positioned supine with the injured knee flexed 90 degrees and the hamstrings relaxed. The examiner sits on the patient's foot, and the tibia is pulled forward. This test is not very sensitive for an acute ACL injury (5). The pivot shift test is performed with the supine patient's knee fully extended. When the tibia is internally rotated and a valgus force is applied to the knee as it is flexed, the knee “shifts” or reduces from the subluxated position. This test reproduces the giving-way phenomenon the patient experiences. Because this test can be painful and cause apprehension, the patient must be relaxed and cooperative. Typically, the pivot shift cannot be tested in the painful, acutely injured knee. Joint-line tenderness associated with an ACL injury may represent meniscal injury, collateral ligament injury, or bone bruising.
The MCL and LCL are easily palpated, and the site of injury can be localized. The integrity of the collateral ligaments is tested by applying valgus and varus force with the knee in 0 degrees and 15 degrees flexion. In the painful, acutely injured knee, this examination is best accomplished with the patient in the supine position, the affected hip abducted, and the affected thigh resting on the examination table. With the patient in this position, the thigh is supported and the patient is more relaxed. Valgus force is administered to the medial leg to test the MCL, and a varus force is administered to the lateral leg to test the LCL. At 15 degrees flexion, the collateral ligaments are the isolated primary stabilizers. Collateral ligament injury can be categorized in three degrees: first degree, varus or valgus force generates pain but does not elicit any joint-line opening; second degree, the joint line gaps but has an end point; and third degree, the joint opens widely without an end point, indicating complete disruption of the ligament. At 0 degrees flexion, the cruciate ligaments provide additional stability against varus and valgus stress. Medial or lateral joint-line opening at 0 degrees flexion indicates a severe injury involving rupture of at least one collateral and one cruciate ligament.
The PCL is best tested with a posterior drawer test. With the patient in a supine position, the affected knee is flexed 90 degrees, and the examiner sits on the patient's foot to stabilize it. The knee is observed for posterior sagging. The examiner then exerts a posteriorly directed force on the proximal tibia. If the anterior lip of the tibial plateau extends beyond the anterior edge of the femoral condyles, the patient has sustained a severe PCL injury. If the tibia stays anterior or equal to the femoral condyles, the patient has a minor PCL injury (6,7). The quadriceps active drawer test also can demonstrate PCL insufficiency (7). In the same position as for a posterior drawer test (described above), the patient pushes the stabilized foot down on the examination table. In the PCL-injured patient, the quadriceps contraction pulls the proximal tibia anteriorly.
If the examination indicates that two or more ligaments are injured, one must consider that the patient has had a knee dislocation that spontaneously reduced. The clinician should perform a detailed distal neurovascular examination to assess possible injury to the popliteal artery and peroneal nerve.
Treatment and Prognosis
These ligamentous injuries are best treated with the RICE protocol, which reduces pain and swelling. NSAIDs are a useful adjunct. Additionally, the knee should be placed in a knee immobilizer for support. Radiographs should be obtained to rule out fracture. The presence of a Segond fracture, a small avulsion fracture of the proximal lateral tibial plateau, is pathognomonic for an ACL injury. Additionally, each collateral and cruciate ligament can fail by pulling off of its bony insertion. Almost always, MRI is required to assess completely the damage to the knee before a treatment plan is developed.
A patient with an ACL injury should be referred to an orthopedic surgeon for complete evaluation and treatment. Isolated MCL injuries are treated nonoperatively and require protective bracing until healed. If a patient has an MCL injury from a noncontact injury, an ACL injury should be suspected. Treatment of a PCL injury depends on its severity: low-grade PCL injuries are treated nonoperatively, but high-grade PCL injuries may require surgery in high-demand patients. LCL injuries almost always occur in conjunction with a cruciate ligament injury. Isolated or associated LCL injuries almost always are repaired or reconstructed.
Because the natural history of an ACL-deficient knee is not completely understood, there is much discussion and controversy about its treatment. In young, active patients, an ACL-deficient knee is prone to recurrent giving way, with more damage to the knee, particularly to the menisci and articular surfaces, which can lead to posttraumatic
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arthritis. ACL reconstruction is recommended for these high-risk patients. Many low-demand, typically older patients can function well without an ACL if they observe proper activity modification, such as eliminating pivoting and jumping activities. Some patients without an ACL are disabled, even in terms of activities of daily living, and are candidates for reconstruction. Although an ACL reconstruction is safe, reliable, and predictable, it represents a big decision for the patient and surgeon. An extensive preoperative and postoperative rehabilitation program is essential for an excellent result.
Knee dislocations should be given an urgent referral to an orthopedic surgeon because such injuries almost always require extensive surgery.
Preoperative rehabilitation (improving ROM, obtaining quadriceps function, and reducing swelling) is valuable in preparing patients with ligamentous injury for surgery because it decreases postoperative stiffness and weakness.
Patella Dislocations
Definition and Mechanism of Injury
Dislocation of the patella is a common injury and represents the second most common cause (after ACL injury) of a traumatic knee hemarthrosis. The mechanism is very similar to that of a noncontact ACL injury: a quick, pivoting motion on a planted foot, with the knee relatively extended. The patella dislocates laterally with a pop. It may reduce spontaneously (with another pop) or remain dislocated lateral to the lateral femoral condyle. Medial patellar dislocations are extremely rare and usually are iatrogenic, secondary to overvigorous surgical treatment of lateral patellar instability (8).
There are two distinct types of patella dislocations: (a) traumatic, which results from a severe injury to the knee and has limited increased risk of reinjury after appropriate treatment; and (b) atraumatic, which results from a relatively minor trauma or after a traumatic dislocation and is more likely to recur. Patients at risk for reinjury are those with patellar malalignment, long patellar tendons (patella alta), generalized ligamentous laxity, or a deficient vastus medialis obliquus. Examining the contralateral uninjured knee helps identify patients at risk for reinjury.
