Chapter 43. Assessment and Treatment of Pain in Sports Injuries

As our knowledge increases regarding the health benefits of exercise, more and more people attempt to stay healthy and physically fit with sports-related activities. As a result, sports injuries are no longer confined to a small group of competitive athletes but affect an ever-growing segment of the population. Improper training techniques, over-ambitious routines, and the use of faulty equipment have led to an increase in sports injuries (especially overuse injuries) and resultant pain syndromes. In the pediatric population, younger and younger children engage in highly competitive sports with training schedules that put them at increased risk for injury. Elite athletes, under the pressure of commercial interests and more widely disseminated knowledge about exercise physiology and training methods, are driven to greater extremes in order to gain small but significant advantages over the competition. This has led to overambitious workouts with inadequate rest periods. Many athletes suffer from chronic pain and injury as a result.

This chapter presents a brief review of the essential elements of bone, joint, tendon, ligament, and muscle physiology to lay the foundation for understanding both acute and repetitive stress injuries that are commonly seen in athletics. We then give an overview of treatment strategies for both acute and more chronic pain syndromes.

Bone

Bone is composed of organic proteins, matrix, and cells. The organic component of bone is 90% collagen type I and provides the tensile strength. The mineral phase of bone matrix accounts for 50% of the volume and 65% of the weight of bone and is composed of highly structured hydroxyapatite crystals and amorphous calcium phosphates. Bone cells account for only 3% of bone volume and include osteoblasts, osteoclasts, and osteocytes. Bone remodeling is ongoing throughout life and occurs predominantly at the trabecular part of the skeleton. Wolff’s law of adaptation states that mechanical remodeling of bone occurs in response to deforming strain. Both osteoblasts (responsible for erosion of existing bone) and osteoclasts (responsible for repair and remodeling of erosions) are involved. The exact mechanism of how mechanical strain activates osteocytes to initiate remodeling is still unknown, but both chemical messengers (dependent on the prostaglandins PGI2 and PGE2, IGF-1, and parathyroid hormone) and piezoelectric effects are believed to be involved.1

High levels of physical activity and stress loading in athletes increase bone density. The degree of increase in bone density is proportional to the level of stress loading accomplished in the athletic activity. For example, the bone mineral density (BMD) of the distal femur is found to be highest in world-class weightlifters followed by throwers, runners, soccer players, and then swimmers. This positive effect on BMD from mechanical loading is also observed in young women skaters and may counter the adverse estrogen-deficient effects on bone density seen in woman who are thin and amenorrheic.

Studies on both the elderly and young confirm that strength training at higher loads increases BMD more when compared with endurance training at low weights with high repetitions.2

Joints

Diarthrodial or synovial joints are capable of large degrees of motion and, under normal circumstances, tolerate high levels of friction, shear, and wear with little deterioration throughout a normal life span. A typical knee or hip joint may withstand loads up to six times body weight on a repetitive basis for up to a million times a year.3 Synovial fluid and soft connective tissue are common to all diarthrodial joints. The soft connective tissue includes the articular cartilage, joint capsule, meniscal cartilage, and ligaments. The primary load-bearing structure of the joint is the articular cartilage. Cartilage is primarily made up of type II collagen with up to 150 proteoglycan (PG) monomers linked to a central core of hyaluronic acid (Fig. 43-1). The link between PG and hyaluronic acid is essential for the structural integrity of cartilage. These macromolecules are highly hydrophylic, but, because they are confined in the semirigid collagen matrix, reach only 20% of their theoretical swell volume. The swelling pressure caused by the embedded PG is resisted by the tension that develops in the collagen matrix, and it is this balance of forces that is essential for modulating the compressibility of the structure under various loads.

Immobilization of a joint for prolonged periods causes significant loss of PGs in the cartilage, which in turn causes a loss of resistance to compression. In the recovery process after injury, both joint range of motion and stress loading is necessary to reverse the above changes.

