Metatarsal Stress Fracture

Background

With an increase in public interest in physical fitness, clinical practitioners are diagnosing stress fractures with greater frequency.[1, 2, 3] First described by Aristotle in 200 BC, stress fractures were initially recorded in the medical literature in 1855 by the Prussian military physician Breithaupt, who described what is now known as a march fracture, or stress fracture of the metatarsals. See the images below.

Radiograph of the feet. This image depicts a stress fracture of the left second metatarsal with exuberant callus. Radiograph of the left foot. This image depicts a stress fracture of the fifth metatarsal. Bone scan of the lower extremities. This image depicts a right fifth metatarsal stress fracture.

Metatarsal stress fractures are not limited to high-level athletes or military recruits. This type of injury is seen in runners of all levels, as well as ballet dancers and gymnasts and patients with rheumatoid arthritis (RA), metabolic bone disease, and neuropathic conditions.[4, 5, 6] Metatarsal stress fractures are also seen with increasing frequency in patients who engage in aerobics activities, particularly high-impact aerobics.

NextEpidemiologyFrequencyUnited States

The incidence of stress fractures in the general population is unknown, as virtually all literature on the subject is derived from a military population or advanced-level athletes. Stress fractures are estimated to constitute up to 16% of all injuries that are related to athletic participation; running is the cause in most of these cases. Most stress fractures (95%) involve the lower extremities, particularly the metatarsals.

PreviousNextFunctional Anatomy

The second and third metatarsals are relatively fixed in position within the foot; the first, fourth, and fifth metatarsals are relatively mobile. More stress is placed on the second and third metatarsals during ambulation; thus, these bones are at increased risk for stress fractures.

The fifth metatarsal, which is approximately 1.5 cm from the proximal pole of the bone, bears greater stress in those who oversupinate when they walk or run. The fifth metatarsal also has a diminished blood supply and, thus, a decreased ability to heal.[7, 8]

Stress fractures of the proximal fifth metatarsal must be distinguished from proximal avulsion fractures ("pseudo-Jones" fractures) and Jones fractures. The proximal avulsion fracture is usually associated with a lateral ankle strain and occurs at the insertion of the peroneus brevis tendon. The true Jones fracture is an acute fracture of the proximal diametaphyseal junction.

PreviousNextSport-Specific Biomechanics

Queen et al investigated whether foot type (flat or normal) resulted in loading differences during four sport-specific tasks (cross-cut, side-cut, shuttle run, and landing from a simulated lay-up).[9] Of 22 healthy individuals, 12 had normal feet and 10 had flat feet, and each completed 5 trials per condition. In-shoe pressure data were collected at 50 Hz, and analyses of the entire foot and 8 regions of the foot were carried out on contact area, maximum force, and the force time integral. The investigators' findings included the following statistically significant (P [9] :

Flat feetDuring the cross-cut task, there was an increase in medial midfoot contact area.During the side-cut task, an increase in contact area, force time integral, and maximum force in both the medial and lateral midfoot were demonstrated. During the shuttle run task, an increase in force time integral in the lateral midfoot and increases in maximum force in both the medial and lateral midfoot were present During the landing task, an increase in maximum force in the medial midfoot was present. However, flat feet showed a decrease in middle forefoot maximum force.

Queen et al concluded that individuals with a normal foot may have a lower risk for medial and lateral midfoot injuries such as metatarsal stress fractures. Thus, foot type should be assessed when determining an individual's risk for metatarsal stress fractures.[9]

PreviousProceed to Clinical Presentation , Metatarsal Stress Fracture

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Navicular Fracture

Background

The navicular plays an important role in maintaining the medial longitudinal arch of the foot. Commonly, fractures of the navicular are not evident on plain radiographs. This often leads to a delay in diagnosis, which may result in prolonged disabling foot pain in individuals, particularly young athletes. The 4 types of navicular fractures are (1) cortical avulsion, (2) tuberosity, (3) body, and (4) stress.[1, 2, 3, 4, 5]

Cortical and tuberosity avulsion fractures

Avulsion fracture, the most common fracture of the navicular, is often associated with ligamentous injuries and results from twisting forces on the mid foot. These fractures are commonly treated conservatively, except for avulsion of the posterior tibial tendon insertion (tuberosity fracture), which may be repaired operatively, especially if a proximal dislocation of 1 cm or more is present. An avulsion of the posterior tibial tendon insertion must be differentiated from an accessory navicular (see Other Problems to Be Considered).

Fractures of the navicular body

Fractures of the body are commonly associated with other injuries of the midtarsal joint. Sangeorzan et al categorized navicular body fractures into 3 types, as follows[6] :

Type 1 is a coronal fracture with no dislocation.Type 2 is a dorsolateral to plantomedial fracture with medial forefoot displacement.Type 3 is a comminuted fracture with lateral forefoot displacement and carries the worst prognosis.

All navicular body fractures with 1 mm or more of displacement require open reduction and internal fixation.

Stress fractures

The rest of this article primarily discusses the diagnosis and treatment of navicular stress fractures, which are usually sports-related injuries.

In 1855, Brehaulpt first described stress fractures in military recruits who were subjected to long marches. As more civilians took up physically demanding sports, the incidence of stress fractures has increased in the general population. Towne et al first described stress fracture of the tarsal navicular in 1970.[7]

In athletes, navicular stress fractures are of particular concern because they are underdiagnosed and can lead to significant disability if the diagnosis is delayed.[1, 2, 3, 4, 5, 8] In a study by Torg et al in 1982, the average time between the fracture and diagnosis was estimated to be 7 months.[9] Given the significant improvement in outcome with early diagnosis and proper treatment, navicular stress fractures should be considered in any athlete with midfoot pain. In a 2006 study by Saxena and Fullem, navicular stress fractures took up to 4 months to heal posttreatment.[10]

Fracture-dislocation of the navicular may occur in athletes.[11, 12, 13, 14, 15, 16, 17, 18] This uncommon injury generally requires reduction and examination for stability via fluoroscopy, with the patient under general anesthesia. If the postreduction examination findings confirm stability of the navicular, treatment with a non–weight-bearing cast may be sufficient; otherwise, internal fixation is required.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education articles Broken Foot and Cast Care.