Signs and Symptoms
Patients may present acutely to the emergency room with the patella still dislocated. With relaxation and gentle straightening of the knee, the patella can be pushed gently back into place. Many dislocated patellas spontaneously reduce, and the patient presents with large, tense hemarthroses and medial retinacular pain, indicating rupture of the MPFL complex, which courses from the medial epicondyle (just anterior to the proximal MCL attachment) and inserts along the superior medial corner of the patella. In addition to pain over the ligament, blood leaking into the medial patellar retinacular provides a “doughy” feel to the soft tissue in this area. With a laterally directed force on the patella, one can elicit apprehension in the patient. Special attention should be given to overall limb and patellar alignment and tracking. Patients with femoral anteroversion, tibial torsion, patella alta, and a large quadriceps angle (Q angle, Fig. 72.2) are at risk for recurrent dislocation.
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FIGURE 72.2. The Q angle is constructed by a line connecting the anterior superior iliac spine with the center of the patella to a second line connecting the center of the patella with the tibial tubercle (left). The normal angle is up to 20 degrees. Right: Abnormal Q angle. |
Treatment and Prognosis
Patients with a patellar dislocation should be treated with the RICE protocol to reduce pain and swelling. NSAIDs are an appropriate adjunct. Use of a brace or cast is extremely controversial (9). Although knee immobilization
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is not an unusual treatment for a patellar dislocation, the patella is more unstable in an extended knee than in a flexed knee; therefore, a lateral buttress brace that allows knee flexion and provides a buttress to lateral patellar displacement may be a better choice than immobilization bracing. Additionally, prolonged immobilization leads to quadriceps atrophy and weakness, which is counterproductive; quadriceps strength is the main stabilizer of the patella. Radiographs, including a tangential view of the patella, should be obtained to identify loose fragments that may have occurred with the patellar dislocation or reduction. Use of MRI is helpful but is not indicated for every patellar dislocation. MPFL repair and/or reconstruction is gaining popularity, particularly with patients who have recurrent dislocations. If surgery is contemplated, MRI can identify the area of MPFL injury. MRI can document chondral loose bodies not seen on plain radiographs but which are suspected if the traumatic effusion does not clear in 3 weeks. MRI also should be ordered if an injury in addition to the patellar dislocation, such as an ACL injury, is suspected.
The mainstay of treatment for patella dislocations is physical therapy, which provides most patients with quick resolution of the effusion and improvement in ROM and quadriceps function. Patients with recurrent patella dislocations, atraumatic dislocations, or loose bodies should be referred to an orthopedic surgeon for definitive evaluation and treatment. Surgical treatment may include arthroscopy, open or arthroscopic lateral release, distal patellar realignment, proximal patellar realignment, proximal and distal realignment, and MPFL repair or reconstruction.
Extensor Mechanism Disruption
Definition and Mechanism of Injury
The extensor mechanism, which consists of the quadriceps tendon, patella, and patella tendon, actively extends the knee joint and stabilizes it for locomotion. Rupture of the quadriceps or patellar tendon can result from a forceful quadriceps concentric contraction (such as occurs in jumping) or eccentric contraction (such as occurs when landing from a jump). A direct blow to the patella with the knee in flexion can result in a patella fracture. Tendon rupture also can occur from a corticosteroid injection (e.g., given for tendinitis) in or around the quadriceps or patellar tendon.
Signs and Symptoms
A patient with an extensor mechanism disruption has pain, swelling, inability to extend the knee completely, and difficulty bearing weight. In addition to an effusion and soft-tissue swelling, there is a palpable defect at the site of disruption. With a quadriceps tendon rupture, the patella migrates distally, whereas with a patellar tendon rupture, the patella retracts proximally. A patient with a complete rupture cannot extend the knee, whereas a patient with an incomplete rupture or an intact patellar retinaculum can extend the knee from a partially flexed position.
Treatment and Prognosis
Radiographs should be obtained to document the site of injury to the extensor mechanism. MRI is helpful (but not necessary) for making the diagnosis. The knee should be placed in a knee immobilizer, and the patient should be referred urgently to an orthopedic surgeon. Treatment consists of primary repair of the ruptured tendon or open reduction and internal fixation of a patellar fracture. In rare circumstances, such as a <50% tear in a low-demand patient, partial patellar or quadriceps tendon injuries can be treated with immobilization.
Patellofemoral Pain
Definition and Mechanism of Injury
The extensor mechanism is subjected to magnified forces by many activities, such as ascending/descending stairs, running, squatting, and jumping. Repetitive overuse from such activities can cause pain. In the adolescent, this pain can be localized to the tibial tubercle, the distal insertion of the patellar tendon, causing a traction apophysitis. In adults, such repetitive overactivity may lead to patellar or quadriceps tendinitis. Additionally, patients with malalignment and maltracking have increased patellofemoral pain with repetitive overuse.
Signs and Symptoms
A patient with patellofemoral pain from any of the causes listed has pain around the patella with ascending/descending stairs, running, jumping, squatting, kneeling, or prolonged sitting. Swelling seldom occurs, but there may be crepitus over the patella or quadriceps tendon. Close attention should be paid to patellar stability, alignment, and tracking. A patient with subtle patellar instability has increased patellar mobility, moving more than two quadrants medially or laterally. Patients may have decreased patellar motion and lateral patellar compression. Additionally, patients with chronic patellofemoral pain may have hamstring and hip flexor tightness and core muscle weakness and imbalance. Radiographs should be ordered to rule out rare conditions such as osteochondritis desiccans (osteochondral defect) of the patella, tumor, and bipartite patella, but otherwise they seldom are helpful. Adolescent patients with traction apophysitis may have increased separation or fragmentation of the apophysis. Chronic tendinitis may show tendon calcification. MRI is recommended only for the most recalcitrant cases.
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Treatment and Prognosis
Most patellofemoral pain is self-limiting and will respond to the RICE protocol and reduced activity. If symptoms persist, patients should be afforded a trial of physical therapy, consisting of core strengthening, stretching, and quadriceps open and closed concentric and eccentric strengthening. Additionally, a therapist may use a battery of modalities, including ultrasound, cryotherapy, phonophoresis, iontophoresis, electrostimulation, and cross-friction massage. Patellar malalignment, instability, and maltracking can be improved after treatment with McConnell taping (application of tape to the patella) to improve patellofemoral mechanics (10).
