Abstract
Overuse and traumatic distal lower extremity conditions are common among physically active individuals, and the incidence rate is an order of magnitude greater than that reported in the general population. With frequent impact and heavy load-bearing activity, military servicemembers have unique occupational demands that may further exacerbate inherent risks of leg, ankle, and foot injuries. A thorough endocrine, nutritional, and multisystem clinical work-up is warranted to evaluate certain overuse conditions. Furthermore, mechanical alignment and soft tissue integrity should always be scrutinized when considering a range of nonoperative or surgical treatment options. Modifications in training regimen, the use of external restraints or orthotics, and physical therapy with targeted neuromuscular, strength, and/or gait interventions may be effective preventative measures in selected patients with distal lower extremity injuries.
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Keywords
Lower Leg
Tibial Stress Fracture
Introduction
Stress fractures and the broader spectrum of stress-related injuries occur on a continuum in response to overuse activity. With repetitive impact and loading forces, these injuries arise from cumulative microtrauma that results in mechanical compromise with eventual fatigue-related failure. While also occurring in the midfoot, metatarsals, femur, pelvis, and vertebrae, the tibial stress fracture is most common, particularly among active cohorts [1].
When evaluating stress-related conditions of the tibia, two discreet entities should be considered. Medial tibial stress syndrome (MTSS), or “shin splint syndrome,” is a broad-based stress-related injury of unclear etiology involving the posteromedial tibial shaft. Proposed theories identify periosteal traction at sites of muscular attachment and deformation with mechanical bending as potential contributors to its development, although a complex interplay of biomechanical, biological, and morphological factors are likely present. Alternatively, true tibial stress fractures are less common but higher risk. These fractures develop at the anterior tibial cortex in response to continuous tensile loads and may manifest radiographically with a “dreaded black line” and thickened anterior cortex in a chronic situation (Figs. 11.1–11.3).
Tibia stress fracture. (Note: dreaded black line)
Bone scan with focal uptake of tibia stress fracture
Tibia stress fracture status post intramedullary nail at 6 months
Epidemiology
With a reported incidence of 0.5 %, tibial stress fractures can be found among a well-defined, broad demographic population [2]. More classically, distance runners and military recruits have sustained higher rates of stress injuries, particularly those involving the tibia [3–5]. However, these injuries are not specific to these cohorts as tibial stress fractures have been described in a variety of sports such as ballet, volleyball, rowing, basketball, and gymnastics [6].
Among military populations, tibial stress injuries typically occur in untrained service members undergoing repetitive, intense physical activity and/or training programs for combat readiness, such as in basic training or advanced specialized military courses. Several studies have demonstrated that 1–31 % [4, 7] of military recruits will incur a stress fracture, while up to 53 % may experience MTSS [8]. Cosman et al. demonstrated that the cumulative 4-year incidence of single-stress fractures among US Military Academy (USMA) cadets was 5.7 % for males and 19.1 % for females, with approximately 50 % of injuries occurring within the first 3 months of enrollment [9]. Among the broader US Armed Forces, Lee and colleagues [10] determined that the mean annual incidence rate of tibial stress fractures was 3.24 per 1000 person-years between 2004 and 2010. In the largest sample of US Army recruits, the incidence rate of tibial stress fractures was 19.3 and 79.9 cases per 1000 male and female recruits, respectively [5]. In addition to the medical burden of injury, the financial repercussions of stress fractures is not negligible, with the estimated cost approximately US$34,000 per US service member [11].
Many factors may contribute to the development of a tibial stress fracture. These are typically separated into intrinsic and extrinsic risk factors. However, more recently, the medical and public health community has been increasingly focused on the identification of modifiable risk factors as a means to improve injury prevention. Intrinsic factors for tibial stress fractures, including female sex, white race, older age, increased bone turnover, anatomic malalignment, and decreased tissue or bone vascularity have been identified and are largely non-modifiable. General physical fitness, muscle endurance, bone density, steroid or tobacco use, excessive alcohol consumption, and hormonal deficiencies are among the intrinsic factors that may be alternatively considered modifiable variables. Extrinsic factors include training regimen, dietary or nutritional profile, footwear, and training surface, and these factors may also be considered as targets for intervention and risk mitigation [12, 13].
Female sex is among the more notable risk factors associated with stress fractures, particularly within the military, in general, where they are at up to a 2- to 12-fold greater risk of stress injury than males [14–21]. While classically associated with the female athlete triad (i.e., eating disorders, functional hypothalamic amenorrhea, and osteoporosis), stress fractures can arise as a result of a multitude of factors. Known risk factors include underlying differences in bone geometry (e.g., smaller and more narrow tibia) and microarchitecture (e.g., decreased bone mineral density, greater trabecular volume), altered hormonal regulation, nutritional deficiencies, reduced muscle mass, and diminished physical fitness [20]. Given communal training within the military setting, lower levels of physical fitness among women lead to greater comparative physical effort, earlier fatigue, and altered gait or running mechanics, which could further exacerbate the risk of overuse injuries in the lower extremity [14, 22].
Training regimens, primarily dramatic increases in vigorous impact and running activity, contribute significantly to the development of tibial stress injuries. As a result, the study among military cadets and recruits during basic training is ideal and has helped develop the existent body of literature. In contradistinction to athletics where physical activity is more consistent throughout adolescence and adulthood, military enlistment is often preceded by a period of sedentary lifestyle or decreased general fitness, which may heighten secondary risk of stress fracture. Cosman and colleagues [9] demonstrated that cadets at USMA were at a twofold greater risk of stress injury when they had exercised less than 7 h per week in the year prior to matriculation. Furthermore, the rate, duration, and intensity of military training (e.g., marching, running) have been associated with rates of tibial stress fracture [10]. Consequently, redesigned training programs with decreased cumulative exposure, implementation of minimum sleep requirements, and greater emphasis on agility exercises and cross-training have been successful at mitigating the rates of tibial stress fracture without compromising unit readiness [10, 23, 24].
While there have been several attempts at preventative treatment, few measures have led to a decrease in rates of tibial stress injury. Adjusted training schedules and individualized risk stratification have been most successful in injury reduction [10, 25]. There is also limited evidence that suggests a relative risk reduction with the use of shock-absorbing insoles when compared with controls. However, the optimal insole design and shoe wear modifications are undetermined. Calcium and vitamin D supplementation have been widely promoted for the prevention of fragility fractures, and recent evidence certainly supports its use within a military population at risk for tibial stress fractures, particularly when deficiencies or other risk factors exist [26]. Conversely, pre-exercise stretching and medial arch supports for excessive pronation have not been found to demonstrate a protective effect from stress-related fracture [27].