Tendons and Ligaments

Tendons and ligaments are made up of highly organized collagen fibers (predominantly type I) arranged in a linear fashion. Tendons transmit the force generated by muscle actions to bones and generate movement about a joint. Ligaments are capsular if they extend off of the joint capsule, or accessory when extending between bones. In contrast to tendons, ligaments prevent excessive movement and contribute to joint stability. Both tendons and ligaments are made up of collagen fascicles that spiral on each other with successive folds or crimps that permit stretch and buffer elongation. The blood supply to tendons and ligaments is sparse when compared with joints, muscle, and bone. For example, avascular regions are found in the central region of the anterior cruciate ligament of the knee and the supraspinatus tendon of the shoulder.

Tendons are often surrounded by synovial sheaths when there is a significant pulley action present (e.g., the digit flexor tendons of the hand). At the junction with the bone, or enthesis, small synovial bursa are often present to prevent friction (e.g., greater trochanter bursa, retrocalcaneal bursa, and subacromial bursa).

Golgi and Pancinian organs lie at the myotendinous junction and transmit information to the central nervous system about muscle tension and pressure. Tendons demonstrate nonlinear deformation in response to stress. In the first phase, collagen fibers straighten and elastic fibers elongate. The second phase requires much greater force, and is characterized by breaking of collagen cross-links and disruption of smaller collagen fibers. Finally, increased forces will result in tendon rupture and failure occurs when a tendon is stretched 5% to 8% beyond its resting length (Fig. 43-2).

Changes in activity significantly affect tendons and ligaments. Physical training increases the weight and size of tendons and ligaments and increases the cross-links between collagen fibers. Immobilization decreases these cross-links and thus diminishes the tensile strength.

Muscle

Skeletal muscle makes up approximately 40% to 45% of the total body weight. There are two major types of muscle fibers (type I and II), which were originally identified with basic histochemical staining techniques (Fig. 43-3). These staining differences correlate with underlying differences in structural, contractile, and biochemical properties. Subtypes of type I and II have been characterized as well, and Table 43-1 summarizes the differences among fiber types.

The response of muscle to changes in levels of physical activity can be profound. There are two basic forms of muscle actions: static (or isometric), in which there is no joint movement, and dynamic in which there is a change in the length of the muscle and joint movement occurs. Dynamic actions can be further divided into concentric, in which the muscle shortens during the increased load (triceps in a shotput hurl), and eccentric, in which the muscle lengthens during the increased load (quadriceps when landing from a jump). Eccentric actions have lower energy requirements but carry an increased risk of muscle damage and tearing due to higher forces.

Increases in muscle mass with resistance training are primarily brought about by type II fiber hypertrophy (with a contribution from type I hypertrophy) rather than by muscle fiber proliferation. It has been found in animal models that repetitive stretching of muscle fibers alone is sufficient to cause massive increases in gene expression of contractile proteins causing muscle hypertrophy. The resistance to fatigue that develops with endurance training results from a number of factors including increases in capillary supply and mitochondrial content (i.e., increase in oxidative capacity) of the muscle fibers and metabolic adaptations favoring fat metabolism and glycogen sparing. It is still a contested question whether transformation of fiber types contributes to the adaptation of muscle to various training stimuli. The predominance of type I fibers in distance runners probably results from genetic influences, environmental factors such as training, and the interaction between the two. Some studies have shown changes in type IIB to type I with high-intensity interval training, but others did not show such changes or have only shown a shift from type IIB to type IIA with endurance training. In disuse atrophy, the reduction of muscle bulk can be profound, with up to 30% reduction in cross-sectional area after 1 month of immobilization. Both type I and II fibers are reduced in size to varying degrees depending on the individual.4

