N

13

Muscle Injuries

Steven J. Svoboda and Dean C. Taylor

In This Chapter

Delayed-onset muscle soreness Muscle strains

Surgery—repair of hamstring avulsion Muscle contusion Myositis ossificans

MUSCLE STRUCTURE AND FUNCTION, INJURY AND REPAIR

Muscle-tendon units originate from bone and usually insert onto another bone through a second tendon. Muscle contraction serves to produce torque about a joint leading to limb motion. Muscle consists of both contractile proteins including myosin, actin, troponin, and tropomyosin and a connective tissue matrix.2 A muscle fiber is a syncytium of fused, multinucleated muscle cells and is the basic structural element of skeletal muscle. The muscle fibers can be arranged in parallel to a muscle's direction (unipennate) or oblique to the muscle's direction (bipennate; Fig. 13-1). The surrounding connective tissue includes the endomysium, which invests the individual fibers, the perimysium, which surrounds fascicles of muscle fibers, and the epimysium, which surrounds the entire muscle.2

The sarcolemma is a plasma membrane surrounding the muscle fiber whose nuclei are eccentrically located immediately beneath the sarcolemma. Also along the periphery of the fiber are satellite cells whose predominant function is to provide stem cells during times of muscle proliferation and regeneration. There are two major fiber types of skeletal muscle. Type I fibers are considered slow twitch and fatigue resistant due to their high mitochondrial and myoglobin content; however, they have the slowest contraction time and the lowest concentration of glycogen and glycolytic enzymes. Type II fibers are considered fast twitch with type IIA consisting of fast-twitch oxidative glycolytic fibers and type IIB consisting of fast-twitch glycolytic fibers. Type II fibers contract with the highest velocity and are most at risk of fatigue. Fiber composition, among other properties, has been implicated as a critical factor in susceptibility to certain muscle injuries.3

Regardless of which mechanism of injury to muscle one considers, there is a common response. The initial injury to muscle fibers stimulates mononucleated cells that typically reside within muscle to release chemotactic factors that initiate a three-stage inflammatory response. First, neutrophils invade the injury site, releasing cytokines that attract additional cells to the area. In addition to promoting inflammation, these neutrophils release oxygen free radicals that cause further damage to the cell membrane. The second stage is represented by an increase in macrophage migration to the injury site to phagocytose cellular debris. The third phase of inflammation begins when a subpopulation of macrophages increases in number. These macrophages are associated with muscle regeneration. Substances released by the injured muscle and attracted inflammatory cells have been likened to "wound hormones."4 Muscle regeneration occurs within this milieu, with satellite cells providing the necessary stem cells. In a mouse model, this process appears to be limited to muscles weighing less than 1.5 g and, therefore, does not play a significant role in human muscle healing. In the case of human muscle healing, repair by connective tissue fibrosis or scar often predominates, beginning at 2 days after injury and increasing over the next 2 weeks with fibroblasts the important cell type. Satellite cell proliferation that accounts for muscle regeneration peaks at 2 to 4 days after injury, implying that there is a fine balance between the two processes.2 The remainder of the chapter analyzes specific subtypes of muscle injuries to highlight their similarities and differences as they apply to the clinical situation.

INDIRECT MUSCLE INJURY

Indirect muscle injuries occur in response to too much strain or force within the muscle without direct contact. These injuries occur near the muscle-tendon junction despite distant application of force, whereas injury occurs at the site of force application in direct injuries.5

Delayed-onset Muscle Soreness

Pain localized to a muscle that occurs 24 to 48 hours after a bout of unaccustomed exercise and resolves over 5 to 7 days without

INTRODUCTION

• Muscle composes 40% to 45% of total body weight and represents the single largest tissue mass in the body.1

• Common types of muscle injuries can be broken down into several categories (Table 13-1).

• The purpose of this chapter is to discuss the most common forms of muscle injury presenting within a sports medicine practice.

• Indirect injuries include delayed-onset muscle soreness and muscle strain injuries.