Patients with recalcitrant or recurrent patellofemoral pain should be referred to a physiatrist or orthopedic surgeon for additional evaluation. These conditions seldom require surgery.
Bursitis
Definition and Mechanism of Injury
A bursa is a synovial-lined space that separates adjacent moveable structures, such as tendon or skin and bone, to reduce friction. Overuse can create chronic friction and fluid within the bursa. The bursa can collect fluid from direct trauma and inflammatory processes such as gout and infection.
The bursae commonly located about the knee include the prepatellar bursa (anterior to the patella), retropatellar bursa (posterior to the patellar tendon), pes anserinus bursa (between the distal medial hamstrings and the proximal medial tibia), and iliotibial band (ITB) bursa (located between the ITB and the lateral femoral condyle). ITB bursitis usually results from ITB tendinitis, which commonly develops from a change in a running routine, training errors, real or functional limb-length discrepancies, core weakness, and core muscle imbalance. Prepatellar bursitis can arise from chronic irritation to the anterior part of the knee, as occurs with prolonged kneeling by plumbers or commercial carpet installers.
Signs and Symptoms
Prepatellar bursitis usually presents with painful swelling anterior to the patella. Because the fluid is in front of the patella, the patella is not ballotable. Traumatic bursitis may be accompanied by ecchymosis, and the contained fluid is hemorrhagic. Inflammatory bursitis is painful and presents with warmth and redness. Aspiration may be needed to differentiate a septic process. Septic bursitis has marked warmth, cellulitis, and usually a portal of entry (folliculitis or insect bite). Advanced cases may be associated with lymphangitis and fever.
ITB bursitis/tendinitis presents with localized tenderness over the distal ITB at the lateral epicondyle and possibly down to its insertion on the Gerdy tubercle. ITB tightness can be elicited by the Ober test (11). The Ober test is performed with the patient lying in the lateral decubitus position with the affected limb up. The examiner uses his/her forearm and hand to cradle the patient's knee, flexes and then abducts the patient's hip, and then extends that hip. If the ITB is tight, the leg will remain suspended above the horizontal. Flexing and extending the knee from 15 to 40 degrees in this position elicits pain, crepitance, or snapping at the lateral femoral epicondyle. (At 30 degrees, the ITB typically lies over the lateral femoral condyle. Extended from this position, it is anterior to the lateral femoral epicondyle; flexed from that position, it is posterior to the femoral epicondyle.)
Pes bursitis presents with pain and swelling along the distal insertion of the medial hamstrings, gracilis, semimembranosus, and semitendinosus along the proximal medial tibial plateau. The hamstrings may be tight. Chapter 74 discusses anserine bursitis and its treatment.
Treatment and Prognosis
Bursitis and tendinitis can be treated effectively with the RICE protocol. A short course of NSAIDs may be a helpful adjunct (see Chapter 74). If tendinitis is associated with the bursitis, a physical therapy evaluation is warranted. In addition to traditional stretching and strengthening, the therapists will assess the patient for underlying alignment problems and imbalances and may use modalities such as cryotherapy, iontophoresis, phonophoresis, cross-friction massage, or electrical stimulation to reduce symptoms and improve healing.
If the bursitis persists despite nonoperative treatment, the fluid can be aspirated and a compression dressing can be applied to prevent reaccumulation of the fluid.
If nonoperative treatment (including a well-documented program of physical therapy) for ITB tendinitis and bursitis has failed, referral to an orthopedic surgeon is indicated. Surgery would include excision of the bursa, with lengthening and/or partial sectioning of the ITB to reduce friction at the lateral femoral epicondyle.
Septic bursitis should be treated with aspiration to obtain fluid for culture and sensitivities, and then appropriate parenteral or intravenous antibiotics should be administered. If the septic bursa is associated with fever or lymphangitis, the bursa should be incised, drained, and packed open. This intervention should be performed in an operating room or procedure room setting, which would necessitate a referral to an orthopedic surgeon.
Baker Cysts
Definition and Mechanism of Injury
A popliteal cyst, commonly called a Baker cyst (see Chapter 74), is a synovial cyst that forms in the popliteal space contiguous to the knee-joint cavity. Typically, it is seen with
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degenerative meniscal tears. It also can occur with arthritis of the knee and other inflammatory conditions. The knee joint produces fluid in response to mechanical or biologic inflammation and, as the knee is flexed, the fluid is forced posteriorly. Over time, a popliteal cyst may develop.
Signs and Symptoms
Most Baker cysts are asymptomatic and are noted incidentally on physical examination or MRI. As the cyst grows, it produces a sensation of fullness behind the flexed knee. If the Baker cyst becomes extremely large, it can produce compressive symptoms, particularly of the posterior tibial nerve.
Treatment and Prognosis
Most popliteal cysts resolve or reduce with appropriate treatment of the knee effusion. If a cyst accompanies a degenerative meniscus tear, excision of the tear will decompress the cyst. Occasionally, the cyst requires aspiration or, more rarely, excision. Aspiration or excision without addressing the intra-articular problem may result in cyst recurrence.
Popliteal cysts in preadolescent patients usually resolve spontaneously and do not need treatment unless an intra-articular problem is present.
If a large popliteal cyst ruptures, it may be accompanied by intense pain and swelling in the patient's posterior calf. The symptoms mimic deep venous thrombosis, and a vascular study may be required to rule out deep venous thrombosis.
Septic Knee
Definition and Mechanism of Injury
A deep-space knee infection represents an orthopedic emergency. The knee can be seeded from direct inoculation (knee aspiration or penetrating trauma), hematogenous spread (from a distant infection), or local adjacent tissues. Predisposing factors include arthritis, gout, intravenous drug abuse, alcoholism, diabetes, systemic steroids, or immunosuppression.