Aging alone has been thought to lead to the loss of muscle mass and strength. There is a loss of both cross-sectional area and total number of muscle fibers with age, predominantly affecting type II. This loss in muscle mass coincides with loss of bone density. However, recent studies have supported that many of the changes seen are not inevitable but are the result of decreased activity. The positive training effects seen on muscles in the young also occur in the elderly. Even in the 10th decade of life, an elderly person can make significant increases in muscle mass and strength if given a progressive resistance-training program. Similar positive changes in muscle respiratory capacity seen in the young can occur with endurance training in the elderly.5

Finally, the central nervous system also changes with training. This is evidenced by the marked improvement in performance that can occur with training in a specific activity over time, with much less dramatic changes in peripheral muscle strength. For example, during a 12-week period of training that included lifting boxes from the floor to the waist by knee extension, a 200% increase in weight was achieved with only a 15% increase in absolute isometric strength of the quadriceps muscle group. Also, the untrained contralateral limb will show an improvement in performance when the ipsilateral limb is repetitively trained, suggesting that the central mechanism plays a role. These changes are felt to result from neural adaptations including synchronization of motor units in the trained activity with a more advantageous balance of agonist versus antagonist muscle activation.2

Injuries in sports can be caused by a sudden overload to structural components of the bones, joints, and soft tissue or from chronic overuse. The forces that various structures must withstand during athletic activity are enormous. For example, a runner weighing 165 pounds will absorb a total of nearly 500,000 pounds of force on each foot during a 1.6-km run. There are various extrinsic and intrinsic factors that influence the type and severity of injury listed in Table 43-2. In the majority of injuries that are not traumatic, there has usually been a sudden change in the training routine that underlies the onset of pain. Typically, either there was a recent initiation of a new sport activity or there was a recent marked increase in training load involving changes in frequency, duration, and intensity.

Bone and Joint

Bone injury can occur with the extremes of repetitive forces seen in athletics and is characterized by the formation of stress fractures. The incidence of stress fractures in athletic populations of men is approximately 2% and of woman from 3.8% to 10%. Up to 49% of woman track runners with fewer than five menstrual periods a year develop stress fractures, suggesting that a hypoestrogenic state increases the risk. In runners, stress fractures account for nearly 25% of all injuries.6 Stress fractures are seen more commonly in different bones depending on the athletic endeavor7 (Table 43-3).

The most common joints injured in sports are the shoulder and the knee. The shoulder is the most unstable joint in the body and depends almost exclusively on ligaments and the tendons of the intrinsic muscles to maintain a balance between the extremes of range of motion and stability. As a result, these ligamentous and tendinous structures are commonly injured in sports where this tenuous balance is tested to achieve optimal performance. Both acute and chronic repetitive injuries are seen. Table 43-4 lists some less common shoulder injuries in the athletic population.8

The knee is typically injured acutely because of sudden forces that overwhelm the supporting ligaments. Often, if the loads are sufficient to disrupt the relatively tough intrinsic ligaments of the knee, the cartilagenous structures such as the menisci will also be torn. Common causes of knee pain in the athlete include meniscal tears, patellofemoral pain syndrome, ligamentous injuries, patellar tendinitis, and osteochondral injury. In the juvenile population apophysitis of the tibia (Osgood-Schlatter’s syndrome) is often seen. Table 43-5 lists some less common injuries to the knee in the athletic population.9

Spine

Just as in the occupational arena, low back pain (LBP) is common in sports. Pain can develop as a result of any of the causes seen in nonathletes. Of particular interest to adolescent athletes is the development of symptomatic spondylolysis with pars interarticularis defects. Spondylolisthesis can occur with bilateral pars defects. Excessive loading of spinal elements during growth in adolescence is felt to be harmful and puts athletes in this age group at greater risk for developing LBP than sedentary controls. The cumulative prevalence of LBP in juveniles is 30% with only 8% having more chronic or recurrent problems.10 Among adolescent athletes referred for evaluation of LBP, up to 47% have been found to have spondylolysis. Stress loading in extension and rotation is felt to be particularly problematic, and as a result, there is a higher prevalence of spondylolysis in sports such as soccer, tennis, wrestling, gymnastics, football, volleyball, and rugby. The level most frequently involved is L5 (88.6%) with L4 seen less often.11 Spina bifida occulta has been found to be more prevalent in patients with spondylolysis.