• Direct injuries include contusions and myositis ossificans.

Table 13-1 Common Types of Muscle Injury

Indirect

Delayed-onset muscle soreness Muscle strain

Direct Contusion Laceration

Vascular Traumatic Tourniquet

Exercise-induced compartment syndrome

Infectious

Neurologic Denervation Central or peripheral Viral or traumatic

Neuropathic Metabolic Viral Genetic

Myopathies

From Beiner JM, Jokl P: Muscle contusion injuries: Current treatment options. J Am Acad Orthop Surg 2001;9:227-237.

intervention is the hallmark of delayed-onset muscle soreness (DOMS).6 DOMS occurs more frequently with eccentric exercise, meaning that the involved muscle is lengthening while it is being activated.5 After DOMS develops, passive stretching and resumption of activity aggravate the pain. Palpation of the muscle is painful and is associated with a reduced range of motion and prolonged strength loss. Laboratory testing reveals an elevated level of creatine kinase. This increase is thought to

TA EDL

Figure 13-1 Muscle architecture varies from fusiform (TA, tibialis anterior) and unipennate (EDL, extensor digitorum longus) with muscle fiber direction and pull in line with the muscle-tendon unit to bipennate (RF, rectus femoris) and multipennate (G, gastrocnemius) with muscle fiber direction and pull oblique to the muscle-tendon unit. Arrows indicate fiber length and orientation. (From Garrett WE Jr, Nikolaou PK, Ribbeck BM, et al: The effect of muscle architecture on the biomechanical failure properties of skeletal muscle under passive extension. Am J Sports Med 1988;16:7-12.)

be due to increased permeability or breakdown of the sar-colemma due to the excessive eccentric loads that disrupt the z lines within the fibril.7 Calcium ions accumulate within the muscle due to the disrupted sarcolemma and this results in activation of calcium-dependent proteolytic enzymes that allow release of the creatine kinase. The creatine kinase attracts monocytes that convert to macrophages, contributing to local inflammation.7 The inflammatory mediators contribute to pain perception, as they are noxious to nociceptors within muscle. Further, the acute clinical finding of generalized swelling of the affected muscle is significant and thought to be due to this inflammatory process. Interestingly, a recent study has described a persistent loss of muscle volume of 7% to 10% between 2 and 8 weeks after exercise. A small population of "susceptible" muscle fibers is thought to be injured initially and necrose, leading to fewer muscle fibers within the muscle. This loss of volume persisted after recovery and after a second bout of eccentric exercise at 8 weeks.8

Individuals who are in excellent general aerobic condition are susceptible to DOMS if they engage in novel, eccentric exercise just the same as generally untrained individuals. However, training of a muscle group eccentrically confers a highly specific protective effect on that muscle for a prolonged period of time. This protective effect manifests itself as decreased pain reporting, decreased muscle swelling, and decreased serum creatine kinase levels up to at least 8 weeks after the initial bout.8 Muscle fiber type is also a factor in DOMS with type II muscle implicated as more susceptible to such injuries.

Treatment

No single therapy has been shown to unequivocally resolve DOMS faster than the currently understood natural history of the condition. Nonsteroidal anti-inflammatory drugs (NSAIDs) have shown early subjective benefit that is minimized by prolonged administration that tends to inhibit the healing process. Exercise is thought to be the single intervention with the most promise of ameliorating the symptoms of DOMS. The mechanism by which exercise reduces symptoms is unclear but is thought to be due to breaking up adhesions within the muscle, increasing noxious waste removal from the area by improved local blood flow, or endorphin release, which decreases the perception of pain.7

Muscle-Tendon Strains

Muscle-tendon strain injuries are stretch-induced injuries that are noncontact in nature. While understanding of this class of injuries is incomplete, much basic science as well as clinical research has been completed to assist in their management.