NextEpidemiologyFrequencyUnited States

Navicular stress fractures may account for up to 35% of stress fractures in athletes. Because navicular stress fractures are not easily observed on plain radiographs, the reported incidence rates vary widely. The overall incidence may appear to be increasing due to advances in imaging.[19, 20, 21, 22, 23, 24, 25]

Among track-and-field athletes, up to 21% may experience a stress fracture in the course of a year.[26, 27] In these athletes, up to 15% of stress fractures are of the navicular.[26] Other studies have demonstrated similar findings.[28, 29, 30, 31] The highest incidence of stress fractures is in jumping and sprinting events.

Among military recruits, the incidence is approaching that of athletes, as the training of military recruits more closely mirrors the training of athletes.[28, 32, 33, 34]

International

Worldwide, the incidence of navicular stress fracture is related to the sport of participation and to the training that is involved rather than to geographic location.

PreviousNextFunctional Anatomy

The tarsal navicular is a disk-shaped bone that articulates distally with the 3 cuneiforms, proximally with the talar head, and, occasionally, laterally with the cuboid. The distal articulation with the 3 cuneiforms is by means of 3 facets that have a common synovial cavity. The plantar and dorsal cuneonavicular ligaments reinforce the distal articulation.

On the lateral side are the plantar, dorsal, and interosseous cuboideonavicular ligaments and, occasionally, a syndesmotic joint with the cuboid. Medially, the distal articulation serves as an attachment for the posterior tibial tendon and the spring, or plantar calcaneonavicular, ligament. On the proximal side, it envelops the talar head completely. The thickened talonavicular ligaments reinforce the talonavicular joint in a plantar and dorsal orientation. Medially, the anterior fibers of the deltoid ligament add support.

Along with the calcaneocuboid joint, the talonavicular joint forms the transverse tarsal joint, which allows motion of the forefoot on the hindfoot. The ligamentous structure is such that when the hind part of the foot is everted, the joint is mobile, and when the hind part of the foot is inverted, the joint is fixed.

The blood supply of the navicular comes from small branches of the posterior tibial and dorsalis pedis arteries. This supply leaves the medial and lateral areas of the navicular relatively well supplied compared with the central section of the navicular. This relative difference correlates with the common site of stress fractures.

PreviousNextSport-Specific Biomechanics

The navicular is part of 2 important structures that are essential for normal gait: (1) the medial longitudinal arch and (2) the transverse tarsal joint (also called the midtarsal or Chopart joint).

The medial longitudinal arch is composed of the navicular, calcaneus, talus, 3 cuneiforms, and 3 medial metatarsals. This arch provides support for normal gait, in particular from mid stance until push-off.

The transverse tarsal joint is essential for normal gait and is composed of the talonavicular joint and the calcaneocuboid joint. At heel strike, this joint is flexible and plays an important role in absorbing ground impact and accommodating the foot to the ground. At push-off, the transverse tarsal joint is locked and is helpful in forward propulsion.

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Plantar Fasciitis

Background

Plantar fasciitis is the pain caused by inflammation of the insertion of the plantar fascia on the medial process of the calcaneal tuberosity. The pain may be substantial, resulting in the alteration of daily activities. Various terms have been used to describe plantar fasciitis, including jogger’s heel, tennis heel, policeman’s heel, and even gonorrheal heel. Although a misnomer, this condition is sometimes referred to as heel spurs by the general public.

There are many diagnoses within the differential of heel pain; however, plantar fasciitis is the most common cause of heel pain for which professional care is sought. Approximately 10% of the United States population experiences bouts of heel pain, which results in 1 million visits per year to medical professionals for treatment of plantar fasciitis.[1] The annual cost of treatments for plantar fasciitis is estimated to be between $192 and $376 million dollars.[2] The etiology of this condition is multifactorial, and the condition can occur traumatically; however, most cases are from overuse stresses.

The typical presentation is sharp pain localized at the anterior aspect of the calcaneus. Plantar fasciitis is often associated with a heel spur (exostosis); however, many asymptomatic individuals have bony heel spurs, whereas many patients with plantar fasciitis do not have a spur.[3]

Plantar fasciitis can be a difficult problem to treat, with no panacea available. Fortunately, most patients with this condition eventually have satisfactory outcomes with nonsurgical treatment.[4] Therefore, management of patient expectations minimizes frustration for both the patient and the provider.

NextAnatomy

The plantar fascia is a thickened fibrous aponeurosis that originates from the medial tubercle of the calcaneus, runs forward to insert into the deep, short transverse ligaments of the metatarsal heads, dividing into 5 digital bands at the metatarsophalangeal joints[5] and continuing forward to form the fibrous flexor sheathes on the plantar aspect of the toes. Small plantar nerves are invested in and around the plantar fascia, acting to register and mediate pain.