Soft Tissue

Tendons

Tendinitis and muscle strains account for 30% to 50% of all sports injuries. A recent review of the literature on the etiology and treatment of tendinitis suggests that there are few well-controlled prospective studies that can guide care.12 Nevertheless, some basic concepts are generally accepted. The forces that injure a tendon can be either extrinsic to the tendon itself, causing an impingement on the tendon, or intrinsic, related to excessive stretch forces on the tendon during activity. A common example of an extrinsic tendinitis is shoulder impingement syndrome, where there is inadequate space between the humeral head and the acromion for free passage of the rotator cuff tendons during overhead activity (throwing and swimming), leading to direct tendon trauma. Intrinsic tendinitis commonly results from repetitive overuse or sudden excessive loading as is seen with weightlifting. Eccentric loading of the tendon applies greater forces and under many circumstances can be more traumatic. This occurs when the muscle tendon complex is lengthening during an action. An example of acute eccentric loading to the patellar tendon occurs when landing from a jump as the knee bends and the quadriceps muscle lengthens to absorb the shock. In addition, a lengthening of the muscle to maximize force generation briefly precedes most concentric actions. This puts the maximum force on the tendon when the tendon is elongated, potentially causing damage.

Ligaments

Ligament injuries, or sprains, commonly occur in the knees and ankles of athletes. The etiology of such injuries is almost always the result of a sudden excessive force on the ligament. Examples include a sudden valgus stress to the knee with a football tackle at the knees causing disruption of the medial collateral ligament, or a sudden change in direction on a tennis court or football field with the foot firmly planted, which can lead to anterior cruciate ligament injury. Joint stability may be significantly impaired with serious ligamentous injury and, if improperly treated, can lead to chronic stresses to the joint and supporting muscles and tendons.

Muscles

Muscle injuries occur either from an acute excessive load or from excessive chronic use. Myotendinous failure is a function of the force applied and the strength and level of fatigue of the muscle. The myotendinous junction is highly infolded, increasing the contact surface area by 20 times to provide added strength. As a result, tears occur near but not at the true histologic junction. If severe enough, muscle and tendon tears can occur and be associated with hematomas. Muscles that cross two joints or have a higher percentage of type II fibers are more prone to strain patterns. Examples of such muscles include the hamstrings, rectus femoris, and the gastrocnemius.

Eccentric actions put muscles at greater risk for strain and can cause the disruption of contractile elements at the Z lines. Delayed onset muscle soreness is more common after eccentric loading.13 This condition usually appears 24 to 48 hours after an exercise bout and is associated with high serum levels of intramuscular enzymes such as creatine kinase.

Other causes of muscle pain in sports include muscular contusions by blunt trauma. Myositis ossificans is a complication of muscle contusion characterized by intramuscular calcifications. Exertional rhabdomyolysis can also occur, with or without direct trauma, and is potentially fatal. Complications include compartment syndrome in the affected limb due to excessive muscle swelling and renal failure.14 Compartment syndrome can also occur in chronic situations and results from repetitive injury to a muscle group, leading to swelling and increased pressures in the muscle with exertion (often seen in the lower extremities of runners).

History

Historically, it is important to determine if there has been a recent change in duration, intensity, and frequency of the training regimen. Symptoms usually present approximately 2 to 4 weeks after a training regimen change. In addition, other common risk factors for injury include changes in environment or terrain and changes in equipment such as new running shoes or tennis racquets. The exact mechanism of injury (inversion sprains or decelerating injuries) contributes to establishing a diagnosis. Associated disease states should be looked for, including arthritis, circulation problems, and prior history of injuries. Special considerations for female athletes and athletes in the pediatric and elderly age groups are highlighted later in the chapter.