Mechanism

A muscle-tendon unit can be injured when it is either passively stretched or is stretched while activated. Further, a strain injury frequently occurs in light of eccentric contraction. It is known that forces generated within eccentrically activated muscle are higher than in a concentrically activated muscle.5 Maximal nerve stimulation, which generates concentric loading within a muscle, does not generate enough muscle activation to cause disruption of muscle.5 In order to cause either partial or complete muscle injury, some type of stretch must be added. Pulling passive muscles until failure generates loads several times greater than the maximal isometric force that an activated muscle can generate. This suggests that the passive forces within muscle in addition to the active forces generated by the muscle are impor

tant in muscle strain injury.9 Passive stretching of muscle results in ruptures near to, but not exactly at, the muscle-tendon junction. This location of failure is constant regardless of strain rate or type of muscle being stretched.10 Active muscles, when stretched to failure, generate failure loads only moderately above those generated within stretched resting muscle; however, activated muscle absorbs significantly more energy prior to failure than resting muscle.11 The relevance of this to clinical practice lies in the consideration of muscle as a shock absorber and implies that larger and stronger muscles resist injury better. In addition to these features of muscle undergoing complete disruption, muscle undergoing nondisruptive injury also has unique features. First, muscle strained to 80% of failure load exhibits a change in the linearity of the force-displacement curve that indicates the muscle has undergone plastic deformation and a subsequent change in material structure.12,13 In animal models, muscle-tendon units stretched into plastic deformation are able to generate only 70% of the load of uninjured muscle immediately after injury. At 24 hours after stretch injury, it can generate only 50% of normal load and then begins to improve over the ensuing days and at 7 days following injury can generate loads equal to 90% of controls. Stretching unstimulated muscle to failure 7 days after nondisruptive injury requires only 77% of the force required to rupture uninjured muscle.12 This suggests that healing muscle is at risk of reinjury, which is discussed in more detail later.

Predisposing Factors

There are several factors that have been implicated as predisposing a muscle to injury. These factors can be considered both as intrinsic characteristics of a muscle and extrinsic factors acting on the muscle. Intrinsic characteristics of muscles that predispose them to injury include gross anatomic characteristics, basic functional characteristics, and muscle architecture. Extrinsic factors include a history of injury and the presence of fatigue.

Several muscles by nature of their anatomic origins and insertions are frequently implicated as being at risk of muscle strain injury. Notable among them are the hamstrings (most frequently the biceps femoris), the rectus femoris, the gastrocnemius, the adductor longus, the pectoralis major, and the triceps brachii muscles.14 The former three are the muscles that are most commonly affected by strain injuries. One theory as to why these three muscles are selectively involved is their common characteristics of muscle-tendon units that span two joints from origin to insertion and their more superficial location.2,15 It has been suggested that the adductor longus owes its increased risk of muscle strain injury to its complex architecture.10

With respect to basic muscle function, it must be understood that these two-joint muscles act predominantly as limiters of joint range of motion. For example, the hamstring muscles during sprinting, rather than acting to actively flex the knee, work more to decelerate knee extension.14 Another example is the quadriceps muscle group during running that acts to limit knee flexion after heel strike rather than powering knee exten-sion.5,14 Referring back to the basic science of muscle injury, we see that this role as a limiter of joint motion forces the muscle to activate eccentrically and as a result puts it at increased risk of muscle strain injury.

Muscle architecture also has been found to be a factor implicated in muscle strain injury. Injured muscle, regardless of architectural type (i.e., fusiform, unipennate, bipennate, and multipennate) fails at the musculotendinous junction.9 Typically, the affected muscle-tendon junction is the distal one except in the case of the gastrocnemius, which fails variably at the distal or proximal junction or even at the musculotendinous junction between the medial and lateral heads. This variability is thought to be due to the complex multipennate architecture of the gas-trocnemius.9 More pennate muscles (such as the tibialis anterior, extensor digitorum longus, and rectus femoris) were found to have a greater percentage of elongation prior to failure than less pennate muscles. In one specific case of muscle strain injury, rectus femoris injuries occurring at its proximal end were investigated as they represented a different pattern of injury than that of the typical distal rectus femoris injury.16 Anatomic dissections confirmed that the classic description of the proximal rectus femoris anatomy was imprecise and that, indeed, these proximal injuries were adjacent to the musculotendinous junction, like other muscle strain injuries.17 The fiber type composition of a muscle also affects a muscle's susceptibility to strain injury. Muscles with a high percentage of type II (fast-twitch) fibers are more commonly injured, which may be due to the fact that type II fibers are preferentially recruited during high-speed activities.3,18

