Define the muscle-tendon unit.
Describe the stages of tissue healing and the importance of application of this knowledge in rehabilitation.
State the mechanism of injury for strains.
Identify characteristics of the different grades of strains and application of this to rehabilitation.
Describe the classifications of tendon pathology.
State key aspects of the clinical evaluation.
Identify rehabilitation principles for acute and chronic injuries and design appropriate rehabilitation interventions.
Describe rehabilitation treatment techniques for common muscle-tendon pathologies.
Injury to muscle and tendon structures can substantially affect individual joint mobility and stability. Furthermore, muscle and tendon injuries can alter movement of the entire body and ultimately limit functional participation in life activities. The goal of this chapter is to aid the clinician in identifying and treating muscle and tendon injuries. Specifically, the objectives of this chapter are to (1) identify basic science components and healing parameters of the muscle-tendon unit, (2) differentially diagnose muscle and tendon pathologies, and (3) discuss evaluation considerations and rehabilitation principles for muscle and tendon injuries.
Anatomic components and tissue response to injury
Muscles are composed of contractile tissue and are responsible for creating and dissipating force while enabling voluntary movement of the body. Movement of the skeletal system is made possible through the connection of muscle to bone via tendons. Together, muscles and tendons form a complex unit known as the muscle-tendon unit.
“What is the location, duration, and intensity of your pain?”
“What factors make the pain worse, and what factors make the pain better?”
“Has the pain progressively gotten better or worse over time?”
“Have you had any treatment for the current medical issue?”
“Have you had a similar injury in the past?”
“Are you currently taking any medications for the problem?”
“What are your functional limitations?”
The muscle-tendon unit is composed of a muscle with tendons at each end, and each tendon is attached to bone ( Fig. 7-1 ). The point of connection between muscle and tendon is the myotendinous junction (MTJ), and the point of attachment of tendon to bone is the osseotendinous junction (OTJ). The entire muscle-tendon unit works to produce controlled movement, as well as to stabilize and protect joints. Therefore, when the musculotendinous unit sustains an injury, it often has an impact on joint stability and functional mobility. Injury to the muscle-tendon unit can occur within the body of the muscle or tendon or at their points of attachment. Frequently, the site of injury in the musculotendinous unit is at the MTJ. When injury occurs near the OTJ, an avulsion fracture may result, with the bony insertion separated from the bone ( Fig. 7-2 ).
A commonly seen clinical pathology, Osgood-Schlatter disease, occurs when activation of the quadriceps muscle-tendon unit causes the infrapatellar tendon to pull excessively at the OTJ on the tibia. The OTJ becomes inflamed, and contraction of the quadriceps muscle-tendon unit, especially against resistance, causes pain. The pull of the quadriceps muscle-tendon unit causes a small separation at the tibial tubercle, which then results in additional bone growth. Osgood-Schlatter disease is often seen in children who participate in running and jumping activities in which the quadriceps muscle is repeatedly activated. This pathology is also commonly seen during periods of rapid growth when appropriate flexibility of the quadriceps musculotendinous unit is not maintained. The enlargement of the tibial tubercle that occurs with Osgood-Schlatter disease remains even after the symptoms subside.
When treating a patient with Osgood-Schlatter disease, care must be taken to prevent further tissue damage and protect the irritated structures until they heal. Initial treatment consists of rest and modification of activity to allow the inflammation to subside. Gentle, progressive stretching, particularly of the quadriceps musculature, will help improve musculotendinous flexibility. Use of a counterforce brace on the infrapatellar tendon may also be considered toward the end of the rehabilitation program to alter the application of force at the OTJ as the patient attempts to return to endurance activities and functional, sport-specific workout drills.
Stages of Healing
It is important to have a fundamental understanding of healing time frames before discussing pathology and ultimately deciding on appropriate treatment because knowledge of tissue-healing phases will help guide the decision-making process during patient progression. The stages of soft tissue healing consist of the inflammatory response phase, the fibroblastic-repair phase, and the maturation-remodeling phase. Although the literature reports variations in the exact time frames for each phase, these phases of healing overlap and the time frames serve as general guidelines for the clinician because each soft tissue injury varies in severity and in the individual’s response to injury.