Signs and Symptoms
Patients present with pain, swelling, warmth, redness, difficulty with weight-bearing, and painful and limited ROM.
Treatment and Prognosis
A knee-joint aspiration is indicated for all painful, nontraumatic knee effusions. It is important to aspirate the knee through noncellulitic skin to avoid inoculating the knee joint. In addition to culture and sensitivity, a cell count of the aspirated fluid is important. Although white blood cell counts >50,000 can be found with gout, such levels are suspicious for infection. White cell counts >100,000 represent a septic process. If the patient is sexually active, a diagnosis of gonorrhea should be investigated. In Lyme-endemic geographic areas, the patient should be assessed for Lyme disease with appropriate cultures and titers.
Treatment almost always requires incision and drainage, historically via arthrotomy followed by inflow/outflow drains. Arthroscopic lavage and synovial resection are adequate for most septic knees. If surgical treatment is delayed, repeat aspirations and intravenous antibiotics are appropriate initial interventions.
The Lower Leg
Anatomy
The principal anatomic components of the leg and their function are as follows:
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important dynamic stabilizers for the ankle. This compartment does not contain an artery, but the peroneus muscles receive their blood supply via branches of the peroneal artery, a tributary of the posterior tibial artery.
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FIGURE 72.3. Leg anatomy. Left: Coronal view. Right: Cross-sectional view showing compartments. |
Knowledge of lower-limb neuroanatomy, lumbar root source, nerve course, muscle innervation, and sensory components is invaluable to the evaluation and diagnosis of leg pain.
General Evaluation
As with the knee, injuries to the leg can be caused by a single traumatic event or chronic, repetitive stress. An appropriate history is essential (see Chapter 68). The clinician must define the mechanism of injury. If no acute trauma has occurred, then stress injury from chronic repetitive activity or increase in the frequency or duration of the activity is the likely cause. Pain in the leg may be referred pain from back, pelvis, or hip abnormalities. As with the knee, the general principles of inspection, palpation, and evaluation of ROM and strength are addressed:
Differential Diagnosis of Acute Leg Pain
Trauma is a common cause of acute leg pain. Blunt trauma can result in a contusion or, if severe enough, fracture of the tibia and fibula. Because of the superficial nature of the medial border of the tibia, high-energy injuries usually result in an open fracture. Acute pain can result from muscle strain and/or rupture. Rupture (partial or complete) of the proximal medial or lateral head of the gastrocnemius or plantaris can result in severe pain and swelling, mimicking deep venous thrombosis. Delayed-onset muscle soreness and tendinitis are the most common causes of acute pain with a sudden increase in lower leg activity. More rarely, such acute pain can be the result of stress fracture or compartment syndrome. Other etiologies of lower leg pain include sciatica (from a herniated disk or other cause), deep venous thrombosis (see Chapter 57), neurogenic and vascular claudication (see Chapter 94), cellulitis
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(see Chapter 32), myopathy and neuropathy (see Chapter 92), and acute monoarthritis (see Chapter 76).
Acute Compartment Syndrome
Definition and Mechanism of Injury
Compartment syndrome not only is a cause of acute leg pain; it also is a surgical emergency that requires early recognition for a favorable outcome. It is associated with a high rate and amount of indemnity payments in malpractice suits (12). The lower leg contains four compartments (anterior, lateral, superior posterior, and deep posterior) surrounded by a dense, unifying fascia. Injury to the tissues of the lower extremity causes bleeding and swelling. As this bleeding and swelling increase, the pressure in the compartment(s) rises. This scenario is compounded when the compartment pressure eclipses the venous pressure, stopping flow out of the compartment while arterial flow into the compartment continues, escalating the rise in pressure. When compartment pressure exceeds mean arterial pressure, an ischemic process begins to develop and, with time, can lead to muscle and nerve injury and necrosis.
A common misconception is that a fracture is needed to create a compartment syndrome. A compartment syndrome can develop from seemingly minor trauma (e.g., muscle contusion or ankle sprain) or prolonged pressure (as can occur in an individual, overdosed with drugs or alcohol, lying on the lower leg). It can also be exercise-induced or chronic. (See Exertional or Chronic Compartment Syndrome).
Signs and Symptoms
In the awake patient, the most common sign of compartment syndrome is pain out of proportion to the injury, pain that cannot be managed even with liberal doses of narcotics. The compartment(s) involved is swollen and tense. Passive stretch of the muscles through the compartment causes severe pain. Typically, the skin over the compartment has a red, shiny sheen and could mimic an early cellulitis. As the compartment syndrome develops, the patient experiences paresthesias in the distribution of the nerve traversing the compartment and paresis or weakness of the involved muscles. Pulselessness is a very late clinical finding. In trauma patients with low systolic pressure, compartment syndrome can develop at low pressures. Any diagnosis of compartment syndrome should be confirmed by pressure measurements in all suspected compartments.
If the patient is unconscious or uncooperative, compartment pressures can be measured easily with a commercially available unit. All four compartments should be measured.
Controversy exists regarding what pressure level constitutes a developing compartment syndrome, but most surgeons recommend surgical intervention when pressures are elevated to within 30 mm Hg of the patient's diastolic pressure (13).
Treatment and Prognosis
Acute compartment syndrome necessitates an emergent referral to an orthopedic surgeon for immediate fasciotomy of the involved compartments, which relieves the pressure. Elevated pressures for 6 to 8 hours can lead to irreversible muscle and nerve damage. Because extensive muscle damage can lead to rhabdomyolysis and renal failure, the clinician should monitor the patient for these possible developments and treat them accordingly.
Any injury to the lower leg that could lead to swelling should be treated with the RICE protocol in an effort to prevent the potential development of a compartment syndrome. Once a compartment syndrome develops, the limb should be kept horizontal because elevation can decrease mean arterial pressure.
Exertional Leg Pain
Leg pain with walking, running, or vigorous activity represents exertional leg pain and is a common presenting condition. Differential diagnoses include stress fractures, shin splints, medial tibial periostitis, exertional or chronic compartment syndrome, vascular or neurogenic claudication, and radicular nerve root irritation.