When muscle has been injured, it is susceptible to further injury if it is placed under high-level stresses too soon. As mentioned earlier, muscle's ability to resist stretch equates to its ability to absorb energy. This resistance derives from its passive connective tissue elements and its active contraction against the lengthening force. Most physiologic activity in eccentrically contracting muscle occurs at small deformations, and this is when the active component of muscle absorbs the most energy. Thus, a weakened muscle from previous injury will be more susceptible to further injury.3 Fatigued muscle has also been found to be at risk of muscle strain injury. While control muscle and fatigued muscle fail at the same length, fatigued muscle has been found to absorb less energy prior to reaching the degree of stretch that causes injuries.19 Further, a fatigued muscle is not as efficient in its function, and this may interfere with the storage and retrieval of elastic energy by muscle, resulting in loss of athletic function.19

Preventive Measures

Various prevention methods exist to minimize the risk of acute strain injuries. While it has been commonly thought that there was a neuromuscular response resulting from stretching, more recent literature has shown that muscle is viscoelastic in nature. This means that if a constant load is applied to muscle passively, the muscle will slowly elongate; similarly, if muscle is repeatedly stretched to a specified length, it will require less load to achieve this length as the number of cycles increases. This effect has been noted to achieve approximately 80% of its maximum level after four cycles in experimental animals and accounts for approximately a 4% increase in length.20 The persistence of this effect has not been well established. It appears that stretching may afford muscle some protective effects due to this phenomenon, although there is no clear consensus in the literature to support this. In fact, preinjury stretching in a mouse extensor digitorum longus muscle model was not effective in preventing muscle injury.21 While there are some distinctions between animal species tested and strain rate applied, static stretching does not appear to be harmful in any study. A warm-up period has also been recommended prior to exercise or competition, with research showing that an increase of 1 degree within muscle increases the peak load at failure compared to muscle that has not been warmed up.22 This study used muscle preconditioning in the form of repeated isometric contractions to raise temperature, and this may also influence the muscle's resistance to injury. Another study used warm (40°C) and cold (25°C) muscle to show that warm muscle has less stiffness and as a result generates lower loads as it is deformed.23 This is protective against muscle strain injury as it is thought that there is a critical load threshold above which muscle will be injured.23 Thus, a prudent strategy prior to exercise would be to include a period of warm-up consisting of moderate activity followed by a period of static stretching prior to initiating intense sport or exercise. Muscle strength also exists as a relative preventive measure owing to the fact that this is typically accompanied by increased muscle bulk, which allows increased energy absorption by the muscle.

Clinical Features and Evaluation History

Muscle strain injuries typically occur to athletes engaged in explosive activities such as sprinting or sports such as football, rugby, or soccer. A complete tear of the muscle can be quite remarkable to witness, and the athlete usually has no difficulty identifying the specific moment that he or she was injured. The athlete will complain of a sudden, intense pain in the affected muscle and occasionally will be able to describe a "pop" with ensuing tightness in that muscle.2 These are typically noncon-tact injuries causing the injured athlete to complain of pain localized to the region of the muscle-tendon junction of the affected muscle. The most commonly affected muscle is the hamstring muscle, specifically the biceps femoris. Hamstring strains occur most commonly during sprinting and during football and rugby. Other muscles commonly affected include the rectus femoris and the adductor longus. This is often associated with kicking a soccer ball. A complete rupture of the hamstrings from their proximal insertion on the ischial tuberosity has been described in water skiers when transitioning from being in the water to being up on skis. It typically occurs in novice skiers and is a result of excessive hip flexion with extended knees.24