The plantar fascia is made up of 3 distinct parts: the medial, central, and lateral bands. The central plantar fascia is the thickest and strongest section, and this segment is also the most likely to be involved with plantar fasciitis. In normal circumstances, the plantar fascia acts like a windlass mechanism to provide tension and support through the arch.[6] It functions as a tension bridge in the foot, providing both static support and dynamic shock absorption.[7]

PreviousNextPathophysiology

Biomechanical dysfunction of the foot is the most common etiology of plantar fasciitis; however, infectious, neoplastic, arthritic, neurologic, traumatic, and other systemic conditions can prove causative. The pathology is traditionally believed to be secondary to the development of microtrauma (microtears), with resulting damage at the calcaneal-fascial interface secondary to repetitive stressing of the arch with weight bearing.[8, 9, 10]

Excessive stretching of the plantar fascia can result in microtrauma of this structure either along its course or where it inserts onto the medial calcaneal tuberosity. This microtrauma, if repetitive, can result in chronic degeneration of the plantar fascia fibers. The loading of the degenerative and healing tissue at the plantar fascia may cause significant plantar pain, particularly with the first few steps after sleep or other periods of inactivity.

The term fasciitis may, in fact, be something of a misnomer, because the disease is actually a degenerative process that occurs with or without inflammatory changes, which may include fibroblastic proliferation. This has been proven from biopsies of fascia from people undergoing surgery for plantar fascia release.

Studies have introduced the etiologic concept of fasciosis as the inciting pathology. Fasciosis, like tendinosis, is defined as a chronic degenerative condition that is characterized histologically by fibroblastic hypertrophy, absence of inflammatory cells, disorganized collagen, and chaotic vascular hyperplasia with zones of avascularity.[11, 12, 13, 14]

These changes suggest a noninflammatory condition and dysfunctional vasculature. With reduced vascularity and a compromise in nutritional blood flow through the impaired fascia, it becomes difficult for cells to synthesize the extracellular matrix necessary for repairing and remodeling.[15]

Biomechanics of running

During running, the vertical forces in the foot at foot strike may reach 2-3 times an individual’s body weight.[16] The plantar fascia and longitudinal arch are also part of the foot’s shock absorption mechanism. During the heel-off phase of gait, tension increases on the plantar fascia, which acts as a storage of potential energy. During toe-off, the plantar fascia passively contracts, converting the potential energy into kinetic energy and imparting greater foot acceleration

PreviousNextEtiology

The cause of plantar fasciitis is often unclear and may be multifactorial. Because of the high incidence in runners, it is best postulated to be caused by repetitive microtrauma. Possible risk factors include obesity, occupations requiring prolonged standing and weight-bearing, and heel spurs.[17] Other risk factors may be broadly classified as either extrinsic (training errors and equipment) or intrinsic (functional, structural, or degenerative).

Extrinsic risk factors

Training errors are among the major causes of plantar fasciitis. Athletes usually have a history of an increase in distance, intensity, or duration of activity. The addition of speed workouts, plyometrics, and hill workouts are particularly high-risk behaviors for the development of plantar fasciitis. Running indoors on poorly cushioned surfaces is also a risk factor.

Appropriate equipment is important. Athletes and others who spend prolonged time on their feet should wear an appropriate shoe type for their foot type and activity (see Treatment).[18] Athletic shoes rapidly lose cushioning properties.[19] Athletes who use shoe-sole repair materials are especially at risk if they do not change shoes often. Athletes who train in lightweight and minimally cushioned shoes (instead of heavier training flats) are also at higher risk of developing plantar fasciitis.

Intrinsic risk factors

Structural risk factors include pes planus, overpronation, pes cavus, leg-length discrepancy, excessive lateral tibial torsion, and excessive femoral anteversion.[18, 20]

Athletes with pes planus (low-arched) or pes cavus (high-arched) feet have increased stress placed on the plantar fascia with foot strike.[19] Pronation is a normal motion during walking and running, providing foot-to-ground surface accommodation and impact absorption by allowing the foot to unlock and become a flexible structure. Overpronation, on the other hand, can lead to increased tension on the plantar fascia.

Leg-length discrepancy, excessive lateral tibial torsion, and excessive femoral anteversion can lead to an alteration of running biomechanics, which may increase plantar fascia stress.

As regards functional risk factors, tightness in the gastrocnemius and soleus muscles and the Achilles tendon is considered a risk factor for plantar fasciitis. Reduced dorsiflexion has been shown to be an important risk factor for this condition.[17] Weakness of the gastrocnemius, soleus, and intrinsic foot muscles is also considered a risk factor for plantar fasciitis.

Aging and heel fat pad atrophy are 2 degenerative risk factors for plantar fasciitis.

PreviousNextEpidemiology

A survey of US professional football, baseball, and basketball team physicians and trainers found that plantar fasciitis was among the 5 most common foot and ankle injuries observed in professional athletes.[21] It is estimated that approximately 1 million patient visits per year are due to plantar fasciitis.[17] Plantar fasciitis accounts for about 10% of runner-related injuries and 11-15% of all foot symptoms requiring professional care. It is thought to occur in 10% of the general population as well. It may present bilaterally in a third of cases.

Age-, sex-, and race-related demographics

The exact incidence and prevalence by age of plantar fasciitis is unknown, but the condition is seen in adults essentially of all ages. A peak incidence may occur in women aged 40-60 years. An increased incidence exists in patients with certain spondyloarthropathies (eg, ankylosing spondylitis), which often present in patients aged 20-40 years.

Women are affected by plantar fasciitis twice as often as men. In young people, the condition occurs equally in both sexes. Race and ethnicity play no role in the incidence of plantar fasciitis.

PreviousNextPrognosis

About 80% of plantar fasciitis cases resolve spontaneously by 12 months; 5% of patients end up undergoing surgery for plantar fascia release because all conservative measures have failed.