Chronic Exertional Compartment Syndrome
Introduction
Chronic exertional compartment syndrome (CECS), or exercise-induced compartment syndrome, is a common source of lower extremity disability among active patients. First described by Mavor in 1956, CECS has historically referred to involvement of the leg, although cases affecting the shoulder, upper arm, forearm, hand, gluteus, thigh, and foot have also been described [28].
As with other overuse conditions of the lower extremity, the pathophysiology of CECS is only partially understood. During normal exercise, the muscle volume increases by up to 20 % or up to 20-fold greater than its resting size, with pressures exceeding 500 mmHg [29]. In response to increased metabolic demands, blood perfusion rises in turn with accumulation of interstitial fluid. However, when this is coupled with chronic fascial thickening, limited tissue compliance [30], diminished capillary density [31], and/or elevated baseline intracompartmental pressures, patients with CECS are unable to accommodate exercise-related changes and experience symptoms as a result of relative tissue ischemia and nerve compression [32]. In response to these changes, patients complain of pain and neurovascular symptoms, which often precipitate early cessation of athletic activity and military training. Alternatively, acute compartment syndrome represents a surgical emergency where tissue ischemia occurs following a traumatic injury or other underlying systemic process, and this should not be confused with CECS.
Epidemiology
CECS occurs most commonly in avid runners, military recruits, and competitive athletes involved in sports such as basketball, soccer, and football. The prevalence of CECS varies widely, with reported rates ranging from 10 to 60 % in selected cohorts [33–35]. In a recent evaluation of US military service members over a 6-year time period, the incidence rate of CECS was approximately 0.5 per 1000 person-years [36]. However, given the systematic underreporting coupled with inconsistent diagnostic criteria and specificity, the comprehensive burden of CECS is unknown within the military setting .
Traditionally, CECS has been described among young, active male athletes and military recruits, and the preponderance of cases occur among this demographic [36, 37]. However, limited research may suggest disparate epidemiological trends among patients with CECS, particularly among nontraditional cohorts recently exposed to the rigorous physical demands of the military. As military enlistments and athletic involvement have both continued to increase among females, there has been greater parity in at-risk exposure between males and females. Recent studies demonstrate increased risk among females including one study in US military service members [31, 36]. By contrast, multiple earlier studies suggest no difference in the incidence among men and women [30, 33, 37]. When evaluating by age, Waterman and colleagues [38] also showed a positive association between increased age and the incidence rate of CECS, with patients over 40 years demonstrating a nearly ninefold greater rate of CECS versus those under 20.
Non-commissioned service members, primarily those of junior rank and Army service, showed the highest rates of CECS. This likely reflects the unique physical demands of the junior enlisted service members, often serving in ground military forces with frequent exposure to organized physical fitness training, dismounted field activity, and prolonged marching with a combat load. Overtraining has been implicated, and junior service members may be less able to moderate these intense occupational demands to accommodate physical limitations arising from CECS [38, 39].
In addition to demographic variables, several modifiable factors may also serve as targets for intervention. Abnormal gait patterns and/or prolonged muscular contraction during aerobic exercise may exacerbate the underlying pathophysiology of CECS, by limiting peripheral vascular perfusion during muscle relaxation and increasing intracompartmental pressures. Additionally, repetitive eccentric exercise may diminish fascial compliance with continued exposure, as occurs with the anterior compartment during running [40]. As a result, newer literature has investigated the role of running technique, specifically a forefoot contact pattern, in reducing intracompartmental pressures and mitigating the symptoms related to CECS [41, 42]. In an evaluation of a 6-week forefoot training program for cadets with CECS at USMA, Diebal and colleagues [43] demonstrated significant reductions in anterior compartment pressures (78.4 +/− 32 vs. 32 +/− 11.5 mmHg) and vertical ground-reaction forces, while improving running distance, speed, exertional pain, and patient-reported outcome measures at up to a year after intervention. Furthermore, all patients avoided surgery and remained on active duty without physical activity restrictions. Creatine and anabolic steroid use can also lead to increased intramuscular fluid volume and hypertrophy, thus diminishing potential space for normal volume expansion and increasing intracompartmental pressures with exercise activity .
While certain anatomic features mentioned previously have been associated with the development of CECS, the role of fascial defects of the leg remains uncertain. Between 10 and 60 % of patients presenting for treatment of CECS also had clinically evident fascial defects [39], compared with less than 5 % among asymptomatic individuals [28]. While only 1–2 cm2 in size, this fascial defect may serve as a site for adjacent superficial peroneal nerve entrapment when localized to the anterolateral intermuscular septum. With continued exercise, muscle and neurovascular herniation may occur, leading to further, localized inflammation and/or micro-ischemia. Further studies are required to better elucidate the underlying contribution of these fascial defects, as well as the underpinnings of disrupted arteriolar homeostasis thought to be central to the development of CECS [28].
Ankle
Ankle Sprain
Introduction
The so-called ankle sprains can often collectively represent a spectrum of traumatic soft tissue injuries about the ankle and hindfoot, but the diagnosis classically denotes ligamentous instability about the tibiotalar joint with varying degrees of severity [44]. Traditionally, ankle instability comprises three discreet categories of injury, including lateral, medial, and syndesmotic ankle sprain. However, combined ligamentous involvement and other associated injuries, particularly those involving the chondral surface of the talar dome and peroneal tendons, are common. Sprains involving the lateral ligament complex, including the anterior talofibular ligament, calcaneofibular ligament, and posterior talofibular ligament, account for at least 85 % of all ankle sprains [45] (Figs. 11.4 and 11.5). Conversely, syndesmotic, or “high ankle sprains,” and medial ankle sprains are diagnosed in only approximately 10–15 % of patients with ankle sprains, and the epidemiological literature is fairly limited [46]. The focus of the current review will further elaborate largely on lateral ankle instability.
Axial T2 MRI—anterior talofibular ligament (ATFL) disruption
Coronal T2 MRI—CFL disruption
Epidemiology
In active , athletic populations, ankle sprains account for up to 30 % of single-sport injuries. Nearly 1.2 million ankle-sprain-related health-care visits occur per year, with an estimated cost of up to US$3.8 million for both treatment and rehabilitation [47, 48]. The incidence rates of ankle sprain may vary , with between 2 and 7 individuals per 1000 in the general population injured per year [49–51]. However, the risk of ankle sprain is an order of magnitude greater in military cohorts, with reported incidence rates ranging from 35 to 58.4 per 1000 person-years in previous studies [46]. Among military personnel, paratroopers are at a particularly elevated risk. Lillywhite [52] identified that between 0.6 and 1.2 % of Royal Army paratroopers sustained ankle injuries per year, with increases up to 7.9 % on mass descents. Further studies have shown that ankle sprain accounts for 9–33 % of parachute-related injuries and have an incidence rate between 1 and 4.5 per 1000 jumps [53, 54].