Examination

When examining an athlete, even with a specific, well-localized pain problem, it is important not to focus too narrowly on the problem. Biomechanical factors that underlie an injury can only be determined by viewing the relationship of the various joints involved at least one level above and below the area of pain, both at rest and dynamically in the sports-related activity. Side-to-side comparisons of muscle strength and mass should be made to get a better understanding of muscle imbalances. In sports that involve the asymmetrical use of an extremity (such as tennis), one should expect to find significant differences, but, in many cases, large differences can be problematic. Strength testing of antagonist and agonist muscle groups (such as hamstrings and quads) should also be made in the injured and noninjured side to help with future training recommendations. Finally, grading of the ligamentous sprains and overuse injuries is important to help with clinical decision making regarding immobilization, rehabilitation, and the need for surgical interventions (Tables 43-6 and 43-7). Assessment of problems in the upper or lower extremities should include a thorough examination of the peripheral vascular and nervous system integrity.

Imaging

In most injuries, imaging can be delayed until treatment response is assessed. Of particular concern in an athletic population is the increased prevalence of stress fractures. Stress fractures can be observed under ideal circumstances as little as 3 weeks and at times up to 3 months after injury with conventional radiology. Initial plain films will be negative up to 67% of the time. Classic findings include periosteal new bone formation with sclerosis and radiolucent lines called DBLs (dreaded black lines) that are transverse cortical striations. The three-phase bone scan is the gold standard with virtually 100% sensitivity, but poor specificity. For example, infection and arthritic conditions will also cause positive findings requiring other tests to provide clinical correlation. Changes in bone scan can be seen as early as 48 to 72 hours after the onset of symptoms and can remain positive for 6 months to 2 years after injury. Only 10% to 25% of bone scan positive stress fractures show evidence of fracture on plain films. By using the technetium 99 methylene diphosphonate three-phase technique (angiogram, blood pool, and delayed image phases), other stress injuries can be observed in addition to stress fractures. For example, stress fractures will be positive in all three phases, whereas medial-tibial stress syndrome (shin splints) will only be positive in the third or delayed image phase. In up to 50% of athletes with positive bone scans, asymptomatic sites of uptake will be seen and are felt to be areas of subclinical bone strain (Table 43-8).15

Magnetic resonance imaging (MRI) has excellent sensitivity and superior specificity for bone abnormalities. The advantage over CT scanning is in being able to differentiate between stress fractures and bone tumors or infectious processes. Single photon emission computed tomography (SPECT) is more sensitive for the early detection of spondolytic changes in the spine than bone scan or plain films, but may not be effective for detection 3 months after symptomatic onset.

Imaging of muscles in athletes is rarely indicated. If there is concern over severe muscle tears or soft tissue masses, MRI is the technique of choice, although there is a growing literature about the positive sensitivity and specificity of diagnostic ultrasound in soft tissue injury.16

Female Athletes

After puberty, significant differences emerge between male and female athletes. Females maintain a higher percentage of body fat, gain less muscle mass, have lower lung capacities, and lower oxygen-carrying capacity than men. In addition there are biomechanical differences that may put female athletes at more risk for injury. For example, woman have a higher incidence of genu valgus, which can lead to patellar tracking disorders and injury.

Perhaps more important than these differences are the effects that excessive training can have on normal endocrine function in the female population. Recognition of problems related to athletic ammenorrhea has improved among trainers and physicians. Up to 28% of women participating in college varsity athletics will be ammenorrheic. The prevalence increases to 57% in cross-country runners and is high in dancers, swimmers, and cyclists. The most significant physiologic consequence of this is the effect on bone density, and as a result, stress fractures are more common in this group. Special attention must be given to the risk factors for anorexia athletica, which can in some cases be fatal17 (Table 43-9).