Stress Fractures
Definition and Mechanism of Injury
A stress fracture occurs when a bone undergoes excessive or suddenly increased cyclic loading. This mechanical stress stimulates osteoclastic activity, with eventual osteoblastic bone remodeling in an attempt to meet the increased load. If the bone remodeling cannot keep pace with the mechanical loading, the bone will fail with a microfracture or stress fracture. With continued loading, a stress fracture can progress to a complete fracture.
Stress fractures typically are seen in training athletes and military recruits (14). Although many physiologic and biomechanical factors (e.g., cross-sectional area of the tibia, bone mineral density, pes cavus or valgus, and excessive hip external rotation) have been suggested as etiologies of increased risk for stress fracture, training errors are the most common—and most treatable—causes. Training errors include improper footwear, excessive running mileage, and excessive speed work.
Insufficiency fractures are stress fractures that occur in weakened bones under normal loading stress.
Signs and Symptoms
A patient with a stress fracture typically notes the onset of pain with high-impact activity and abatement of the pain with rest. As the stress fracture evolves, the patient
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experiences pain with daily activities or even at rest. Detailed questioning usually can identify a training error, and on physical examination the patient usually has well-localized tenderness over the stress fracture site, with or without swelling or periosteal callus.
With excessive repetitive activity, a stress fracture can develop in almost any bone, including the sacrum, pubic rami, femoral neck (hip), femur, tibia, fibula, tarsals, and metatarsals. In the lower leg, stress fractures usually occur distally in the fibula and almost anywhere in the tibia (medial, proximal, and distal): in the tibial plateau (mimicking knee pathology), medial malleolus (mimicking ankle pathology), and anterior cortex of the tibial shaft.
Treatment and Prognosis
Typically, anteroposterior and lateral radiographs of the tibia and fibula do not show a stress fracture within the first 2 to 3 weeks of symptoms. Early radiographic findings actually represent early healing of the stress fracture, including periosteal callus and sclerosis across an invisible fracture line. An advanced stress fracture can display a radiographic fracture line, which indicates a risk for complete fracture and displacement.
A technetium bone scan allows one to identify stress fractures early (24 hours) in most patients; in the elderly, positive identification on bone scan may be delayed for 48 hours or more. MRI is an expensive but sensitive imaging study for identifying stress fractures. Short T1 inversion recovery (STIR) sequences can provide greater prognostic capability for stress fractures, which would be important in a competitive athlete.
Stress fractures should be referred to an orthopedic surgeon or physician who specializes in sports medicine. Most fractures heal uneventfully with “active rest” (i.e., reduction of activity to below-pain level) without immobilization, but some are prone to progression and/or nonunion (15,16). Initial treatment should limit activity to the point at which the pain begins. If the patient experiences pain with walking, crutches are prescribed. If no pain is associated with normal daily activity, some light, low-impact training is permissible as long as it occurs below the threshold of pain. Smoking should be discouraged to promote bone healing (see Chapter 27).
Training errors should be identified and corrected. If the patient with a stress fracture is a young woman, it is important to inquire about eating habits and menstrual irregularities. There is such a high correlation between stress fractures, amenorrhea, and eating disorders that this complex is referred to as the female triad (17). These patients may require additional referrals for bone density scanning, gynecologic evaluation, and psychological counseling (see Chapters 11, 101, and 103).
Stress fracture prevention includes proper training methods with cyclic or periodic rest to allow the bone an opportunity to remodel. As a general rule, runners should not increase their mileage by >10% per week. Other methods for reducing the risk of stress fracture include varying the exercise programs (cycling, swimming, elliptical trainers), wearing shock-absorbing shoes and/or insoles, and (especially for an individual in training) paying special attention to proper nutrition to support the increased physical needs.
Shin Splints
Definition and Mechanism of Injury
Shin splints are another common cause of exertional leg pain. They often occur with jogging, running, or sustained walking in poorly conditioned individuals and, as do stress fractures, can occur secondary to training errors, including improper shoe wear. Shin splints have been identified as medial tibial periostitis (18). Pain is thought to result from periostitis at the attachment of the posterior tibial muscle and/or the medial soleus on the midshaft of the medial tibia (Fig. 72.4).
Signs and Symptoms
Patients with shin splints have poorly localized tenderness at the junction of the middle and distal medial tibia. Swelling or crepitus may or may not be present.
Radiographs usually are negative but are obtained (after 2–3 weeks of symptoms) to rule out a stress fracture. MRI or a bone scan can be used to image recalcitrant cases and usually show vertical uptake above the medial tibial cortex.
Treatment and Prognosis
Shin splints respond to the RICE protocol and NSAID medication. As symptoms improve, activity can be advanced to the level of the pain threshold. Training errors should be identified and corrected. Patients will improve with formal physical therapy, which should address limb alignment, eccentric and concentric strengthening of the muscles of the lower leg, core strengthening, and modalities such as electrical stimulation, phonophoresis, iontophoresis, and ultrasound (19,20). If the patient has pes planus or cavus, orthotics should be prescribed (see Chapter 73).
Exertional or Chronic Compartment Syndrome
Definition and Mechanism of Injury
In the lower leg, there are four well-described muscle compartments encapsulated by fascial sheaths. When muscles are exercised, they swell. The fascia adjusts to muscle swelling. However, muscle swelling with activity can result in an exercise-related compartment syndrome, although the direct cause remains elusive. Some patients are unable to exercise vigorously for extended periods because of leg pain; other patients develop symptoms with activities they previously could perform without pain.
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FIGURE 72.4. Sites of pain and relevant anatomy for shin splints, anterior compartment syndrome, and lateral compartment syndrome. |
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Signs and Symptoms
Patients with exertional compartment syndrome complain of cramping and aching in the affected lower leg with a predictable level of physical activity. For example, a patient may have no symptoms after running 1 mile but may develop pain after running 1.5 miles. As exercise and symptoms persist, the patient may develop lower leg weakness and distal paresthesias. Symptoms gradually resolve over time with rest.