To better understand and anticipate the epidemiology of this injury, several authors have sought to identify modifiable risk factors associated with lateral ankle sprain [46, 55–57] (Table 11.1). Non-modifiable risk factors can be useful in identifying high-risk populations for injury prevention, while modifiable risk factors such as body mass index (BMI), proprioception or postural stability, and the absence of external restraints to inversion (e.g., prophylactic bracing) can be the targets for intervention [57]. Within the context of this framework, several risk factors for ankle sprain will be discussed.
Non-modifiable Risk Factors
Gender
With the increasing popularity and involvement of female athletes in sports, gender-related studies of musculoskeletal injury have become important in determining potential health disparities. The underpinnings of these gender-based discrepancies are likely multifactorial, with several postulated associations including inherent hormonal differences, lower extremity anatomy, limb alignment, ligamentous laxity, neuromuscular control, and the extent and type of athletic exposure [57, 58].
Gender studies on ankle sprain incidence, however, have yielded mixed results. A study of military cadets showed incidence rates (IR) of ankle sprain as 96.4 and 52.7 per 1000 person-years for women and men, respectively (incidence rate ratio (IRR) of 1.83 (95 % confidence interval (CI) 1.52–2.20)), while no differences were detected between the male and female intercollegiate athletes [51]. In a separate study of collegiate athletes, Beynnon et al. showed IRs of 1.6 and 2.2 per 1000 person-days for men and women, respectively, although the difference was not statistically significant [59]. Hosea et al. subsequently found that while female athletes had a 25 % greater risk of sustaining a grade I ankle sprain compared with their male counterparts in both high school and intercollegiate basketball, there was no significant difference in the risk for the more severe ankle sprains [60].
Further studies in the general population of the USA show no overall differences by gender, although male individuals between the ages of 15 and 24 and female individuals over the age of 30 had higher rates of ankle sprain than their opposite sex counterparts [51]. A population-based study of active duty military personnel revealed that female service members experienced an incidence rate that was 21 % higher than that of male service members [46]. Based on the available literature, gender appears to be associated with risk of ankle sprain, although additional factors such as exposure to and level of at-risk activity may directly influence this complex relationship.
Age
Younger age, particularly when associated with increased exposure to at-risk activity, is also associated with the risk of ankle sprain. Studies of the general population of the USA [46] and Denmark [50] yielded a mean and median patient age of 26.2 and 24.4, respectively. A recent population-based study within an active duty military population reported the highest incidence rates for ankle sprain in the group of those under 20 years old for both male and female subjects, and rates generally declined with increasing age [57]. These studies suggest that peak incidence rates for ankle sprain occur during the second decade of life, with male and female peak incidence rates occurring between the ages of 15 and 19 and 10 and 14, respectively [49, 51].
The mechanism of injury for ankle sprain also varies by age, with a greater preponderance of injuries occurring during recreational or competitive sports in young, active populations [46]. Patients under 25 years of age were more likely to sustain ankle sprains while engaging in athletics and physical activity, while patients over 50 were more likely to incur ankle sprain in their own homes or during activities of daily living [50].
Previous Ankle Sprain
Ankle sprain produces damage to ligaments that maintain the stability of the ankle joint, thereby creating potential functional limitations. Some of this damage, such as that resulting in proprioceptive or neuromuscular impairment, is modifiable through exercise. However, the initial inflammatory response following injury can also lead to scar tissue formation, which is more likely than normal tissues to fail due to a 60 % reduction in energy-absorbing capacity [61].
Functional instability and increased risk of reinjury may still occur after primary ankle sprain in athletes and military recruits undergoing basic training even if the primary sprain is on the less severe end of the injury spectrum [62–65]. A recent study on track and field athletes and rates of reinjury within 24 months demonstrated that athletes with a grade I or II lateral ankle sprain were at higher risk of reinjury (14 and 29 %, respectively) than high-grade acute lateral ankle sprains (5.6 %) [65]. However, this may also be related to inadequate rehabilitation of less severe injuries and earlier perceived healing despite persistent proprioceptive impairment, which ultimately increases further risk of recurrence .
Modifiable Risk Factors
Weight and BMI
With increasing weight and BMI , an increasing mass moment of inertia acts about the ankle, potentially increasing the risk of ankle sprain. In a study on high school football players, Tyler et al. [66] showed that the incidence of ankle sprain was significantly increased in patients with BMI categorized as above normal or overweight when compared to players with a normal BMI. Waterman et al. [46] reported similar findings in military cadets with ankle sprains who had higher mean weight and BMI than their uninjured counterparts. Interestingly, in the same study, no statistically significant differences in height, weight, or BMI were observed between the injured and uninjured female cadets, but this may have been due to the limited female representation within the studied cohort .
Despite the evidence that weight and BMI are associated with an increased risk of ankle sprain, other studies have failed to demonstrate that these anthropometric measures are independent risk factors for ankle sprain [59, 67]. Certain athletic cohorts or player positions with elevated BMI may be at a greater predisposition for ankle sprain; further research is required to discern these subtle differences.
Neuromuscular Control/Postural Stability
Proprioception and broader neuromuscular control were first proposed as a risk factor for ankle sprain by Freeman et al. [68] in 1965. Subsequent studies have extensively and rigorously evaluated proprioceptive deficits after primary ankle sprain and described their resultant effects on strength, postural balance, and ankle stability, particularly in athletic populations [69–71]. Furthermore, McGuine et al. [72] demonstrated that high school basketball athletes who subsequently sustained ankle sprains had significantly greater measures of pre-injury postural sway when measured with stabilometry than their uninjured counterparts, indicating an underlying neuromuscular predisposition. Other studies have reported similar results with clinical assessments of postural stability [73].
However, while gross morphologic changes and disrupted afferent nervous networks have been noted with ankle sprain and resultant postural instability, its causal link with chronic ankle instability is less clear [74–76]. Muscular fatigue or diminished baseline strength may potentiate neuromuscular impairment and contribute to subsequent ankle instability [77].
Sport
Certain athletic activities increase the likelihood of ankle sprain, particularly those that involve frequent running, cutting, and jumping movements. Analysis of the National Electronic Injury Surveillance System (NEISS) for all ankle sprain injuries presenting to emergency departments over a 5-year time period revealed that 49.3 % of ankle sprains were caused by participation in sports; basketball (41.1 %), football (9.3 %), and soccer (7.9 %) accounted for more than half of all ankle sprains during athletic activity [51].