For athletes in particular, the slow resolution of plantar fasciitis can be a highly frustrating problem. These individuals should be cautioned not to expect overnight resolution, especially if they have more chronic pain or if they continue their activities.[22] . Generally, the pain resolves with conservative treatment.[22, 23]

Although no mortality is associated with this condition, significant morbidity may occur. Patients may experience progressive plantar pain, leading to limping (antalgic gait) and restriction of activities such as walking and running. In addition, changes in weight-bearing patterns resulting from the foot pain may lead to associated secondary injury to the hip and knee joints.

PreviousNextPatient Education

Patients should be informed that improvement often takes many weeks or months and requires considerable effort to maintain a heel-cord stretching program or to wear a night splint. They should also be taught proper performance of a home exercise program involving stretching the plantar fascia.

The following recommendations are appropriate:

Wear shoes with adequate arch support and cushioned heels; discard old running shoes and wear new ones; rotate work shoes daily Avoid long periods of standingLose weightStretch the plantar fascia and warm up the lower extremity before participating in exerciseFor increased flexibility, stretch the plantar fascia and the calf after exerciseDo not exercise on hard surfacesAvoid walking barefooted on hard surfacesAvoid high-impact sports that require a great deal of jumping (eg, aerobics and volleyball)Apply ice for 20 minutes after repetitive impact-loading activities and at the end of the dayLimit repetitive impact-loading activities such as running to every other day, and consider rest or cross-training for nonrunning days PreviousProceed to Clinical Presentation , Plantar Fasciitis

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Hip Fracture

Background

Although sports injuries to the knee, ankle, and shoulder have been well documented, injuries to the pelvis, hip, and thigh get little attention because of their low prevalence. Unfortunately, severe consequences may result if these injuries are improperly managed.[1, 2, 3]

Femoral neck stress fractures were mainly seen in military recruits due to a triad of activity that is new, strenuous, and highly repetitive. However, as a result of self-imposed fitness regimens of recreational athletes, over the last 20 years the number of these injuries has been increasing in nonmilitary populations. In contrast, contact sports such as football, rugby, and soccer are usually the cause of most fractures of the hip. Stress fractures occur in normal bone undergoing repeated submaximal stress. As the bone attempts to remodel, osteoclastic activity occurs at a greater rate than osteoblastic activity. When these cumulative forces exceed the structural strength of bone, stress fractures occur.[4, 5, 6]

Stress fractures occur mainly at the femoral neck and are classified as either tension (at the superior aspect of the femoral neck) or compression (at the inferior aspect of the femoral neck). See the images below.

A subcapital femoral neck fracture. Slight compression of the femoral head onto the femoral neck can be seen. Note the cortical break medially. This fracture could be missed if not closely evaluated. A view of the contralateral hip for comparison.

Hip fractures are classified as intracapsular, which includes femoral head and neck fractures, or extracapsular, which includes trochanteric, intertrochanteric, and subtrochanteric fractures. The location of the fracture and the amount of angulation and comminution play integral roles in the overall morbidity of the patient, as does the preexisting physical condition of the individual. Fractures of the proximal femur are extremely rare in young athletes and are usually caused by high-energy motor vehicle accidents or significant trauma during athletic activity. Other causes may be an underlying disease process such as Gaucher disease, fibrous dysplasia, or bone cysts.

Identification and initiation of treatment is imperative in attempts to avoid complications, such as avascular necrosis (AVN). AVN is more common in patients in the pediatric and adolescent age groups. This outcome is due to the precarious nature of the blood supply to the subchondral region of the femoral head, which does not stabilize until years after skeletal maturity, after which collateral flow develops.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education article Total Hip Replacement.

NextEpidemiologyFrequencyUnited StatesAn estimated 340,000 hip fractures occur each year. Estimates indicate that in 2040, approximately 500,000 hip fractures will occur. Nine of 10 hip fractures occur in patients aged 65 years and older, and 3 of 4 occur in women.White females have been reported to be twice as likely to fracture their hips than black and Hispanic females. This frequency has been associated with a metropolitan setting, increased caffeine use, alcohol use, sedentary lifestyle, psychotropic drug use, and senile dementia. The rate of fractures is low in adolescent and young athletic populations, estimated to be less than 2% of all hip fractures (one hundredth of adult hip fractures). PreviousNextFunctional Anatomy

The hip is a ball-and-socket joint composed of the acetabulum and the head of the femur. The femoral head is connected to the shaft by the femoral neck. These are supported by a network of trabecular bone.

Two other important landmarks on the proximal femur are the greater and lesser trochanters. These 2 structures are the main muscle attachment sites for the proximal bone. The iliopsoas muscle is connected to the lesser trochanter, and the abductors and short rotator muscles act through their insertion on the greater trochanter. In addition, many additional muscles attach along the intertrochanteric line, and, along with the muscles, they bring with them an abundant and redundant blood supply, which is conducive to healing. This is in contrast to the intercapsular femoral neck, which is prone to healing complications.

The blood supply to the femoral head has been studied extensively and has been found to change substantially during development. Until the cartilaginous growth plate forms a barrier at age 4 years, the major blood supply comes from the medial and lateral circumflex arteries (metaphyseal arteries), which arise from the deep femoral artery. After age 4 years, the posterosuperior and posteroinferior arterial branches of the medial femoral circumflex bypass the growth plate and form the main blood supply to the femoral head. During adolescence, the growth plate fuses and the metaphyseal vessels again become significant, traveling along the femoral neck. Fractures in this area can disrupt this delicate blood supply, leading to AVN, the most severe complication of this fracture.