Elderly Athletes

Acute injuries are common in the elderly participating actively in sports. The safety margin of an exercise routine is much narrower and puts this population at greater risk. Changes in the cardiovascular and neurologic system will inevitably compromise aerobic capacity and coordination of the athletic elderly and should be taken into account when recommending training regimens. Injury rates vary from 14% to 57% in the athletic elderly in different series. Common sites of injuries involve the shoulder or knee and are often due to preexisting orthopedic problems in those joints. In general, lower extremity injuries are most common.18

Muscle strains occur frequently and rupture of muscle and tendons is more likely to occur than in younger populations. Acute injuries related to falls are a common scenario seen in this group. Overuse injuries typically involve tendons and muscles rather than bone, and recovery can be extended up to 2 years in some studies. Stress fractures are rare, but it should be noted that the sensitivity of bone scan may decrease to 80% to 95% in patients older than 65 years of age.

Pediatric Athletes

In children and adolescents, the muscles and tendons are stronger than the bone, and thus bone avulsions are seen more frequently than in adults. The growth plates at the apophyses in the pelvis and hips are particularly at risk and are common sites of acute avulsion. In addition, skeletal immaturity puts the pediatric population at greater risk for stress fractures if overambitious training routines are followed.

Exercise performance is limited compared with adults partly because of lower anaerobic capacity. During exertion, children use more oxygen per kilogram of body weight and thus will experience a higher metabolic cost than adults for an equivalent, absolute exercise level (i.e., walking at a given speed). The response to strength training in children is also different than in adults. In the prepubescent population, the muscle responds to training with central neurogenic adaptations in firing rate and recruitment, but not by muscle fiber hypertrophy, and increases in lean muscle mass. As a result, aggressive strength training with high weights and low repetitions should not be attempted in this population because it increases the risk of tendon and bone trauma without benefit. However, strength training is safe in children if the program is properly designed and supervised by individuals experienced with this age group. In addition, during growth spurts, the apophyses (the site of tendon insertion into the bone) are particularly at risk for injury and training regimens should be reduced19 (Table 43-10).

Treatment of injured athletes has three primary goals: (1) control pain and inflammation, (2) restore normal pain-free range of motion, and (3) return individuals to prior levels of strength, endurance, and optimal biomechanical coordination for the sport-specific activity. There have been studies suggesting that highly trained athletes may have a decreased sensitivity to noxious stimuli.20 Athletes as a group tend to be highly motivated and often overaggressive in the implementation of a treatment plan. Recognition of this phenomenon is important to prevent further injury during the recovery phase. One must also take into account that athletes may not have a normal response to pain during training and fail to appropriately limit activity in response to nociceptive input. There is still debate about the etiology of this phenomenon. Whether training produces sustained effects on raising the pain threshold, or whether competitive athletics preselects individuals with high pain thresholds, not enough is currently known to decide. Clearly, the culture of highly competitive athletics is to endorse the notion that without pain there will be no significant gains made in performance. This can engender repetitive injuries and a balance must be struck between encouraging normal soreness of aggressive conditioning and strengthening routine versus pain caused by a repetitive injury associated with the athletic activity.

Acute Injuries

A useful acronym for managing an acute sports-related injury is RICE: rest, ice, compression, and elevation of the injured part. With grade II or III sprains, appropriate immobilization will be necessary. Treatment can be broken up into three phases for grade I and II injuries: acute, subacute, and chronic. Briefly, in the acute phase, ice should be applied to the inflamed structure for 15 to 20 minutes several times a day with range of motion allowed within the limits of pain. Relative rest is preferred rather than complete lack of activity to avoid severe deconditioning. If the injury involves a weight-bearing structure, crutches should be used when active. This phase can last from a few to several weeks, up to 2 to 5 weeks depending on severity. After the acute inflammatory phase of the injury, ice is not necessary and heat can be applied to improve circulation to the area of injury and can ease stretching of the affected area to prevent dense scar tissue formation in the injured tissue. During this phase, atrophy is prevented with isometric or static muscle actions. Functional electrical stimulation (FES) can also be used to maintain muscle mass. In the subacute phase, gradual increases in range of motion and progressive, active strengthening and endurance training of the involved muscles as well as cardiovascular conditioning should be attempted. Finally in the final phase of rehabilitation, sport-specific training should occur. Initially, training should begin at 25% of the preinjury level and then increase by 10% to 20% each session if no symptoms are provoked during the first two thirds of the training session.21