A more expansive systematic review of ankle sprain epidemiology revealed that incidence rates varied depending on the unit of measurement [78]. When evaluating for incidence per 1000 person-hours, rugby had the highest incidence (4.20), followed by soccer (2.52). Conversely, when considering incidence more accurately in terms of athletic exposure, lacrosse had the highest incidence rate (2.56) of sprains per 1000 person-exposures, followed by basketball (1.90). Similarly, Waterman et al. [46] found that basketball (men’s, 1.67; women’s, 1.14), men’s rugby (1.53), and men’s lacrosse (1.34) were among the highest incidences per 1000 person-years among intercollegiate athletes.
Level of Competition
As a broad category, level of competition has also been identified as a potential risk factor for ankle sprain. Traditionally, level of competition has been synonymously used to describe both intensity of competition (i.e., practice vs. game) and level of skill (e.g., recreational, intercollegiate, and professional). However, both of these components represent distinct variables that should be separately considered and evaluated.
When considering intensity of competition, there is a positive relation between higher level of play and increased risk of ankle sprain, with approximately 55–66 % of injuries occurring during games when compared to training sessions [79–82]. This is likely attributable to the increased risk-taking activity and pace of play .
There is less of a consensus on the impact of skill level on the incidence of ankle sprain. Our previous work has revealed that ankle sprain incidence in intercollegiate athletes was seven times that of intramural athletes in terms of injuries per 1000 person-years [46]. However, when more specifically controlling for the extent of athlete exposures, no significant differences between intramural and intercollegiate athletes were noted. Other prior studies evaluating skill level are conflicting; one report notes an increased risk in higher-level intercollegiate athletes [60]. Conversely, two additional studies have revealed an increased risk of sports injuries in lower-skill soccer athletes than their higher-skill cohorts [83, 84].
Several more specific, predetermining factors may more predictably explain the different rates of ankle sprain. These include higher cumulative numbers of athlete exposures, greater match exposure [85], low training-to-match ratio [86], and limited warm-up or stretch period [86–88].
Preventative Measures
Reasonable measures may be implemented to mitigate modifiable risk factors and reduce the risk of ankle sprain. Several interventions have demonstrated success in achieving these goals without significant effects on quality of life or athletic performance. By increasing passive restraints to ankle inversion and enhancing postural stability, prophylactic bracing in high-risk athletes and selected military personnel can be effective in reducing the risk of primary and recurrent ankle sprain by up to 50 % [27, 67, 89]. In one prospective randomized trial, Sitler et al. [67] showed a threefold increased risk for ankle sprain among unbraced basketball players when compared to braced athletes over a 2-year time period at the USMA. Among paratroopers, a recent systematic review revealed that an external parachute ankle brace reduced all ankle injuries, including ankle sprain, by approximately half while saving between US$0.6 and 3.4 million in direct and indirect costs [54].
Furthermore, neuromuscular training programs have also shown merit in reducing the risk of ankle sprain. In a meta-analysis, McKeon et al. [76] confirmed that prophylactic and targeted balance control training resulted in a 20–60 % relative risk reduction for sustaining lateral ankle sprain, particularly in those individuals with prior history of ankle sprain. With more consistent screening of high-risk athletes and better-instrumented measures for diagnosis, prophylactic interventions may gain more widespread popularity and effectively reduce the incidence of ankle sprain .
Osteochondral Lesions of the Talus
Introduction
Osteochondral lesions of the talus (OLTs) encompass a broad spectrum of terms previously used to describe injury to the articular talar dome, including osteochondritis dissecans, transchondral talus fractures, and osteochondral talar fractures (Figs. 11.6–11.8). An OLT can occur in association with a severe, acute ankle sprain, and the majority of patients will note an acute injury or remote history of trauma. Alternatively, an OLT can also arise from chronic ankle instability due to the repeated shear stress or edge loading of the articular surface. An estimated 50 % of all acute ankle injuries have articular cartilage injury of the talus, while up to 73 % of ankle fractures are associated with chondral lesions [90, 91]. Early descriptions identify a strong association between lateral lesions of the talus and traumatic injury. Berndt and Harty [92] proposed that compression injury happens to a dorsiflexed and inverted ankle, while medial lesions can arise from inversion and external rotation onto a plantarflexed joint. However, the pathogenesis of medial OLTs is less clear and may also be associated with chronic instability, other mechanisms of injury, or atraumatic etiologies [93]. Other proposed causes include degenerative ankle arthropathy, heritable predispositions, underlying metabolic or endocrine disorders, systemic vasculopathy, joint malalignment, and excessive alcohol use [94, 95]. Due to their extensive cartilage surface, tenuous vascular supply, and limited capacity for repair, OLTs lead to chronic pain, swelling, and mechanical symptoms, while the lesion may become unstable, enlarge, or ultimately progress to osteoarthritis if left untreated [93]. Additionally, ankle synovitis, osteophyte formation, loose bodies, and peroneal tenosynovitis or tears may be present in up to 93 % of patients with chronic OLTs [96].
Coronal CT—osteochondral lesion of the talus
Coronal T1 MRI—osteochondral lesion of the talus
Coronal T2 MRI—osteochondral lesion of the talus
Epidemiology
OLTs comprise approximately only 0.1 % of all fractures of the talus and up to 0.09 % of all fractures. Approximately 6.5 % of all ankle sprains had OLTs when evaluated arthroscopically, while between 23 and 95 % of patients undergoing lateral ankle stabilization for chronic instability demonstrated chondral lesions of the talus with increased risk among athletic populations [96–99]. In a study of OLTs among the US military over a 10-year period, Orr et al. [94] reported that the unadjusted incidence rate was 27 per 100,000 person-years, with increased risk among individuals of female sex, white race, enlisted military rank, Army or Marine Corps service, and increasing chronological age. The authors suggest that cumulative exposure to intense occupational demands, particularly among the enlisted ranks and ground forces during a time of war, may explain the temporal and age-related trends observed in their study. Prior studies have also emphasized the increased risk of OLTs in the second to fourth decade of life, spurned by a combination of peak physical activity and age-related diminution of the biomechanical properties of articular cartilage [94, 100, 101].
As with ankle sprains, the treatment and preventative strategies for OLTs should be targeted at mitigating further ankle instability. Physical therapy, bracing, and symptomatic management with nonsteroidal, anti-inflammatory medication may limit OLT propagation or osteochondral fragment displacement, where surgical considerations for chondral restoration are more immediately appropriate (Figs. 11.9 and 11.10). However, nonoperative management has limited success, with reported rates of acceptable outcomes ranging from 45 to 59 % [102, 103].