On physical examination, the patient at rest may have no localized pain. Because the anterior compartment is the one most commonly affected, a patient usually describes pain lateral to the crest of the tibia over the anterior or, less commonly, the lateral compartment. Careful palpation of the anterior and lateral compartments may reveal fascial hernias, that is, palpable defects in the fascia that can be associated with exertional compartment syndrome. Examining the patient after exercise to recreate the threshold of symptoms is extremely helpful. The affected compartments are tight and painful, and subtle fascial hernias are more obvious.
The diagnosis of exertional compartment syndrome can be made with a series of compartment pressure readings: before exercise, immediately after exercise, and later after exercise. Normal at-rest compartment pressure usually is <4 mm Hg. A patient with exertional compartment syndrome usually has elevated at-rest compartment pressure (>8 mm Hg). Immediately after exercise that produces the symptoms, the pressure typically is >30 mm Hg and slowly decreases over time.
Treatment and Prognosis
Patients with exertional compartment syndrome should be referred to an orthopedic surgeon or sports medicine specialist. Because the cause of this syndrome is unknown, it is hard to recommend specific treatment. Nonoperative treatment should include reduced activity, eccentric and concentric muscle strengthening, and accommodative shoe inserts. If symptoms continue, an elective fasciotomy of the involved compartment(s) is recommended. If symptoms with activity are neglected, exertional compartment syndrome can evolve into acute compartment syndrome.
Other Causes of Exertional Leg Pain
Vascular and neurologic claudication is a cause of exertional leg pain in the older patient (>50 years). Frequently, the physical examination with the patient at rest is not very helpful. Vascular studies, including Doppler, are indicated (see Chapter 94). In addition, if spinal stenosis is suspected for neurologic claudication, MRI of the lumbar spine is indicated (see Chapter 71).
Bone and Soft-Tissue Tumors
Patients with a primary bone tumor typically complain of constant, deep, aching pain. Night pain is a common
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feature of malignant tumors. Osteoid osteoma is a benign bony tumor that can cause night pain, which is often relieved by NSAIDs. A sudden increase in pain after mild trauma should raise the possibility of a pathologic fracture and an underlying malignancy. On the other hand, a growing mass, not pain, is the typical presenting complaint of soft-tissue tumors. Constitutional symptoms such as fever, malaise, weakness, and recent weight loss are important symptoms that might be associated with a malignant bone tumor.
The patient should be examined for any local masses, focal tenderness, pain with palpation or weight-bearing, and any peripheral nerve deficit secondary to entrapment. Plain radiographs and other imaging modalities, if needed, should be obtained. Computed tomography is useful for bone tumors, and MRI is useful for soft-tissue tumors. Laboratory studies include a complete blood cell count; calcium, magnesium, and phosphorus levels; alkaline phosphatase activity; and erythrocyte sedimentation rate. Although the results of these tests are nonspecific, they may offer clues regarding bone turnover, an increased inflammatory state, and systemic illness. Patients suspected of having a bone tumor should be referred to an orthopedic surgeon.
Deep Venous Thrombosis
Deep venous thrombosis often presents in a nonspecific manner but is an important potential explanation for lower extremity pain. Chapter 57 provides a full discussion on the management of deep venous thrombosis.
The Ankle
Anatomy
The ankle joint (Fig. 72.5) consists of articulations of the distal tibia and fibula with the talus. The principal anatomic components and their function are as follows:
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FIGURE 72.5. Ankle joint. A: Anterior view. B: Posterior view. C: Lateral view. (From Ramamurti CP, Tiner RV. Orthopedics in primary care. Baltimore: Williams & Wilkins, 1979:245 , with permission.) |
General Evaluation
A focused history is essential (see Chapter 68). As with the knee, ankle injuries can be caused by a single traumatic event or by multiple and chronic stresses. The clinician will need to define the mechanism of injury in order to effect a satisfactory outcome. If no acute trauma has occurred, then stress injury from chronic repetitive activity or increase in the frequency or duration of the activity is the likely cause of injury. As with the knee, the general principles of inspection, palpation, and evaluation of ROM and strength in the ankle are addressed.
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Ankle Sprains
Definition and Mechanism of Injury
Ankle sprains are one of the most common conditions that cause a patient to present to a physician or emergency room. The most common mechanism is an inversion injury to the ankle as the foot begins the foot-strike part of the gait cycle. (Once the foot is planted fully, the ankle mortise provides much of the ankle's stability.) The most commonly injured ligament is the lateral anterior talofibular ligament. The calcaneofibular ligament and the posterior talofibular ligament also can be injured, but usually only by high-energy trauma. All sprains are graded with a ligament grading system (Table 72.1). Medial ankle sprains represent severe ankle injuries. Finally, injury to the syndesmosis results in a “high-ankle” or syndesmosis sprain. This injury usually occurs with rotation of the ankle on a planted foot, with the talus acting as a crowbar to pry open the syndesmosis between the tibia and fibula.
Signs and Symptoms
The patient usually can recall the specific mechanism of injury. Pain and swelling usually develop immediately. Depending on the magnitude of the injury, the patient may or may not be able to bear weight. Physical examination reveals swelling, tenderness, and (later) ecchymosis over the injured ligaments. Reproducing the mechanism of injury exacerbates the pain. Increased laxity may be shown by an anterior drawer test. With the patient's knee flexed over the examination table and the ankle plantarflexed by gravity, the clinician stabilizes the patient's anterior tibia with one hand and uses the other hand to apply forward pressure on the back of the patient's heel, drawing the ankle forward. Increased anterior translation represents ligament injury. Pain along the medial deltoid ligament represents a more severe injury.
Special attention should be directed to the ankle syndesmosis. These injuries present with tenderness at the syndesmosis or proximal fibula, which can be elicited with direct palpation, compression of the syndesmosis, or rotation of the talus within the ankle mortise.