Physical Examination

Athletes sustaining a muscle strain injury can have variable presentation, from requiring assistance off the field to nearly being able to return to immediate play. Pain will be localized to a specific region, typically near the muscle-tendon junction. There may be a palpable defect, as in the case of a complete rupture, or there may be no palpable defect, just localized pain. Passive extension of the muscle is painful as is active contraction of the same muscle. After 24 hours, significant ecchymosis may be evident over the muscle within the subcutaneous space as a result of the intermuscular hemorrhage. This ecchymosis can propagate distally along the subcutaneous plane. In the case of a hamstring strain, this ecchymosis may extend to the foot over time.

Imaging

Imaging studies have shown that in the vast majority of muscle strain injuries, only a single muscle is affected.15 Plain radiographic imaging may show soft-tissue swelling and in the case of a complete rupture may suggest a defect. Computed tomography imaging can also show soft-tissue swelling and define the extent of a complete tear, but magnetic resonance imaging (MRI) is the preferred method of imaging a muscle strain injury.15 Most muscle strains will not require imaging. Such imaging is rarely indicated in an acute muscle strain unless there is a need for greater information in situations in which time to return to sports is critical as in professional or high-level college athletics.25 MRI performed immediately after injury may also be difficult to interpret as the acute hemorrhage may not have the increased T2 signal typically noted after 24 hours following injury.15 MRI may be most helpful in those muscle strain injuries that do not initially respond to usual therapy in order to rule out concomitant injuries and to most objectively define the location and extent.15

Classification

There is no classification scheme that is predictive of outcome and no evidence-based research has been performed to assist in treating these injuries. The most easily communicated classification was established by the American Medical Association and consists of three grades: I, mild interstitial strain; II, moderate partial muscle disruption; and III, severe complete disruption.26

Treatment Options

The vast majority of muscle strain injuries will require nonoperative management with operative management being reserved for selected complete ruptures. The basic scheme for nonoperative treatment includes the RICE mnemonic, which stands for rest, ice, compression, and elevation, and, additionally, a short course of NSAIDs2'3'5'18'27,28 (Table 13-2).

While relative rest is paramount in the treatment of muscle strain injuries, the degree of rest should not be taken to the extreme as this may hasten atrophy and loss of strength. Taylor et al29 determined that, immediately after a severe strain injury, muscle had 63% of the peak tensile load and 79% of the elongation to failure of control muscle. This relative preservation of muscle integrity supports the notion of functional rehabilitation to preserve range of motion and muscle tone in the affected muscle.

The use of NSAIDs can be advocated over the first 48 to 72 hours after injury; however, their long-term effects would suggest that they delay healing of the injured tissue and result in lower peak failure loads. Their use should be closely monitored and discontinued as early as appropriate. The use of judicious physical therapy cannot be overemphasized. Early active assisted range of motion exercises should be instituted, but forced passive range of motion beyond the pain-free extremes of motion should be avoided.

Criteria for Return to Sports

Return to sports should not be attempted until the following three criteria are met: full, pain-free range of motion; return of strength; and ability to perform the sporting activity without pain. An acceptable rule of thumb for the degree of strength required to return to activity is at least 80% of the contralateral side, although for some athletes, it may be more appropriate to delay activity return until nearly 100% strength is attained.

Complications

The most common complication after a muscle strain injury is reinjury and the most significant predictor of reinjury is premature return to competitive activity before full pain-free motion, strength, and pain-free activity are attained. Adequate rest and supervised physical therapy with frequent reevaluation can ensure that return to activity is not done too early.

Table 13-2 Treatment Protocol for Hamstring Strains*

Table 13-2 Treatment Protocol for Hamstring Strains*

AAROM, active-assisted range of motion; AROM, active range of motion; NSAIDs, nonsteroidal anti-inflammatory drugs; PROM, passive range of motion. ♦Concentric high speeds at first, proceeding to eccentric low speeds.