Repetitive Injuries

In repetitive or overuse injuries, correction of underlying external and internal risk factors are essential. In addition to a careful analysis and correction of the biomechanical factors that may underlie the injury, changes in training routines will also have to be made. Treatment must be more cautious than in acute traumatic injuries and is often more prolonged, but many of the same principles of treating acute injuries apply. If there is an acute exacerbation of a chronic problem, ice in the first 48 hours can be helpful to reduce inflammation and swelling. Subsequently, heat is likely to be of more benefit. Initially, flexibility training is more important than is strength training. When strength training is introduced, the focus should be directed at muscle imbalances observed during the examination. When the pain has subsided, eccentric exercises for chronic tendinitis have been found to be extremely effective to increase the strength of the involved structure and can help prevent re-injury.22

The treatment of stress fractures is somewhat different from that outlined above for chronic soft tissue injuries. There are two phases to the treatment of stress fractures. Phase I involves modified weight bearing (ADLs allowed but not sports) and time to allow the bone to heal. Active treatment includes use of NSAIDs and ice for pain control (ultrasound is contraindicated), with stretching and cross training to maintain aerobic fitness using a method that avoids stress to the affected limb (upper extremity bicycle if lower extremity is injured). Use of casting or immobilization is not necessary unless there are hormonal or other factors that may lead to late nonunion of the fracture. When the athlete has been pain free for 2 to 3 weeks, percussion tenderness is negative, and plain films show bone healing, phase II can begin. Here the focus is on the gradual reintroduction of sport with a focus on better controlling any biomechanical and training factors that may have led to the original injury.

Stress fractures of the spine are in general more difficult to treat than other bones given the difficulty in isolating the structure for rest. The treatment of spondylolysis of the lumbar spine is focused on limiting extension of the spine to promote healing. If there is a normal plain film but positive bone scan or SPECT, many advocate treatment without bracing of the spine. Mean time for fracture healing is about 7 months. Specific spine stabilization exercises have been shown to be superior to rest and general conditioning exercises.23 When braces are used after failure of more conservative measures, they must immobilize both the thoracolumbar and the lumbosacral segment. Recommendations are to remain immobilized for 23 to 24 hours a day for up to 6 months. Surgery is needed if this approach fails.10

Medications

The use of medications for controlling pain and inflammation in sports-related injuries is not without controversy. Many injuries seen in sports are associated with swelling and inflammation, and this makes the use of anti-inflammatory medications for pain control an obvious choice. Both nonsteroidal anti-inflammatory medications (NSAIDs) and corticosteroids are known to have suppressive effects on the inflammatory response to injury. Tissue injury causes the release of cell membrane phospholipids, which degrade to arachidonic acid. This in turn leads to a cascade of enzymatic reactions that release pro-inflammatory substances including the prostaglandins, thromboxanes, and leukotrienes (Fig. 43-4). Corticosteroids act early in the cascade to inhibit phospholipase A2. This limits the production of inflammatory mediators by both the cyclooxygenase and the lipoxygenase pathways and underlies the greater potency of corticosteroids and the adverse effects retarding normal tissue repair. Most NSAIDs inhibit cyclooxygenase (COX-1 and COX-2) nonspecifically, thereby limiting production of both PGE1 and PGE2. PGE1 is a constitutive enzyme involved with normal housekeeping activity in the body, including the maintenance of normal renal and gastric function. PGE2 is an inducible form of the enzyme and is expressed only in inflamed tissue. There has been great interest in the recent marketing of more specific COX-2 inhibitors. It is still unclear whether they will provide any additional safety or benefit when used to control pain and inflammation in sport-related injuries. Both NSAIDs and corticosteroids also have other cellular and noncellular effects on suppressing the response to inflammation.