Intraoperative arthroscopic image of lateral osteochondral lesion of the talus
Intraoperative open image of lateral osteochondral lesion of talus
Peroneal Tendon Pathology
Peroneal tendon pathology is associated with ankle instability or other acute ankle injury and should be suspected in any patient with chronic lateral ankle pain. Normally restrained by the superior peroneal retinaculum in the retromalleolar sulcus, the peroneus longus and brevis primarily act to plantarflex the great toe and evert the foot, respectively. In addition to these functions, the peroneal tendons also act as dynamic lateral stabilizer of the ankle, particularly during the midstance phase of gait [104]. However, the peroneal tendons can become unstable with forced dorsiflexion and eversion upon an inverted ankle, leading to tendon subluxation, longitudinal tears, and other post-traumatic tendinopathy. A low-lying peroneus brevis muscle belly, an anomalous peroneus quartus, hypertrophied peroneal tubercle, or specific anatomic variants of the retromalleolar sulcus (i.e., absent or convex morphology, calcaneal tunnel) can predispose patients to mechanical symptoms or instability, and assessment of hindfoot alignment should also be performed to rule out varus deformity as a contributing factor [105–108]. Other underlying comorbidities, including diabetes mellitus, hyperparathyroidism, rheumatoid arthritis, and psoriasis, may also contribute to peroneus longus tears, although the majority of these injuries occur during athletic injuries or other acute trauma [104] (Fig. 11.11).
Axial T2 MRI—peroneus brevis tear
Unfortunately, preventative strategies for peroneal tendon injuries are limited. Careful clinical screening and treatments focusing on the prevention of further ankle instability are the hallmarks of treatment for peroneal tendon pathology, particularly with a previous history of ankle sprain or specific underlying disease (Figs. 11.12 and 11.13).
Lateral ankle intraoperative image—longitudinal peroneus brevis tear
Lateral ankle intraoperative image—longitudinal peroneus brevis tear
Foot
Achilles Disorders
The gastrocnemius–soleus complex serves as a powerful plantarflexor of the ankle and provides a pivotal link to the normal gait cycle through the Achilles tendon. Given its critical importance and peak forces up to 12.5 times body weight, the Achilles tendon is often subject to several inflammatory, degenerative, and traumatic conditions, particularly with age and cumulative activity [109].
With age and repetitive loading, the microscopic architecture of the Achilles tendon undergoes characteristic changes (Fig. 11.14). The collagen fibril diameter and density decrease while becoming increasingly disorganized and disoriented. Additionally, intrasubstance degeneration occurs with microtears, focal necrosis, calcification, and a relative absence of neovascularization indicative of tendinosis at the calcaneal attachment (insertional) or more proximally (non-insertional). Alternatively, tendonitis implies an underlying inflammation and is frequently a misnomer for tendinosis on histopathological analysis. Paratenonitis is an inflammatory entity that arises from mechanical irritation and manifests as edema, increased vascular response, and perivascular infiltration of inflammatory cells. Lastly, Achilles ruptures typically occur in the watershed area of limited vascularization and often vis-à-vis preexisting tendinosis .
Palpable Achilles tendon defect
Epidemiology
Achilles injuries are prevalent among active cohorts, particularly with running and competitive athletes, and by extension, military service members. Conservative estimates place the incidence rate of Achilles ruptures as 7 injuries per 100,000 in the general population, with increases up to 12 per 100,000 when isolating competitive athletes [110]. Although not infrequent, the epidemiology of Achilles ruptures is not completely borne out given the difficulty in quantifying a population at risk. However, certain risk factors have been articulated, including advancing age [111], male gender [112], athletic participation, involvement in selected sports (e.g., basketball) [113, 114], marked changes in training or physical activity [115], preexisting tendinopathy, steroid [116, 117] and fluoroquinolone use [118, 119], and underlying baseline comorbidities. Raikin et al. [113] conducted a descriptive epidemiological study of 406 Achilles tendon ruptures presenting to a tertiary referral setting in the USA. The patient population was middle-aged (mean, 46.4 years), male (83 %), and involved in sporting activity (68 %); basketball (48 %) and tennis (13 %) were the most commonly involved sports in related ruptures. The incidence rate among military service members is approximately 0.24 % [120]. Participation in basketball has resulted in the predominance of acute Achilles ruptures, particularly among African-Americans. In their study over a 3-year time period, Davis and colleagues [114] identified that individuals of the black race were at nearly a twofold higher risk (1.82; 95 % CI, 1.58, 2.10) of Achilles rupture than non-black patients .
Overuse Achilles injuries, including paratenonitis and symptomatic tendinopathy, are more prevalent. Both can occur with recreational or competitive athletics, although there appears to be a stronger association with endurance running. In a retrospective study of Achilles injuries, approximately 53 % of athletes were active runners at the time of injury, while an additional 27 % were involved in running sports. Of all injuries, 66 % of individuals had paratenonitis and 23 % had insertional tendinopathy. Achilles paratenonitis and symptomatic tendinopathy occur largely as a result of training errors or changes in distance, intensity, terrain, technique, or fitness. Whereas some risk factors such as misalignment, limb length inequality, and muscle imbalance or weakness are non-modifiable, other risk factors may be targets for intervention, including heel running, training surfaces, environmental conditions (e.g., wet, slippery, or uneven surfaces), footwear, and equipment [121].
Numerous approaches to conservative treatment have been postulated, although few other than an Achilles stretching and strengthening regimen have demonstrated consistent success. This preserves the mobility and function of the normal ankle and Achilles tendon, while decreasing strain. Mafi et al. [122] and Silbernagel et al. [123] demonstrated significant improvements with an eccentric, load-bearing training protocol, particularly with non-insertional tendinopathy. However, other authors have demonstrated moderate success with a limited-dorsiflexion, eccentric program in patients with insertional Achilles tendinosis as well [124].
Plantar Fasciitis
Introduction
Plantar fasciitis , an inflammatory condition affecting the attachment of the plantar fascia at the calcaneal tubercle, is the most common source of heel pain in the ambulatory setting [125]. Its hallmark pathological findings reflect the cycle of degeneration and microtrauma followed by intrinsic attempts at repair. As a result, angiofibroblastic hyperplasia, chondroid metaplasia, and varying levels of collagen necrosis are evident on histological analysis. Largely thought to result from chronic overload to the plantar fascia, plantar fasciitis can occur alongside or dovetail into other causes of heel pain, namely, nerve entrapment of the first branch of the lateral plantar nerve (i.e., Baxter’s nerve). However, the pathophysiology and potential association between these conditions, as well as plantar heel spurs, remains unclear [126]. In addition to those mentioned, other sources of heel pain must also be entertained, such as seronegative enthesopathies (e.g., ankylosing spondylitis, Reiter syndrome), heel pad atrophy, infection, calcaneal stress fracture, osteoarthritis, and compressive neuropathies (e.g., tarsal tunnel syndrome).