The acute inflammatory phase begins immediately after tissue injury and is characterized by redness, swelling, increased temperature, and pain. The inflammatory phase involves capillary injury and vasodilation, which results in increased blood flow to the injured area. Neutrophils and macrophages are attracted to the site of injury to remove foreign debris and damaged tissue from the area and thereby improve the healing environment. The events in the inflammatory response phase last approximately 2 to 4 days. During the fibroblastic-repair phase, which typically begins 3 days after injury and lasts approximately 2 weeks, new blood vessels form and fibroblasts migrate to the area to synthesize new ground substance and collagen. The wound margins begin to contract in size and weaker type III collagen is deposited in an unorganized fashion to form scar tissue. Finally, during the maturation-remodeling phase, ongoing synthesis and reorganization of collagen fibers take place. The continued collagen deposition transitions to mainly type I collagen, and the collagen fibers in the scar tissue become parallel in alignment as a result of tensile forces applied to the injured soft tissue. The parallel alignment of collagen fibers is usually achieved by 2 months after injury and allows the tissue to endure higher tensile loads. However, this final healing phase is a long-term process that begins approximately 3 weeks after injury and may last up to 1 year. While remodeling, the tensile strength of the wound continues to increase and at 3 months will have approximately 80% of normal tissue strength. When the remodeling phase is complete, the damaged tissue has often not achieved the same tensile strength as uninjured tissue. Luckily, the limitation in tensile strength does not typically affect function. The three phases of tissue healing overlap and represent a continuum of soft tissue healing ( Fig. 7-3 ).
Injuries to muscles involve a similar process as just described, but unique to muscles are satellite cells, which are muscle-specific stem cells located on the border of muscle fibers. With injury to muscle, the ruptured myofibers contract and the gap is filled with edema and eventually scar tissue. On the ends of the retracted muscle fibers, satellite cells are activated to proliferate and cause muscle regeneration. The newly regenerated myofibers on the end of the torn muscle project into the forming connective tissue scar.
When compared with muscle, tendons have less vascularity and therefore less oxygen and nutrition after injury. As a result, tendons may be slower than muscles to recover after injury. With tendons it is thought that healing may occur through intrinsic and extrinsic pathways. The extrinsic mechanism involves inflammatory cells and fibroblasts from the surrounding area that enter to assist in tendon repair, whereas the intrinsic mechanism involves inflammatory cells and fibroblasts from within the tendon. Within the tendon the reparative cell is the tenocyte, which may be activated to produce collagen. Although collagen is needed to help repair the damaged tendon, fibrosis may develop and result in the formation of adhesions to surrounding tissue if excessive collagen synthesis occurs. Clinically, this is not ideal because limited mobility may occur as a consequence of the scar tissue adhesions.
A muscle strain refers to pathology that involves some extent of disruption in the continuity and function of the muscle-tendon unit. The mechanism of injury of muscle strains may be related to passive overstretching, excessive active loading, or repetitive loading of fatigued musculature. In other words, the strain occurs when the amount of stretch exceeds the limits of flexibility, the amount of force exceeds the level of strength, or the duration of force exceeds the level of endurance of the involved muscle-tendon unit. In particular, eccentric repetitive loading is often a cause of muscle strain because muscle forces can be higher during the lengthening activation and lead to microscopic damage to the contractile element of the muscle. A muscle strain can also be the result of an acute impact (direct blow) to the involved musculature, known as a contusion.
Clinically, strains are frequently seen in certain muscle groups. Strains commonly involve muscles that have a large percentage of type II fast-twitch muscle fibers and muscles that cross two joints, such as the hamstrings, gastrocnemius, and rectus femoris. Muscles that span two joints are placed at risk through lengthening loads at both joints simultaneously and mixed demands during function. In sports medicine, muscle strains commonly occur in “speed athletes,” such as sprinters and football, basketball, and soccer players. Muscle strains also tend to occur during strenuous exercise, particularly during eccentric muscle activation or when the muscle is fatigued. At the end of practice or a training session, the musculature is more likely to be fatigued and the athlete is at an increased risk for an acute strain, especially if proper conditioning is not maintained.
Muscle strains should be differentiated from the exercise-induced muscle soreness that occurs after eccentric exercise or physical activity in naïve/unaccustomed individuals. Although both strains and exercise-induced muscle soreness occur with eccentric exercise and both produce pain with passive stretching or muscle activation (or both), a muscle strain is a painful event that is acute in nature and identified at the time of injury. In other words, the patient will report knowledge of the moment when the muscle strain was felt. In contrast, delayed-onset muscle soreness (or DOMS) typically peaks 24 to 72 hours after exercise. Importantly, DOMS occurs after bouts of eccentric exercise, especially in untrained muscle, but it typically resolves without intervention within a few days to a week.