PreviousNextSport-Specific Biomechanics

The ball-and-socket joint provides most of the inherent stability of the hip joint, while allowing for a large range of motion. Additional stability is provided by the thick capsule and strong ligamentous structures that actually enforce the capsule, namely the iliofemoral, pubofemoral, and ischiofemoral ligaments. These ligaments are taut with internal rotation, which limits motion, and become lax with external rotation.

Motion about the hip occurs in the sagittal, frontal, and transverse planes. During normal gait, motion occurs in all 3 planes, and normal activities occur within the range of 120 º flexion, 20 º extension, 40 º abduction, 25 º adduction, and 45 º external and internal rotation.

The biomechanics of the neck-shaft angle, which averages 135 º and 10-15 º of anteversion, allows for a unique arrangement. This permits angular movements of the thigh to be converted to rotatory hip motion.

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Hip Pointer

Background

A hip pointer is a contusion to the iliac crest, the surrounding soft-tissue structures, or the greater trochanter of the femur. Typically, the injury is caused by a direct blow or fall.[1, 2, 3, 4] Hip pointer injuries occur most commonly in contact sports (eg, football, hockey), but they can also occur in noncontact sports (eg, volleyball) as a result of a fall onto the hip or side. Pain and tenderness in this region can limit an athlete's participation in sports.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education article Repetitive Motion Injuries.

NextEpidemiologyFrequencyUnited States

No specific statistics for the frequency of hip pointer injuries are available; however, hip injuries generally comprise 5-9% of high school athletic injuries.[1, 2, 3, 5]

PreviousNextFunctional Anatomy

The anterior iliac crest region of the hip and the greater trochanter of the femur have a minimal amount of overlying fatty tissue or muscle and are more susceptible to contusion and injury than more protected regions of the body.

The iliac crest has multiple muscle origins and insertions, including the sartorius, the tensor fascia lata, the internal and external obliques, and a portion of the rectus femoris muscle.

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Chronic Exertional Compartment Syndrome

Background

Chronic exertional compartment syndrome (CECS) is a condition in athletes that can occur from repetitive loading or exertional activities. CECS is usually observed in competitive or collegiate athletes; long-distance runners, basketball players, skiers, and soccer players. Although it is most common in the lower legs, CECS can occur in any compartment of the extremities; for example, it has been described in the forearms of motocross racers and other athletes.[1, 2, 3]

CECS is characterized by exercise-induced pain that is relieved by rest. In some cases, weakness and paresthesia may accompany the pain. Onset of symptoms typically occurs at a specific exercise distance or time interval or intensity level (eg, within 15 min of initiating a run). Symptoms tend to subside with rest and are minimal during normal daily activities but return when activity is resumed.

Unlike acute compartment syndrome, which usually results from trauma, the pathophysiology of CECS is not well understood. CECS may result from ischemic changes within the compartment; however, multiple theories and mechanisms have been suggested (see Pathophysiology and Etiology).

Although physicians have been aware of CECS symptoms since the early part of the 20th century, it was not until the late 1950s that the first reports on CECS were documented. Mavor was the first to describe the entity in 1956 in a patient who experienced recurrent anterior leg pain with exertion that was associated with herniation of the muscle and numbness of the affected extremity.[4] In 1975, Reneman defined the clinical manifestations of CECS and identified increased intracompartmental pressure as the cause.

CECS was initially thought to be a form of shin splints (anterior tibial enthesitis).[5, 6] However, with the advent of the fitness boom and the increased popularity of endurance sports, additional research on exercise-induced leg pain has demonstrated that CECS is a well-defined clinical entity.

The literature is somewhat confusing because of the interchangeable use of the terms acute, subacute, chronic, and recurrent compartment syndrome; crush syndrome; and Volkmann ischemic contracture. Compartment syndrome is a condition in which increased tissue pressure within a closed osteofascial compartment compromises blood flow to the muscles and nerves within that compartment, resulting in the potential for tissue and nerve damage (acute compartment syndrome), as well as in symptoms/disability (CECS).

Crush syndrome is distinct from compartment syndrome and occurs when primary muscle necrosis initiates the cycle of events that may lead to an acute compartment syndrome. Volkmann ischemic contracture is a sequela of untreated or inadequately treated compartment syndrome, in which necrotic muscle and nerve tissue have been replaced with fibrous tissue.

Compartment pressure readings with and without exercise are the gold standard for the diagnosis of CECS (see Workup). A trial of conservative treatment may be undertaken for CECS, but symptoms generally recur when the patient returns to exercise.[7] If conservative treatment is unsuccessful, the patient should be referred to an orthopedic surgeon for consideration of fasciotomy (see Treatment).

For patient education information, see the Sports Injury Center.

NextAnatomy

A firm grasp of lower extremity anatomy is central to understanding the pathophysiology, diagnosis, and treatment of CECS. The lower leg is divided into 4 compartments: anterior, lateral, superficial posterior, and deep posterior. A fifth compartment, the tibialis posterior, has been documented, but its clinical significance has yet to be established.

The anterior compartment consists of the tibialis anterior, extensor digitorum longus, extensor hallucis longus, and peroneus tertius. The borders of this compartment are the tibia, fibula, interosseous membrane, and anterior intermuscular septum. Typically, the anterior compartment of the leg is the most frequently affected compartment in cases of CECS.

The lateral compartment includes the peroneus longus and brevis. Within the compartment lie the common peroneal nerve and its superficial and deep branches. This compartment is bordered by the anterior intermuscular septum, the fibula, the posterior intermuscular septum, and the deep fascia.

The superficial posterior compartment is surrounded by the deep fascia of the leg and contains the gastrocnemius, soleus, and plantaris.