Epidemiology
Up to 10 % of the population will be affected by plantar fasciitis during their lifetime [126] and it may occur bilaterally in up to 20–30 % of patients [128]. Plantar fasciitis affects two fairly distinct, yet disparate cohorts. Low-demand, sedentary individuals may develop plantar fasciitis due to cumulative or excessive loading, and obesity has been consistently identified as a potential risk factor for plantar fasciitis [129, 130] and chronic plantar heel pain [131–133] in this population. Additionally, occupations that involve prolonged standing, walking, or other upright, repetitive activity aside from athletics may also precipitate plantar fasciitis, or the British appellation “policeman’s heel” [126, 130].
Plantar fasciitis also commonly affects athletic individuals and military cohorts. A national survey estimated that 83 % of patients presenting for medical treatment of plantar fasciitis were active, adult individuals, with a total of 1 million visits over a 5-year period. Among runners, the prevalence of plantar fasciitis varies from 4 to 22 %, while the extent of its burden among other athletes is not currently known [134]. Among over 12 million person-years at risk in US service members, Scher et al. [135] identified an incidence rate of 10.5 per 1000 person-years, with individuals of the female sex, black race, Army service, senior officer rank, and ages less than 20 or over 40 years experiencing higher rates of plantar fasciitis. The findings presented in this study support the overload theory, with sharp increases in cumulative occupational activity leading to a higher risk of plantar fasciitis, as seen in other studies [136]. Additionally, with increasing age and years of military service, plantar fasciitis may develop in response to age-related increases in heel pad thickness with corresponding loss of elasticity, thereby translating increased tensile loads to the degenerative plantar fascia [137, 138].
While the roles of sex and race have been debated, the current literature is inconclusive. In the only military study, women demonstrated a nearly twofold greater incidence rate of plantar fasciitis [135], while other authors have demonstrated increased prevalence of heel pain among men [139, 140] and women [131, 141]. Similarly, there is no definitive evidence regarding the role of race, although Scher and colleagues [135] postulated that the higher body weights or BMI among African-Americans may lead to higher rates of plantar fasciitis .
In addition to demographic parameters, several other anatomic and dynamic musculoskeletal factors have been established for plantar fasciitis. Limited ankle dorsiflexion and heel cord tightness impart greater stress on the plantar fascia through the windlass mechanism and increased compensatory foot pronation, particularly during the toe-off phase of gait. As a result, individuals with these chronic deficits demonstrate a higher risk of secondary fasciitis [130, 142]. Dorsiflexion night splints and Achilles/plantar fascial stretching exercises are successful first-line treatments and serve as the hallmarks of nonsurgical management [126, 143, 127]. DiGiovanni et al. [144] have shown that an eccentric, non-weightbearing, tissue-specific plantar fascial stretching exercise regimen is superior to standard, weight-bearing Achilles stretching programs for plantar fasciitis, with enduring long-term benefits [145].
Other aspects of foot biomechanics may also play a role in plantar fasciitis. With a subtle cavus foot, the hindfoot and midfoot do not accommodate ground reactive forces normally, leading to increased stress at the plantar fascia. Conversely, with excessive forefoot pronation with pes planus, the plantar fascia is also under continual strain due to deficiencies in other capsuloligamentous support. In response to age-related changes in the heel and these biomechanical variants, several authors have recommended the use of shock absorbing heel cups or pads as a useful complement to activity modification in the treatment of active individuals resuming athletic activity [141, 146, 147]. Additionally, orthotics and shoe modifications have also been utilized for additional shock absorption, arch support, unloading of the plantar fascia, and limitations of the windlass mechanism [148, 149], although their long-term effectiveness [150] and necessity for custom design [146] have been disputed. Given the estimated US$192–376 million spent on the treatment of plantar fasciitis within the USA, further investigation is required to identify the cost-effectiveness and utility of these health-care resources versus other methods of conservative care [151].
Lisfranc Injuries
Introduction
First described by a French surgeon during the Napoleonic Wars in 1815, Lisfranc injuries represent a traumatic form of midfoot instability, characteristically at the second tarsometatarsal joint and further adjacent involvement. Lisfranc injuries can occur both with a high- or low-energy mechanism of injury. In the former, a direct force or crushing injury precipitates injury to the relatively immobile midfoot and strong ligamentous attachments spanning the second metatarsal and medial cuneiform. Associated fractures are common, particularly the so-called fleck sign at the medial base of the second metatarsal [152] (Figs. 11.15–11.18). However, due to the subtle physical exam and radiographic findings with low-energy injuries, a high index of suspicion must be maintained for individuals with midfoot pain and difficulty bearing weight. Lower-energy injuries occur when a fixed forefoot is indirectly loaded with sudden forefoot abduction, dorsiflexion, or more commonly, forced plantarflexion. Axial loading of a plantarflexed foot can occur due to player contact on a planted foot during athletics, floorboard impact during motor vehicle collisions, or toe-first point of contact during a fall from height.
Anterior-posterior (AP) radiograph of foot—Lisfranc injury
Anterior-posterior (AP) radiograph of foot—Lisfranc injury 3 months status post open reduction internal fixation
Anterior-posterior (AP) radiograph of foot—Lisfranc injury
Anterior-posterior (AP) radiograph of foot—Lisfranc injury, 6-month status post open reduction internal fixation
Epidemiology
Lisfranc injuries among athletes and active patients are not infrequent. They comprise up to only 0.2 % of all fractures, and the overall annual incidence of tarsometatarsal (TMT) injuries is roughly one in 55,000 individuals [153, 154]. About 40–45 % of injuries occur as a result of motor vehicle collisions, followed by falls from height, crush injuries, or other high-energy mechanisms [155]. However, low-energy mechanisms can contribute up to 30 %, and up to 20 % of Lisfranc injuries may be missed or misdiagnosed on initial presentation [156]. Injuries have been reported in athletes involved in basketball, football, soccer, gymnastics, running, and horseback riding, and these cohorts may have inherently higher rates of midfoot sprain [156–158]. An estimated 4 % of collegiate football players sustain a Lisfranc injury, and this was the second most common foot injury in this population. Males have a two- to fourfold greater incidence of Lisfranc injury, with peak incidence occurring in the third decade of life [156]. Additional demographic risk factors have not been elucidated, and no modifiable risk factors have currently been identified .