To avoid having to obtain radiographs of all sprained ankles, the Ottawa rules (21) present safe and clear indications for radiographically ruling out fracture with an ankle injury. If the patient has tenderness on direct palpation over the lateral or medial malleolus or proximal fifth metatarsal, radiographs should be obtained. If there is no direct tenderness over these bony prominences with an ankle injury, then radiographs for the acute injury are not indicated. Obviously, if ankle pain does not resolve within the next 6 weeks (the usual time frame for an ankle injury), radiographs are then indicated.
Treatment and Prognosis
Most ankle sprains can be treated with the RICE protocol and protected activity. Although compression with an elastic wrap or immobilization in a cast is commonly used, protection can be provided with a removable fracture boot, stirrup, or lace-up ankle splints that will accommodate increases and decreases in ankle swelling. Crutches
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may be needed to support weight-bearing. Patients with severe, complete, or multiple ankle ligament sprains and syndesmosis sprains (22) should be referred to an orthopedic surgeon or sports medicine specialist.
Most ankle sprains resolve with nonoperative treatment in 2 to 6 weeks. Physical therapy is strongly recommended, particularly for low-energy ankle sprains, to improve not only ROM and strength but also proprioception, or position sense. The therapist can help retrain the ankle and reduce the risk of reinjury.
Medial ankle sprains and syndesmosis ankle sprains represent severe ankle injuries and require prolonged treatment. It may be 2 to 3 months before the patient is symptom-free with full activity. Only chronic, debilitating ankle instability or acute high-grade ankle sprains in the athlete should be considered for surgical repair or reconstruction.
Ankle Fractures
Definition and Mechanism of Injury
Ankle fractures typically occur once the foot is fully planted and the bony mortise is supplying the ankle's stability. Depending on the magnitude and direction of forces, the ankle may fracture. Several systems have been developed for classifying and prognosticating ankle fractures (22).
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TABLE 72.1 Severity of Ligamentous Sprains |
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Signs and Symptoms
The most reliable sign of an ankle fracture is pain with direct palpation over the medial or lateral malleolus. There may or may not be any deformity. Fracture is associated with substantial swelling and ecchymosis. Patients with low-energy ankle fractures may still be able to bear weight.
Treatment and Prognosis
If the patient has pain over the medial or lateral malleoli or proximal fifth metatarsal, anteroposterior, lateral, and mortise (15 degrees internally rotated anteroposterior view) radiographic views of the ankle are indicated. Any fracture of the ankle should be referred to an orthopedic surgeon. If the fracture is nondisplaced and stable, it can be treated with protected immobilization (cast or fracture boot). However, these fractures must be followed closely with serial radiographs to monitor healing and possible displacement. Healing typically takes 8 to 10 weeks in most adult patients; this time frame is twice as long in patients with diabetes. If there is >1-mm fracture displacement or >1-mm mortise widening of the medial joint space, open reduction and internal fixation should be strongly considered because malunion of an ankle fracture predictably leads to posttraumatic arthritis. Open reduction and internal fixation of ankle fractures also provides the patient with early ambulation, reduced immobilization, and a quicker return to full activity. Physical therapy is recommended for improved ROM, strength, and proprioception.
Achilles Tendinitis
Definition and Mechanism of Injury
Achilles tendinitis refers to chronic irritation of the Achilles tendon and its sheath secondary to repetitive use and trauma (23,24). The Achilles tendon is the terminal tendinous attachment of the soleus and gastrocnemius muscles into the calcaneus. Achilles tendinitis commonly is seen in active individuals (adolescents to middle-aged adults) engaging in athletic activities without proper conditioning. However, Achilles tendinitis can occur even in well-conditioned athletes who run on hills or wear shoes with excessively rigid soles. Furthermore, structural abnormalities such as tibia vara (bowed leg deformity), tight hamstrings and calf muscles, cavus foot (high arched foot, often with claw toes), and varus (inverted) heel deformity predispose to Achilles tendinitis. Initially, the peritenon (loose, soft, connective tissue surrounding the tendon) is inflamed, but in chronic cases the tendon itself undergoes mucoid degeneration with formation of longitudinal nodules and fissures in the tendon. This condition can increase the risk of a tendon rupture.
Signs and Symptoms
The patient typically complains of a burning-type pain at the site of tendon insertion onto the calcaneus. The onset of pain usually coincides with the start of the activity; however, it may lessen or disappear completely as the activity continues. The discomfort often recurs at startup or after completion of the activity.
On examination, there is local or diffuse tenderness of the Achilles tendon. A chronic tender nodule may be present in the substance of the tendon with crepitus and swelling. The patient experiences pain with passive stretch of the tendon.
Retrocalcaneal bursitis involving the bursa that lies between the calcaneus and Achilles tendon may produce symptoms similar to those of Achilles tendinitis. On examination a patient with retrocalcaneal bursitis has focal tenderness confined to the calcaneus.
Treatment and Prognosis
The general treatment protocol is like that for any other tendinitis condition. The inciting activity or sport should be stopped initially, and the patient should use the RICE protocol and be placed on a trial of NSAIDs to reduce the inflammation. Runners should not run for several days and should reduce running mileage and avoid hills until symptoms are absent for 10 to 14 days. If symptoms persist after this short rest period, the patient may need to stop the exercises that aggravate the condition for 3 to 4 weeks or longer.
A physical therapy referral is beneficial for refractory cases of Achilles tendinitis because ultrasound and other modalities can be highly effective. A removable heel lift inserted into the shoe may provide some relief. If the
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syndrome is severe, splinting or casting the ankle joint and using crutches may be necessary to immobilize the Achilles tendon. In mild cases, the prognosis is excellent. Patients with conditions that do not respond in 2 weeks should be referred for an orthopedic consultation. Surgery usually is not necessary, but for some cases, operative options include open débridement and repair of the tendon (25). The patient with retrocalcaneal bursitis is best advised to rest from stressful activity, to obtain properly fitted athletic shoes that are not tight around the Achilles tendon, and to use a heel pad in regular shoes. Corticosteroid injection in and about the Achilles tendon should be avoided because it can lead to rupture of that tendon.