The deep posterior compartment lies between the tibia, fibula, deep transverse fascia, and interosseous membrane. The muscles within the deep posterior compartment are the flexor digitorum longus, flexor hallucis longus, popliteus, and tibialis posterior. Also within this compartment lie the posterior tibial artery and vein and the tibial nerve.

The tibialis posterior compartment (a subdivision of the deep posterior compartment) is more recently described. It consists of the tibialis posterior, which has recently been shown to have its own fascial layer.

PreviousNextPathophysiology

The pathology of CECS is not well established and is still debated; a general discussion follows.

CECS is associated with increased pressure in muscles at rest. Transient increases in compartmental pressure have been demonstrated experimentally as a normal response to exercise. Repetitive muscle contraction alone can increase intramuscular pressure to levels that may cause transient ischemia.

Elevated pressures usually normalize within 5 minutes after cessation of exercise. In CECS, however, the pressure between successive contractions remains high and impedes blood flow. As the pressure rises, arterial flow during muscle relaxation decreases, and the patient experiences muscle cramping.[8] Pressures may remain elevated for 30 minutes or longer in persons with CECS.

Tissue perfusion is proportional to the difference between the capillary perfusion pressure (CPP) and the interstitial fluid pressure. This is also stated by the following formula:

LBF = (PA - PV)/R

In the formula above, LBF is local blood flow, PA is local arterial pressure, PV is venous pressure, and R is local vascular resistance.

Normal myocyte metabolism requires a 5-7 mm Hg oxygen tension, which can readily be obtained with a CPP of 25 mm Hg and an interstitial tissue pressure of 4-6 mm Hg.[9]

When fluid is introduced into a fixed-volume compartment, tissue pressure increases and venous pressure rises. When the interstitial pressure exceeds the CPP (a narrowed arteriovenous [AV] perfusion gradient), capillary collapse and muscle and tissue ischemia occur.

With myocyte necrosis, myofibrillar proteins decompose into osmotically active particles that attract water from arterial blood. One milliosmole (mOsm) is estimated to exert a pressure of 19.5 mm Hg; therefore, a relatively small increase in osmotically active particles in a closed compartment attracts sufficient fluid to cause a further rise in intramuscular pressure.

When tissue blood flow is diminished further, muscle ischemia and subsequent cell edema worsen. This vicious cycle of worsening tissue perfusion continues to propagate. Changes in local vascular resistance (autoregulation) can compensate for some reduction in the local AV gradient. However, compartment tamponade occurs as arterial blood flow is occluded.

Shrier and Magder questioned this traditional hypothesis for the pathophysiology of CS and postulated that a critical closing pressure exists within muscle compartments (similar to West zone II in lung physiology).[10] These authors showed that the increase in this critical closing pressure, which they called Pcrit, rather than an increase in arterial resistance, results in decreased blood flow.

The transmural pressure at which blood flow ceases depends on adrenergic tone as well as the interstitial pressure; the pressure at which this occurs is still under debate. However, in general, compartmental pressures that exceed 30 mm Hg and persist for 6-10 hours result in muscle infarction, tissue necrosis, and nerve injury. For unclear reasons, compartment syndrome that is associated with surgical positioning may manifest later, with a mean time to presentation of 15-24 hours or longer postoperatively.[11, 12]

Pressure-induced functional deficits are likely due to decreased tissue perfusion rather than a direct mechanical effect. Therefore, the amount of pressure a limb can tolerate depends on limb elevation, blood pressure, hemorrhage, and arterial occlusion.

In addition to local morbidity caused by muscle necrosis and tissue ischemia, cellular destruction and alterations in muscle cell membranes lead to the release of myoglobin into the circulation. This circulating myoglobin results in renal injury. Advanced compartment syndrome may result in rhabdomyolysis (acute compartment syndrome); conversely, rhabdomyolysis may result in compartment syndrome.[13, 14]

PreviousNextEtiology

CECS usually results from repetitive microtrauma (overexertion). It is typically observed in long-distance runners, basketball players, skiers, and soccer players.

The pain in CECS has been thought to derive from the same pathologic processes that cause pain in acute compartment syndrome—that is, compromise of the vascular supply, which leads to myoneural ischemia.

Various mechanisms have been suggested as to the cause of this tissue ischemia, including arterial spasm, capillary obstruction, arteriovenous collapse, or venous outflow obstruction. However, a magnetic resonance imaging (MRI) study conducted by Amendola et al showed that significant tissue ischemia does not develop.[15]

Other theories suggest that muscle hypertrophy and/or fascial inflexibility is the origin of pain in patients with this CECS. However, not all athletes with muscle hypertrophy develop compartment syndrome.

Another theory, the mechanical damage theory, posits that exercise results in myofibril damage and release of protein-bound ions. Frequent damage, such as that occurring in the anterior compartment of runners, results in an increased release of ions, increased osmotic pressure, and decreased blood flow within the compartment.

Despite these various explanations for the cause of pain in CECS, no single theory has been overwhelmingly accepted. Further investigation is needed, including that regarding the relationship between pain and compartment metabolites.

PreviousNextEpidemiology

The true prevalence of CECS is uncertain. One United States study found a 14% prevalence rate of anterior CECS in individuals who reported lower leg pain.

Males and females are affected equally, although Kaper et al have suggested that women may be more susceptible than men to lower leg CECS.[16]

CECS usually occurs in well-conditioned athletes younger than 40 years. Athletes with CECS who markedly increase their training are at risk of developing exacerbation of this condition, as are inactive individuals who initiate rigorous training.

PreviousNextPrognosis

Surgical intervention generally has good success in patients with CECS, with success defined as the return to athletics without significant symptoms. For unknown reasons, the deep posterior compartment does not respond as quickly or as well to fasciotomy as the anterior compartment. In the anterior compartment of the leg, success rates usually exceed 85%. In the deep posterior compartment, success rates are approximately 70%.