Metatarsal Fractures
Fifth Metatarsal Base Fracture
Introduction
Fifth metatarsal fractures , either traumatic or stress-related, are typically organized anatomically into three separate groups. Zone 1 fractures represent acute injuries of the fifth metatarsal tuberosity with hindfoot inversion and avulsion of the attachment site of the lateral band of the plantar fascia. Zone 2 injuries, eponymously named Jones fractures after the British surgeon who described them in 1902, involve the metaphyseal junction of the fifth metatarsal with extension into the fourth–fifth intermetatarsal articulation. Also termed “dancer’s fractures,” zone 2 fractures typically occur with forefoot adduction with a plantarflexed ankle. Finally, zone 3 fractures occur at the proximal diaphysis of the fifth metatarsal and are often stress fractures due to repetitive microtrauma. Due to their vascular watershed location, Jones fractures and zone 3 fractures are collectively considered to be high-risk fractures for poor healing and nonunion (Figs. 11.19 and 11.20).
Oblique radiograph of foot—non-healed zone 3 base of the fifth metatarsal fracture at 3 months
Oblique radiograph of foot—6 months after intramedullary screw after non-healed zone 3 base of the fifth metatarsal fracture
Epidemiology
Between 70 and 90 % of high-risk fifth metatarsal base fractures occur in young, active individuals between the ages of 15 and 22 years old. Young athletes involved in high-demand activity are at the highest risk, particularly during a running or jumping sport [159]. Common to soccer, basketball, and football, frequent shifting, pivoting, or cutting motions in a position of plantar flexion impose a higher risk of fracture due to the propensity for lateral missteps during competition. Ekstrand and Van Dijk [160] identified that these fractures accounted for only 0.5 % of injuries among elite soccer athletes, and the incidence rate was 0.04 injuries per 1000 h of at-risk exposure. Of these, 45 % of patients experienced prodromal symptoms and 40 % occurred during preseason activities, suggesting that marked increases in stress loading of the lateral forefoot may also contribute to this injury. Furthermore, some of these fractures in the preseason may be the result of stress changes that go unrecognized prior to complete fracture.
Anatomic alignment and disease comorbidity must also be considered. Cavovarus foot deformity, even subtle changes, may alter normal loading mechanics of the lower extremity, placing disproportionate stress about the more mobile fifth metatarsal base and predisposing it to stress-related injury [161]. As well, genu varum and chronic lateral ankle instability may also affect forefoot loading and should be considered in the patient evaluation [162]. Other neuropathic disorders, namely, hereditary sensorimotor neuropathy and advanced diabetes mellitus, may lead to peroneal weakness, increased adduction forces, and altered midfoot and forefoot alignment, thus leading to increased stress upon the proximal fifth metatarsal [162]. Appropriate recognition and concomitant treatment of these risk factors may facilitate improved rates of healing and diminish chances of recurrence, particularly when coupled with intramedullary screw fixation in the high-demand individual. Additionally, lateral forefoot and hindfoot posting may mitigate reinjury of the proximal fifth metatarsal through varus unloading and may be considered in selected individuals [161].
Metatarsal Stress Fracture
Introduction
The so-called march fractures were first described among the Prussian military during the mid-1800s [162] and continue to be a notable cause of disability among active populations. Lesser metatarsal fractures comprise between 9 and 19 % of all stress fractures [164]. However, Cosman et al. [9] identified that up to 58 % of stress fractures at West Point involved the lesser metatarsals. The second (most common) and third metatarsals account for nearly 80–90 % of all metatarsal stress fracture [3, 164]. In comparison to the high-risk, transverse proximal fifth metatarsal stress fracture, these fractures are typically oblique, diaphyseal injuries that are largely considered low risk (Figs. 11.21–11.24). Great toe metatarsal fractures account for only 10 % of all metatarsal stress fractures and are compression-type injuries predominately seen in elderly populations or young children, sub-populations outside the scope of a typical military population [162].
Anterior-posterior (AP) radiograph of foot—third metatarsal stress fracture
Bone scan showing uptake at third metatarsal
Axial T2 MRI— third metatarsal stress fracture with increased uptake
AP radiograph of foot—third metatarsal stress fracture after 2 months of bone stimulation treatment
Epidemiology
In many ways, lesser metatarsal stress fractures demonstrate a similar inherent pathophysiology, population at risk, and risk profile relative to other stress-related injuries in active patients. Repetitive overloading is implicated in “march fractures,” [163] particularly when training is formed on a hard surface and with inadequate footwear [4, 165]. Military personnel, running athletes, and ballet dancers have a documented history of metatarsal stress injuries [136, 166, 167]. During running, the bending strain of the second metatatarsal is 6.9 times greater than that of the great toe and these tensile strains are adequate to generate fatigue failure with cumulative loading [168, 169]. Sullivan et al. [166] demonstrated that runners had a 16 % incidence rate of second and third metatarsal stress fractures in their study, with a higher risk associated with greater than 20 miles per week, running on a hard surface, and changes in training (e.g., intensity, duration, volume, etc.) within the past 3 months .
Biomechanical risk factors and underlying hormonal or physiologic variables must also be addressed. Forefoot overpronation, low arches, and/or pes planus can contribute to increased transfer of loading forces onto the second metatarsal when compared to a foot with a more normal arch, which may ultimately lead to stress fracture [162, 167, 170]. Similarly, disruption of normal forefoot and great toe function during the toe-off phase of gait may also lead to lesser toe stress fracture [171]. This can occur after a malunion of the first metatarsal or due to iatrogenic causes with hallux valgus surgery or inadvertent dorsiflexion with first metatarsal osteotomy. As with other stress fractures, menstrual irregularities, aberrant hormonal function, and nutritional deficiencies may also accelerate metatarsal stress injuries when exposed to repetitive loading activity [172].
Current interventions have focused on modifiable risk factors for metatarsal stress fractures, particularly training errors among military populations. Greater focus has been placed on gradually progressive increases in fitness training and periodization or strategic variances in training distance and intensity. In a study of 250 military recruits, Greaney and colleagues [165] demonstrated dramatic reductions in training-related stress fractures when converting to grass surface, modified shoe wear, and march gait retraining. Furthermore, Milgrom et al. [169] showed that training with basketball shoes modified with viscoelastic insoles virtually eliminated overuse stress injuries of the foot in the Israeli military. Simkins et al. [170] also showed reductions in stress-related metatarsal fracture within implementation of a prefabricated semirigid orthosis, with rates of injury 0 and 6 % with and without the orthotic, respectively. With disrupted toe-off phase of gait or abnormal great toe contact, a Morton extension or firm medial shank may also be utilized to avoid subsequent stress injury of transfer metatarsalgia to the second and third metatarsals, especially when in conjunction with an adjacent metatarsal pad [162].