The controversy with using anti-inflammatory medications revolves around the concern that the inflammatory response to injury is not purely pathologic, and that it is necessary to remove necrotic tissue and disrupted connective tissue from the injured area. Studies of the effects of NSAIDs on tissue repair in an acute muscle strain injury animal model has shown a delay in the degradation of damaged tissue and slowed muscle regeneration. The majority of the evidence also shows that corticosteroids strongly inhibit tendon and ligament healing following injury.

Nevertheless, in a recent review of clinical studies addressing the benefit of short-term use of NSAIDs for sports injuries, modest benefits were seen with slight decreases in pain symptoms, disability, and inflammation. No clinical evidence for delaying healing was found. Generally, short-term use of NSAIDs (3 to 5 days) is recommended to control pain, to assist in the reduction of swelling, and promote early mobilization of the involved structure. Long-term use is not recommended and vastly increases the risk of potentially lethal side effects including gastric and renal compromise. These side effects can be a serious consequence of overuse of these medications in highly trained athletes during the extremes of competition. Anti-inflammatory medications should not be used to mask a persistent pain problem in the athlete because this will promote further injury and does not address the underlying training or biomechanical issues. There has been no well-controlled study to justify the use of steroids in soft tissue injuries. A list of available NSAIDs and dosing frequency can be found in Table 43-11.

Stronger pain medications are generally not encouraged in athletics, and the International Olympic Committee (IOC) bans most of the opioids. Obviously, use of opioid analgesics in an acute traumatic injury may be appropriate, when the pain is severe. However, in the recovery period, strong analgesics should not be used to mask pain while training.

Injection Principles

Appropriate use of injection techniques into joints, tendon sheaths, bursa, muscle trigger points, and other soft tissue structures can be of great benefit both from a diagnostic and therapeutic point of view in the athlete. It is often useful before injecting to have the athlete provoke the pain by performing the activity that induces the discomfort. This can help with localization of the inflamed tissue. If in doubt about the pain generator, it can be useful to inject with local anesthetic alone initially and then try to provoke the pain 10 to 20 minutes later to determine whether the location was accurate before infusing corticosteroid (Table 43-12).

The risk of tendon rupture with repeated steroid injections is real. The maximum load strength of tendons and ligaments after steroid injection has been demonstrated to be reduced in many animal studies. This effect is particularly predominant immediately after injection. Unfortunately, there is a general lack of well-designed clinical studies to guide the safe use of steroids.24

A conservative approach would permit only 1 to 2 tendon or tendon sheath injections in 1 year, and some would recommend that no vigorous muscle loading should be performed for at least 2 weeks after injection to avoid complications. Many would advocate, however, never to inject a tendon in an athlete, given the potential for loss in tissue durability. Joints can typically be injected up to 3 times in a year. Bursa can be injected more frequently. With injections into superficial structures such as the epicondyles of the elbow or the pes anserine bursa, avoid depositing the steroid into the skin because this can cause depigmentation. One technique is to pinch the skin and pull away from the deeper structures before inserting the needle to avoid such complications. When injecting into perineural areas such as the carpal tunnel, it is safe to touch the nerve if using a 27-gauge needle and then pull back 1 to 2 mm before injecting. Infection or bleeding can be avoided with proper sterile and hemostatic technique. Other risks of steroid use are summarized in Table 43-13.

Treating pain syndromes in athletes can often present major challenges. Although the group as a whole is highly motivated, the goals of treatment are often more difficult to attain than in the general population. The athlete does not only want to be pain-free but to be pain-free while performing an extremely stressful activity that requires a high degree of tissue, biomechanical, and psychological integrity. A complex set of intrinsic and extrinsic factors must be taken into account and corrected in order to be successful and prevent chronic re-injury. As a result, a thorough understanding of both the underlying physiology of the structural elements involved as well as the external factors that are often unique to each sport is essential.