From Clanton TO, Coupe KJ: Hamstring strains in athletes: Diagnosis and treatment. J Am Acad Orthop Surg 1998;6:237-248.

AAROM, active-assisted range of motion; AROM, active range of motion; NSAIDs, nonsteroidal anti-inflammatory drugs; PROM, passive range of motion. ♦Concentric high speeds at first, proceeding to eccentric low speeds.

From Clanton TO, Coupe KJ: Hamstring strains in athletes: Diagnosis and treatment. J Am Acad Orthop Surg 1998;6:237-248.

SURGICAL TREATMENT OF INDIRECT MUSCLE INJURIES

It is beyond the scope of a chapter such as this to discuss all aspects of complete muscle injury as it pertains to each anatomic region and the specifics of diagnosis and management of each. Direct surgical repair of indirect muscle-tendon unit injuries is not commonly advocated; however, bony avulsions of muscle-tendon units are an exception. Distal biceps brachii and proximal hamstring injuries are two examples of injuries that should be considered for surgical repair. Other regions where surgical treatment is an option include the pectoralis major tendon, patellar tendon, quadriceps tendon, and the Achilles tendon.

Repair of Proximal Hamstring Avulsion

The proximal hamstring avulsion injury also represents an uncommon muscle injury that is associated with significant disability. It is included in this chapter as it represents the extreme result of muscle overload injury.

Clinical Features and Evaluation

While most hamstring strains occur at the muscle-tendon junction as discussed previously, the avulsion of the proximal hamstring occurs from the ischial tuberosity involving a fairly predictable mechanism. Forced hip flexion with maintained knee extension is described most commonly.24 When combined with eccentric contraction of the hamstring muscles, avulsion of the common hamstring origin can occur. The largest series of proximal hamstring avulsions described injuries to water skiers. While the aforementioned mechanism was most common among inexperienced water skiers and typically occurred while the skier was attempting takeoff (five of six injuries), experienced water skiers were placed into the position of injury when they caught their ski tip in the water while skiing at high speed and their foot was not released from the binding.24 The role of muscle fatigue in these injuries among the experienced skiers was implicated as all their injuries occurred at the end of a day of skiing. Other activities resulting in rupture of the common hamstring origin include motor vehicle crashes,30 sprinting, falls from heights, horseback riding, volleyball, martial arts, jet skiing, and tennis.24

Patients typically present in a delayed fashion to the orthopedic surgeon. When seen acutely, the surgeon must have a high index of suspicion for these injuries when the patient describes an injury mechanism similar to that described previously. There is often ecchymosis over the posterior gluteal region, and a defect is palpable distal to the ischial tuberosity and proximal to the distally retracted muscle belly. Asking the patient to flex the knee results in retraction of the hamstring muscle belly and tendons of origin distally, with an increase in the length of the defect distal to the ischial tuberosity (Fig. 13-2).

Plain radiographs may reveal a shell of cortical bone avulsed from the ischial tuberosity (Fig. 13-3). MRI should confirm a complete rupture of the origin and in one series was able to identify both proximal hamstring tendon rupture and myotendinous junction injury within the same muscle.24

When seen chronically, patients complain of awkwardness or a sense of poor leg control during walking and running. This may be due to the loss of the hamstring's ability to decelerate the extending knee during the terminal swing phase of gait and the float phase of running.24 These patients often report inability to return to high demand physical activities or athletics despite referral for physical therapy.

Figure 13-2 Clinical photograph of a patient with a chronic complete hamstring tendon avulsion. Note the retracted muscle belly distally and the depression distal to the buttocks accentuated by active knee flexion. (From Sallay PI, Friedman RL, Coogan PG, Garrett WE: Hamstring muscle injuries among water skiers. Functional outcome and prevention. Am J Sports Med 1996;24:130-136.)