Grading of Strains
Strains range from damage to a limited number of muscle fibers or connective tissue to a complete muscle tear or tendon avulsion. Typically, strains are categorized as grade 1, grade 2, or grade 3 ( Table 7-1 ). Determining the appropriate grade of strain will help guide the clinician through the rehabilitation process. A grade 1 strain may leave the athlete with slight discomfort and minimal swelling but full range of motion (ROM) and little functional deficit. A grade 2 strain is characterized by a small to moderate palpable area of involvement along with increased pain and swelling. An athlete with a grade 2 muscle strain will often demonstrate restricted ROM and impaired gait if the lower extremity musculature is involved. A grade 3 muscle strain is typified by a moderate to severe palpable area of involvement and sometimes a defect at the site of injury. The athlete will demonstrate significant deficits in ROM, and functional mobility will be severely impaired.
|Grade||Impairments in Body Structure/Function||Limitations in Ambulation (for Lower Extremity Strains)||Limitations in Participation in Sporting Activities (for Lower Extremity Strains)|
|Structural Fiber Damage/Deformation||Pain||Range of Motion||Strength||Swelling|
|1||Some fibers stretched or actually torn, no gross disruption of the muscle-tendon unit||Pain or tenderness with AROM or stretching||No loss, full ROM possible||No loss, full strength||Minimal, localized edema||Minimal to no limitation in ambulation||Minimal limitations, may be able to participate by using equipment (wraps, bracing, taping)|
|2||Torn muscle/tendon fibers, palpable depression in the area of injury, some degree of disruption of the muscle-tendon unit||Pain with active contraction of the muscle-tendon unit||Loss of ROM because of swelling and bleeding, limitation in AROM||Some loss of strength||Moderate edema||Ambulation with a limp, may need crutches||Unable to participate but should be able to return to sport during the same season with appropriate rehabilitation|
|3||Complete rupture of the muscle belly, MTJ, or OTJ; noticeable defect in the muscle belly or evidence of a torn tendon||Intense pain that diminishes with damage and separation of nerve fibers||Severely limited ROM or total loss of ROM||Moderate to major loss of strength, unable to endure resisted motion||Moderate to major edema||Significant limitation in ambulation, likely to require crutches||Unable to participate; consider sitting out the season for conservative or operative treatment|
A grade 3 strain with a complete muscle or tendon rupture may require surgical repair, so correct assessment of an avulsion injury is critical. For example, a grade 3 muscle strain of the Achilles tendon is best evaluated with the Thompson test ( Fig. 7-4 ). To perform this test, the patient should lie prone with the feet extended off the end of a treatment table while the clinician squeezes the belly of the gastrocnemius muscle. When the Achilles tendon is intact, the foot should move into plantar flexion. However, if the Achilles tendon is ruptured, the foot will not plantar-flex. A patient with an Achilles tendon rupture will often report the feeling of a “pop” or being kicked in the calf. Rupture of the Achilles tendon often occurs around 2 to 6 cm from its insertion site on the calcaneus, where the gastrocnemius and soleus tendons meet and which it is thought to be the area with the poorest blood supply. Early diagnosis and treatment of this pathology are important. Treatment approaches can include either conservative or surgical management; however, surgical repair of an Achilles tendon rupture produces a lower rerupture rate and provides the patient with a quicker and more optimal return to function. One of the evolving rules in the treatment of these injuries is allowing ROM in the postoperative period or even with conservative care because ROM appears to be vital to long-term success.
A contusion injury may be caused by a direct hit or acute blow to the muscle belly. This impact results in muscle cell damage and bleeding into the muscle. Immediately following the injury, an acute inflammatory reaction takes place. Satellite cells on the membrane of muscle cells become new muscle cells, and connective tissue is formed in the damaged area. The damaged tissue continues to progress through the stages of soft tissue healing as described earlier. The extent of muscle tissue damage with a contusion injury will determine the degree to which ROM, strength, and functional activity are impaired.