In a study by Awbrey, 44 of 46 patients undergoing compartment release for lower leg CECS had excellent pain relief and unimpaired running at 1- and 9-year follow-up.[17]

The majority of complications can be attributed to surgical intervention or misdiagnosis. Complication rates of surgery have been reported in the 11-13% range; complications include hemorrhage, wound breakdown, complications from anesthesia, and postoperative infection.

In addition, surgical patients may experience persistent or CECS, Volkmann contracture, and permanent disability. Persistent pain with activity may result from incomplete or incorrect decompression of a muscle compartment. Recurrent CECS is thought to be related to severe scarring and subsequent closing of the compartment release. Mortality may result from renal failure or sepsis from difficult wound management.

PreviousProceed to Clinical Presentation , Chronic Exertional Compartment Syndrome

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MRSA Skin Infection in Athletes

Overview

Nosocomial infections of methicillin-resistant Staphylococcus aureus (MRSA) (ie, hospital-acquired MRSA [HA-MRSA]) have been reported since 1963.[1] Community-acquired MRSA (CA-MRSA) infections are a more recent variant and are becoming more common in athletes[2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14] and active individuals since the first reported cases in a high school wrestling team in 1993[15] and a British rugby club in 1998.[16] CA-MRSA differs from HA-MRSA in its genetic makeup, increased pathogenicity, and susceptibility to antibiotic treatment.[17, 18, 19]

The resistance of MRSA to beta-lactam antibiotics is due to the presence of the mecA gene sequence. The mecA gene produces transpeptidase PBP2a (penicillin-binding peptide) that decreases the bacterial affinity of the beta-lactam antibiotics. The mecA gene is a subset of a larger SCCmec gene that is responsible for the differences seen in HA-MRSA and CA-MRSA bacteria.[18, 20]

Several variations of the SCCmec gene have been sequenced; SCCmec gene types I, II, and III are found in HA-MRSA, whereas CA-MRSA bacteria have the SCCmec type IV gene.[21] The SCCmec gene types I-III are larger genes, and other portions of the gene provide resistance factors against other antibiotic classes. The type IV SCCmec gene is a small gene that has fewer of these additional resistance factors. This difference may explain the continued susceptibility of CA-MRSA compared with HA-MRSA to some oral antibiotics such as trimethoprim-sulfamethoxazole.

For excellent patient education resources, visit eMedicineHealth's Infections Center. Also, see eMedicineHealth's patient education articles MRSA Infection, Sepsis (Blood Infection), Life-Threatening Skin Rashes, and Antibiotics.

NextVirulence

CA-MRSA has been found in some cases to be a more virulent form compared with HA-MRSA. Up to 70% of CA-MRSA strains contain the Panton-Valentine leukocidin (PVL) virulence factor, including the most common form of CA-MRSA isolated from outbreaks in the United States.[22]

PreviousNextPrevalenceMRSA colonization

Studies have shown that approximately 25-30% of the population is colonized with methicillin-sensitive S aureus bacteria. Colonization is usually on the skin or in the nasal passages. One study demonstrated a 3% rate of MRSA nasal colonization in adult patients visiting an outpatient clinic for unrelated medical appointments.[23] A similar study in an outpatient pediatric population detected MRSA colonization rates slightly above 1%.[24]

CA-MRSA infections in the general population

A prospective study in an Oakland, California, emergency department found that 51% of patients with a skin infection who presented for evaluation and treatment had positive culture results for MRSA; 99% of the MRSA infections contained the type IV SCCmec gene that is associated with the CA-MRSA strain, and 94% of MRSA isolates also contained the PVL gene.[25]

CA-MRSA outbreaks in athletes and other populations

Most publicized reports of CA-MRSA infection have been in college or professional football teams.[2, 3, 4, 5, 6, 7] However, outbreaks have also been reported in other sports, such as wrestling, rugby, and fencing. In a study of all Nebraska high schools between 2006 and 2008, Buss et al determined that among the schools that responded, MRSA infections rose from 4.4% in school year 2006-2007 to 14.4% in 2007-2008; the incidence per 10,000 wrestlers rose 3-fold from 19.6 to 60.1 and that per 10,000 football players increased 5-fold from 5.0 to 25.1.[10]

Other populations at risk for CA-MRSA outbreaks include military recruits, children in day care, prison inmates, homosexual men, injection drug users, and veterinarians, particularly those who have contact with farm animals, notably pigs.[5, 26, 27]

PreviousNextClinical Presentation

Most CA-MRSA infections initially manifest as folliculitis or a similar soft-tissue or skin infection. Typically, the athlete may describe his or her presentation as an "infected pimple" or "insect bite." Some CA-MRSA infections may have progressed to abscess formation. In other cases, the infection may manifest as a life-threatening illness, such as a rapidly progressing sepsis or pneumonia.

The initial clinical examination usually reveals a limited area of redness, warmth, and swelling that is consistent with folliculitis. Occasionally, the patient may have swelling and pain in a joint. In more advanced cases, moderate to severe pain at the site of the infection may be reported; the pain may be due to soft-tissue necrosis from PVL activity.

Transmission

In severe cases of CA-MRSA infection, endocarditis, septicemia, necrotizing fasciitis, osteomyelitis, and multisystem organ failure, or death due to overwhelming sepsis may occur. Severe cases may progress extremely rapidly from the initial manifestation of an abscess.