Figure 13-2 Clinical photograph of a patient with a chronic complete hamstring tendon avulsion. Note the retracted muscle belly distally and the depression distal to the buttocks accentuated by active knee flexion. (From Sallay PI, Friedman RL, Coogan PG, Garrett WE: Hamstring muscle injuries among water skiers. Functional outcome and prevention. Am J Sports Med 1996;24:130-136.)

Relevant Anatomy

The semitendinosus and biceps femoris muscles share a common insertion on the posterolateral aspect of the ischial tuberosity. The semimembranosus muscle may form a portion of this common tendon or may be independent, inserting anteriorly and medially to the common tendon. This common origin may be a factor in the hamstring failing in certain scenarios from its tendon-bone interface and not at its myotendinous junction (Fig. 13-4).

Treatment Options

Few comprehensive studies exist to guide decision making with this injury. In a retrospective study of a series of water skiing-related proximal hamstring ruptures,24 12 patients were studied, and it was found that only seven patients (58%) were able to return to most of their preinjury sports at a reduced level. Six of these seven had partial ruptures, and the one complete rupture that returned to preinjury sports did not participate in

Figure 13-3 Radiographic appearance of a complete avulsion injury (arrow) of the common hamstring origin. (From Clanton TO, Coupe KJ: Hamstring strains in athletes: Diagnosis and treatment. J Am Acad Orthop Surg 1998;6:237-248.)

Figure 13-3 Radiographic appearance of a complete avulsion injury (arrow) of the common hamstring origin. (From Clanton TO, Coupe KJ: Hamstring strains in athletes: Diagnosis and treatment. J Am Acad Orthop Surg 1998;6:237-248.)

Figure 13-4 A, Origin of the proximal hamstring tendons on the ischial tuberosity with the biceps femoris (BF) and semitendinosus (ST) in place. B, BF and ST reflected to reveal the origin of the semimembranosus (SM) tendon deeper and more medial. Note that the BF and ST share a common tendon. (From Sallay PI, Friedman RL, Coogan PG, Garrett WE: Hamstring muscle injuries among water skiers. Functional outcome and prevention. Am J Sports Med 1996;24: 130-136.)

high demand, acceleration sports. Only three of these seven returned to regular water skiing. Five of 12 patients (42%) were significantly limited and unable to run or perform agility sports. They had pain, cramping, and poor leg control with attempts to run. All five of these patients had complete ruptures. Notably, only two patients in this series had surgical repair. Both of these were performed chronically, and one patient continued to have pain and weakness with sporting activities, while the second reported no limitation in sporting participation.

While there is no outcome measure commonly accepted to compare methods of treatment, the preceding series highlights the fact that nonoperative management should only be associated with limited goals following treatment. For athletes with complete ruptures desiring return to high-demand sporting activity, injuries can be divided into acute (less than 4 weeks from injury) and chronic (more than 4 weeks from injury). This distinction has been suggested based on the increased scar formation seen within the muscle and degree of scar surrounding the sciatic nerve seen more than 4 weeks after injury.31 For individuals seen acutely, surgery may be recommended for those individuals who are physically fit and desire to return to high-demand activities, especially running activities. For chronic injuries, surgery is indicated if the patient is unable to return to desired activity due to pain or weakness despite physical therapy.

Surgery

After obtaining informed consent and after identifying the surgical site by signing it, the patient is brought to the operating

Figure 13-5 Common skin incisions for repair of proximal hamstring avulsion injuries. Incision A is transverse within the gluteal crease and is most appropriate for acute repairs and incision B is a vertical incision over the posterior thigh and is most appropriate for chronic hamstring avulsions requiring sciatic neurolysis. (From Klingele KE, Sallay PI: Surgical repair of complete proximal hamstring tendon rupture. Am J Sports Med 2002;30:742-747.)