Contusion injuries are commonly seen in individuals engaging in athletic activities, such as football, where an athlete’s helmet or shoulder pad may forcefully impact an opponent’s quadriceps muscle, for example. Contusions can be classified as mild, moderate, or severe based on the amount of ROM allowed by the involved muscle in the adjacent joints ( Table 7-2 ). A mild contusion may cause a loss of one third of normal ROM, whereas a severe contusion may limit motion to less than one third of normal mobility. Like strains, contusions may also lead to deficits in strength and functional limitations. A severe contusion is characterized by significant bleeding and a large palpable area of involvement, and the muscle may herniate through the fascia. Clinically, muscle strains and contusions are some of the most common injuries seen in sports participation.
|Grade||Impairments in Body Structure/Function||Limitations in Ambulation (for Quadriceps Contusions)||Limitations in Function and Participation in Sporting Activities (for Quadriceps Contusions)|
|Structural Fiber Damage/Deformation||Pain||Range of Motion (for Quadriceps Contusions)||Strength||Swelling|
|Mild||Muscle fiber damage, vascular hemorrhage, and hematoma formation||Localized tenderness||Knee ROM greater than 90°||Minimal to no loss of strength||Minimal, localized edema||Normal gait||Able to do deep knee bend, may be able to participate in sports but cautioned against risk for reinjury; protective pad used to cover the injured tissue|
|Moderate||Muscle fiber damage, vascular hemorrhage, and hematoma formation||Tender muscle mass||Knee ROM less than 90°||Moderate loss of strength||Moderate edema||Antalgic gait||Unable to climb stairs or rise from a chair without pain, unable to play sports|
|Severe||Muscle fiber damage, vascular hemorrhage, and hematoma formation; muscle may herniate through fascia||Marked tenderness||Knee ROM less than 45°||Moderate to major loss of strength||Marked edema, may be difficult to identify contours of defined musculature||Severe limp, likely to require crutches for ambulation||Unable to participate in sports, must take extreme caution to prevent aggravating the injury with functional activity|
The clinician should also be aware of a condition known as myositis ossificans (also called heterotopic bone) that can develop after a severe muscle contusion ( Fig. 7-5 ). It commonly occurs in the thigh musculature after a direct blow to the muscle causes tissue disruption and excessive bleeding that leads to ectopic bone formation in the area of the injured soft tissue. Initial radiographs are negative, but after 4 to 6 weeks bone formation can be identified radiographically. Even though myositis ossificans can restrict mobility, it is not always treated surgically because the ectopic bone may not impair function and the body may eventually absorb the ossification. However, if surgical resection is indicated, it is performed only after the bone has fully matured because early surgery can exacerbate the condition.
Proper treatment of a contusion can help decrease risk for the development of myositis ossificans. Immediately after a quadriceps contusion injury, the knee should be immobilized in flexion. During this initial rest period, the knee is kept flexed to provide tension on the quadriceps muscle and inhibit blood pooling and muscle contracture. While the leg is wrapped, ice is applied to the area of injury to limit excessive blood flow to the injured area, and nonsteroidal antiinflammatory medication may help in addressing the inflammation as well. Typically, the leg is initially wrapped in flexion for the first 24 hours. Afterward, the patient can proceed through the rehabilitation process by beginning with isometric quadriceps-strengthening exercises and progressing to gentle, pain-free ROM and stretching. Reinjury, especially shortly after the initial injury, increases risk for the development of myositis ossificans. Therefore, it is important to avoid activities that may reinjure the muscle tissue, including aggressive overstretching, early aggressive massage, or trying to continue typical athletic activity with a grade 2 or 3 contusion. Heat or thermal modalities that increase blood flow to the area should also be avoided initially after injury.
The terminology involved in tendon injury is evolving and requires further clarification. In the past, tendinitis has been used as a catch-all term to describe all tendon pathologies. However, what is now known about the histologic differences in tendon pathologies requires further clarification of the language used when discussing tendon injuries. Several terms are used to describe various tendon pathologies. For example, tenosynovitis refers to inflammation of the synovial sheath that lines some tendons, and enthesopathy refers to a lesion at or near the enthesis or bony attachment. Therefore, new classification systems have been proposed to subgroup tendon pathologies . For clarity, tendinopathy is used in this chapter as a broad term that refers to any pathology involving tendons and, as a result, is inclusive of several different tendon pathologies.
In this chapter, tendinopathies will be classified as tendinitis , paratenonitis , and tendinosis ( Table 7-3 ). Tendinitis and paratenonitis are the earliest signs of tendon pathology and trigger an acute inflammatory response. However, if tendon damage continues, tendinosis, partial tears, or even tendon rupture may occur. Tendinitis, paratenonitis, and tendinosis may occur separately, or these pathologies may occur simultaneously, as is the case with paratenonitis and tendinosis.