Prevention
Exercises that gently stretch the tendon may help condition runners and prevent recurrences. The use of good shoes is important. Shoes should have flexible soles, a well-molded Achilles pad, and a rigid heel wedge.
Achilles Tendon Rupture
Definition and Mechanism of Injury
An Achilles tendon rupture is a disruption of the tendon, usually 2 to 6 cm proximal to its insertion into the calcaneus. It typically occurs in middle-aged adults, usually during athletic activities that require rapid active plantarflexion of the ankle. Patients with Achilles tendinitis are at risk for tendon ruptures, as are patients with systemic inflammatory diseases (such as lupus and rheumatoid arthritis) or with a history of using systemic steroids (26). Achilles tendinitis and tendon rupture have been associated with fluoroquinolone therapy (27). The rupture can be acute or chronic, complete or incomplete.
Signs and Symptoms
A patient with an acute rupture usually recalls a sudden snap and pain in the area of tendon insertion. A patient with a chronic rupture may not recall a particular event but generally has pain in this area. Depending on how complete the rupture is, the patient may not be able to actively plantarflex the ankle or may be able to do so with weakness and pain. On examination, there is local pain and swelling. A palpable defect may be present in the tendon. The Thompson test is positive (28). This test is performed by squeezing the mid to proximal muscular section of the calf. If the tendon is intact or not completely torn, the ankle will plantarflex. If the tendon is completely ruptured, no plantarflexion will occur.
Radiographs should be obtained to rule out an avulsion fracture at the tendon insertion site. If the diagnosis is still not clear, MRI will delineate the degree of the tear and its location. Patients with acute or painful chronic tears or those with avulsion fractures should be referred to an orthopedic surgeon for definitive treatment. For a patient with an acute rupture, referral should be made urgently because delay in treatment beyond a few days may result in retraction of the proximal portion of the tendon.
Treatment and Prognosis
Some controversy exists regarding the management of Achilles tendon ruptures (29,30). Both operative and nonoperative options are available. In the case of operative repair, primary anastomosis at the site of rupture is followed by a period of immobilization to allow for tendon healing. Nonoperative treatment entails immobilizing the ankle joint in plantarflexion to approximate the two ends of the tendon. This position is held for 4 weeks in a below-the-knee cast. Then the foot is brought into more dorsiflexion with another below-the-knee cast, and the process is repeated until the tendon is healed. Most surgeons recommend surgical repair of acute, complete ruptures in young, active patients. The prognosis of Achilles tendon ruptures is varied. Most patients are able to return to routine daily activities, but some may not be able to return to preinjury levels of sporting activities. Generally, compared with nonoperative modalities, surgical repair has a higher success rate of returning patients to preinjury sports levels with a lower chance of recurrence (31).
Prevention
Proper conditioning can prevent a tendon rupture. Appropriate stretching exercises should be performed before and after sporting activities. Appropriate treatment of Achilles tendinitis should be sought to decrease the potential chance of a rupture.
Posterior Tibialis Tendinitis and Rupture
Definition and Mechanism of Injury
Tendinitis of the posterior tibialis tendon is common. This tendon courses posterior to the medial malleolus, inverts the ankle joint, and plantarflexes the foot. Chronic irritation from the malleolus, along with a tenuous blood supply, place this tendon at risk for tendinitis and subsequent rupture. Patients with a history of trauma or previous surgery to the medial aspect of the foot, diabetes, obesity, or local steroid injection are at risk for dysfunction and tearing of this tendon.
Signs and Symptoms
Patients frequently complain of medial foot and ankle pain. The onset of the pain usually is gradual. Examination reveals tenderness along the course of the tendon behind the medial malleolus. Additionally, patients with a torn tendon may have gradual loss of the medial arch of the foot and, eventually, a flatfoot deformity. With complete tendon rupture, the foot abducts and the pain can
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move laterally into the region of the sinus tarsi or beneath the fibula, where bony impingement can occur secondary to the loss of the medial arch. The hindfoot assumes a valgus position, allowing more of the toes to be visible when viewed from behind the patient (“too-many-toes” sign). In the early stages, when only tenosynovitis is present, the tendon is intact and the patient is able to perform a single-heel rise, that is, stand only on the affected limb and raise the heel from the floor with plantarflexion of the ankle. In more advanced stages of tendon attenuation or tear, however, the patient is unable to perform a heel rise. In advanced stages, radiographs show osteoarthritis in the ankle. MRI is valuable in showing posterior tibial tendon attenuation or tear.
Treatment and Prognosis
In the presence of an intact posterior tibial tendon with tendinitis, the standard RICE protocol with NSAIDs can be followed. The ankle joint should be immobilized for 6 weeks with a rigid below-the-knee cast or boot to allow the inflammation to resolve. Subsequently, the patient can progress to a stiff-soled shoe with a medial heel wedge. Patients for whom such nonoperative measures fail may require surgical débridement of the tendon. For patients with incompetent or torn posterior tibial tendons, nonoperative treatment tends to be less effective and does not prevent progression to flatfoot deformity. Surgical options include reconstruction of the tendon, flexor tendon transfer, medial calcaneal osteotomy to displace the calcaneus medially, lengthening the lateral aspect of the foot, and ankle arthrodesis, or a combination thereof (32,33). The prognosis for this form of tendinitis tends to be good, but it may recur. The prognosis for posterior tibial tendon rupture varies and depends in part on the extent of the acquired flatfoot deformity.
Prevention
The best prevention for posterior tibial tendon rupture is to halt the progression of tibialis posterior tendinitis. Often, early treatment of posterior tibial tendinitis with NSAIDs, immobilization, activity modification, and use of orthotics is successful. Once the tendon is ruptured, the foot can develop a flatfoot deformity, and major surgical reconstruction may be necessary.
Specific References
For annotated General References and resources related to this chapter, visit http://www.hopkinsbayview.org/PAMreferences.