Figure 13-5 Common skin incisions for repair of proximal hamstring avulsion injuries. Incision A is transverse within the gluteal crease and is most appropriate for acute repairs and incision B is a vertical incision over the posterior thigh and is most appropriate for chronic hamstring avulsions requiring sciatic neurolysis. (From Klingele KE, Sallay PI: Surgical repair of complete proximal hamstring tendon rupture. Am J Sports Med 2002;30:742-747.)

room and placed prone. For acute injuries, a transverse incision may be made in the gluteal crease as it is more cosmetic; however, for chronic tears or tears with concern for sciatic nerve involvement, an extensile incision made over the posterior thigh should be employed (Fig. 13-5). The inferior border of the gluteus maximus muscle is mobilized superiorly by dividing the posterior fascia. The combined tendon is avulsed from the lateral aspect of the ischium and usually does not contain a bony fragment.31 The tendon can be anatomically reattached using any common method of tendon fixation to bone such as two or three large suture anchors loaded with heavy nonabsorbable sutures31 (Figs. 13-6 and 13-7) or with two or three heavy nonabsorbable sutures via bone tunnels.30 A locking stitch should be used with each suture. In the case of suture anchors, one limb of the suture can be passed through the tendon using a Mason-Allen stitch

Figure 13-6 Appearance of the repaired proximal hamstring origin using two suture anchors. Arrow points to the repaired tendon. (From Klingele KE, Sallay PI: Surgical repair of complete proximal hamstring tendon rupture. Am J Sports Med 2002;30:742-747.)

Figure 13-7 Use of simple and locking stitches through suture anchors to repair the tendon to the ischium. Tension placed on the simple suture reduces the tendon to the insertion site. (From Klingele KE, Sallay PI: Surgical repair of complete proximal hamstring tendon rupture. Am J Sports Med 2002;30:742-747.)

Figure 13-7 Use of simple and locking stitches through suture anchors to repair the tendon to the ischium. Tension placed on the simple suture reduces the tendon to the insertion site. (From Klingele KE, Sallay PI: Surgical repair of complete proximal hamstring tendon rupture. Am J Sports Med 2002;30:742-747.)

while the other limb is passed in a simple fashion. This suture is then tensioned, reducing the proximal tendon end to its insertion site and finally tied to the suture limb that was passed as a Mason-Allen stitch.31

In the event of a chronic avulsion, using an extensile incision, the scarred hamstring tendons are identified from distal to proximal. The sciatic nerve is typically encased in dense scar tissue adherent to the scarred hamstring muscles (Fig. 13-8). In these

Figure 13-8 A, Intraoperative view of a chronic proximal hamstring rupture with the clamp beneath the retracted tendon. Arrow points to the insertion site. B, Suture in tendon reduced to the common hamstring origin. Arrow points to the sciatic nerve. (From Sallay PI, Friedman RL, Coogan PG, Garrett WE: Hamstring muscle injuries among water skiers. Functional outcome and prevention. Am J Sports Med 1996;24:130-136.)

Figure 13-8 A, Intraoperative view of a chronic proximal hamstring rupture with the clamp beneath the retracted tendon. Arrow points to the insertion site. B, Suture in tendon reduced to the common hamstring origin. Arrow points to the sciatic nerve. (From Sallay PI, Friedman RL, Coogan PG, Garrett WE: Hamstring muscle injuries among water skiers. Functional outcome and prevention. Am J Sports Med 1996;24:130-136.)

cases, identifying the normal sciatic nerve distally and then tracing it proximally through the scar region are recommended. A nerve stimulator has been recommended as an adjunct to neurolysis of the sciatic nerve from the scar bed.31 With the sciatic nerve isolated, the tendon can then be repaired as for the acute case. Fractional lengthening of these muscles at the myotendi-nous junction may be required in chronic cases.

Was this article helpful?

0 0
Cure Tennis Elbow Without Surgery

Cure Tennis Elbow Without Surgery

Everything you wanted to know about. How To Cure Tennis Elbow. Are you an athlete who suffers from tennis elbow? Contrary to popular opinion, most people who suffer from tennis elbow do not even play tennis. They get this condition, which is a torn tendon in the elbow, from the strain of using the same motions with the arm, repeatedly. If you have tennis elbow, you understand how the pain can disrupt your day.

Get My Free Ebook


Post a comment