The most common route of transmission of CA-MRSA is though an open wound, such as a superficial abrasion, or from contact with a CA-MRSA carrier. Other methods of transmission include poor hand washing, poor personal hygiene (eg, not showering after workouts), sharing personal items (eg, razors, towels, clothing), or a failure to properly clean and disinfect exercise and training equipment.

PreviousNextTreatment & ManagementOutpatient treatment

The primary method of treatment for CA-MRSA skin and soft-tissue infections includes incision and drainage (I&D) of the abscess and therapy with appropriate antibiotics when indicated. Wound exudates should be cultured to accurately determine the causative organism and appropriate antibiotics for therapy.

The susceptibility of CA-MRSA is dependent on local resistance rates (US Centers for Disease Control and Prevention guidelines [see Antibiotic/Antimicrobial Resistance: Clinical Guidelines and CDC Surveillance Systems and Published Data, as well as Diseases Connected to Antibiotic Resistance: Methicillin-Resistant Staphylococcus aureus (MRSA)]). Typical treatment choices include oral antibiotics.

Oral antibiotics Trimethoprim-sulfamethoxazole (Bactrim DS; available as generic) twice daily, with or without rifampin, at 600 mg/d. Note: Rifampin is not a first-line drug for CA-MRSA, but this agent may be used in conjunction with other antibiotics for infections that do not respond to the initial treatment or for patients who experience recurrent infections. Doxycycline at 100 mg twice dailyClindamycin at 450 mg 3 times a day (96% sensitive): Resistance to clindamycin is increasing because of the inducible macrolide-lincosamide-streptogramin B (iMLSb) phenotype, which may result in cross-resistance to clindamycin. TetracyclineMinocyclineNot recommended due to resistance Ciprofloxacin: This drug has a 33% sensitivity in some areas. Ciprofloxacin is not a good choice in pediatric patients because of concerns about its effect on growth plates. Cephalexin (Keflex; MiddleBrook Pharmaceuticals, Inc, Germantown, Md)Not recommended due to poor oral absorption Oral vancomycinLength of treatment

There are no well-controlled studies that demonstrate an optimal length of antibiotic treatment for CA-MRSA.

Inpatient treatment

Treatment of moderate to severe CA-MRSA infections may require surgical debridement of the abscess, intravenous antibiotics, and hospitalization. The need for hospitalization should be made on a case-by-case basis.

Intravenous antibiotics Vancomycin: Note that reports have described some intermediate vancomycin susceptibility in Japan, Texas, and New York.Some studies also indicate vancomycin treatment failure with MRSA bacteremia is associated with high mortality rates (1) when this agent is initiated after an inappropriate empiric antibiotic was used and (2) when vancomycin itself is the empiric agent in cases when the infective strain had a high vancomycin minimum inhibitory concentration (MIC).[28, 29] Another study demonstrated previous antibiotic exposure is itself a risk for MRSA isolation.[30] Linezolid at 600 mg twice daily: The FDA warns against the concurrent use of linezolid with serotonergic psychiatric drugs, unless indicated for life-threatening or urgent conditions. Linezolid may increase serotonin CNS levels as a result of MAO-A inhibition, increasing the risk of serotonin syndrome.[31] Daptomycin at 4 mg/kg/dQuinupristin-dalfopristin at 7.5 mg/kg every 8-12 hoursInvestigational antibiotics

There are 2 anti-CA-MRSA beta-lactams, ceftaroline (cephalosporin) and ME1036 (carbapenem), that are under investigation. A preliminary study of susceptibility testing indicated that ceftaroline was 64-fold more potent than ceftriaxone, whereas ME1036 was >128-fold more potent than ceftriaxone.[32] All isolates had the PVL genes and type IV SCCmec, and 67.8% showed the USA300-0114 strain, cloned via pulsed field gel electrophoresis (PFGE).

Another agent that is under study and that may hold potential for the prevention of catheter-associated infections, particularly against MRSA, is omiganan pentahydrochloride, a novel topical cationic peptide.[33]

Recurrent infections

If an athlete has recurrent MRSA infections, suspect resistance to the previous antibiotic or nasal colonization, and send a nasal swab for culture. A different antibiotic may also be prescribed if the practitioner is concerned about a poor response to treatment. If the nasal swab culture is positive for CA-MRSA, then treat with mupirocin antibiotic ointment (Bactroban; GlaxoSmithKline, Research Triangle Park, NC) twice a day applied to the nares and oral rifampin at 300 mg twice daily for 7 days.

PreviousNextPrevention

Several key methods can be used for prevention of the spread of CA-MRSA infections.[34] Because the most common source of infection is from close contact or from an open wound, preventive measures should focus on proper hygiene. Hand washing, using soap and water or antibacterial hand gels, should be encouraged by the infected patient and by individuals who come in direct contact with the patient. Additionally, open wounds and abrasions should be covered and protected.

Athletes should be educated and instructed to not share personal hygiene products such as razors or towels. Medical and training staff should continue to practice universal infectious disease protection measures. These personnel should ensure the proper disposal of bandages after dressing changes and the routine cleaning of equipment such as training tables, whirlpools, and exercise mats.

PreviousNextReturn to Play

Athletes with mild cases of CA-MRSA infections may be allowed to return to athletic participation once an appropriate antibiotic treatment has commenced and the risk of transmission to other athletes has been significantly reduced or eliminated. Abrasions should be covered with a protective covering, and the athlete should be reevaluated daily for signs or symptoms of recurrence or worsening of the infection. The athlete and teammates should also be counseled about the need to avoid sharing towels, razors, or other personal items. Training staff should ensure proper disinfection of equipment and surfaces with which the infected athlete may come in contact, such as training tables, protective equipment, or wrestling mats, among other items.

Previous, MRSA Skin Infection in Athletes

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