In summary, lower extremity injuries to the shank, ankle, and foot are common in physically active military and athletic populations. Many of the common injuries that affect the lower extremity in these populations impact the tendons, ligaments, and bones. While some of these injuries are due to acute injury, many are due to chronic overuse or repetitive loading. Some of the modifiable and non-modifiable risk factors for these injuries have been identified; however, we still have a rudimentary understanding of the risk factors for many of these lower extremity injuries. Furthermore, little is known about how baseline factors at the time of injury contribute to important patient outcomes following standard management strategies. As a result, further research is needed to identify those in the military that are at the greatest risk for these lower extremity injuries and to determine which treatment algorithms yield the best outcomes in this patient population .
References
Matheson GO, Clement DB, McKenzie DC, Taunton JE, Lloyd-Smith DR, MacIntyre JG. Stress fractures in athletes. A study of 320 cases. Am J Sports Med. 1987;15(1):46–58.
Bucholz RW, Court-Brown CM, Heckman JD, Tornetta P. Rockwood and Green’s Fractures in Adults. (7th edn, Chap. 55). Philadelphia: Lippincott Williams and Wilkins; 2009.
Harrast MA, Colonno D. Stress fractures in runners. Clin Sports Med. 2010;29(3):399–416.
Milgrom C, Giladi M, Stein M, Kashtan H, Margulies JY, Chisin R, Steinberg R, Aharonson Z. Stress fractures in military recruits. A prospective study showing an unusually high incidence. J Bone Joint Surg Br. 1985;67(5):732–5.
Knapik JJ, Graham B, Cobbs J, Thompson D, Steelman R, Jones BH. A prospective investigation of injury incidence and injury risk factors among Army recruits in military police training. BMC Musculoskeletal Disord. 2013. 14(32).
Caesar BC, McCollum GA, Elliot R, Williams A, Calder J. Stress fracturs of the tibia and medial malleolus. Foot Ankle Clin. 2013;18(2):339–55.
Armstrong DW, Rue JP, Wilckens JH, Frassica FJ. Stress fracture injury in young military men and women. Bone. 2004;35(3):806–16.
Yates B, White S. The incidence and risk factors in the development of medial tibial stress syndrome among naval recruits. Am J Sports Med. 2004;32(3):772–80.
Cosman F, Ruffing J, Zion M, Uhorchak J, Ralston S, Tendy S, McGuigan FE, Lindsay R, Nieves J. Determinants of stress fracture risk in United States Military Academy cadets. Bone. 2013;55(2):359–66.
Lee D. Stress fractures, active component. US Armed Forces, 2004-2010. MSMR. 2011;18(5):8–11.
U.S. Army Research Institute of Environmental Medicine Bone Health and Military Medical Readiness. U.S. Army Research Institute of Environmental Medicine, Natick, MA, USA; 2006.
Jones BH, Thacker SB, Gilchrist J, Kimsey CD, Sosin DM. Prevention of lower extremity stress fractures in athletes and soldiers: a systematic review. Epidemiol Rev. 2002;24(2):228–47.
Zahger D, Abramovitz A, Zelikovsky L, Israel O, Israel P. Stress fractures in female soldiers: an epidemiological investigation of an outbreak. Mil Med. 1988;153(9):448–50.
Knapik J, Montain SJ, McGraw S, Grier T, Ely M, Jones BH. Stress fracture risk factors in basic combat training. Int J Sports Med. 2012;33(11):940–6.
Brudvig TJ, Gudger TD, Obermeyer L. Stress fractures in 295 trainees: a one-year study of incidence as related to age, sex, and race. Mil Med. 1983;148(8):666–7.
Jones BH, Bovee MW, Harris JM, Cowan DN. Intrinsic risk factors for exercise-related injuries among male and female Army trainees. Am J Sports Medicine. 1993;21(5):705–10.
Mattila VM, Niva M, Kiuru M, Pihlajamaki H. Risk factors for bone stress injuries: a follow-up study of 102,515 person-years. Med Sci Sports Exerc. 39(7):1061–6.
Pester S, Smith PC. Stress fractures in the lower extremities of soldiers in basic training. Orthop Rev. 1992;21(3):297–303.
Protzman RR, Griffis CG. Stress fractures in men and women undergoing military training. J Bone Joint Surg Am. 1977;59(6):825.
Wentz L, Liu PY, Haymes E, Ilich JZ. Females have a greater incidence of stress fractures than males in both military and athletic populations: a systemic review. Mil Med. 2011;176(4):420–30.
Kaufman KR, Brodine S, Shaffer R. Military training-related injuries: surveillance, research, and prevention. Am J Prev Med. 2000;18(3):54–63.
Bell NS, Mangione TW, Hemenway D, Amoroso PJ, Jones BH. High injury rates among female Army trainees: a function of gender? 2000. AJPM. 2000;18(3):141–6.
Hauret KG, Jones BH, Bullock SH, Canham-Chervak M, Canada S. Musculoskeletal injuries description of an under-recognized injury problem among military personnel. Am J Prev Med. 2010;28(1):61–70.
Finestone A, Milgrom C, Evans R, Yanovich R, Constantini N, Moran DS. Overuse injuries in female infantry recruits during low-intensity basic training. Med Sci Sports Exerc. 2008;40(11):630–5.
Yeung SS, Yeung EW, Gillespie LD. Interventions for preventing lower limb soft-tissue running injuries. Cochrane Database Syst Rev. 2011;6(7).
Lappe J, Cullen D, Haynatzki G, Recker R, Ahlf R, Thompson K. Calcium and vitamin D supplementation decreases incidence of stress fractures in female Navy recruits. J Bone Miner Res. 2008;23(5):741–9.
Rome K, Handoll HH, Ashford R. Interventions for preventing and treating stress fractures and stress reactions of bone of the lower limbs in young adults. Cochrane Database Syst Rev. 2005;18(2).
Fraipont MJ, Adamson GJ. Chronic exertional compartment syndrome. J Am Acad Orthop Surg. 2003;11(4):268–76.
Fronek J, Mubarak SJ, Hargens AR, Lee YF, Gershuni DH, Garfin SR, Akeson WH. Management of chronic exertional anterior compartment syndrome of the lower extremity. Clin Orthop Relat Res. 1987;220:217–27.
Detmer DE, Sharpe K, Sufit RL, Girdley FM. Chronic compartment syndrome: diagnosis, management, and outcomes. Am J Sports Med. 1985;13:162–70.
Edmundsson D, Toolanen G, Sojka P. Chronic compartment syndrome also affects nonathletic subjects: a prospective study of 63 cases with exercise-induced lower leg pain. Acta Orthop. 2007;78(1):136–42.
Wilder RP, Sethi S. Overuse injuries: tendinopathies, stress fractures, compartment syndrome, and shin splints. Clin Sports Med. 2004;23(1):55–81.
Ovarfordt P. Intramuscular pressure in vascular disease and compartment syndromes. Bulletin of the department of surgery. Lund: University of Lund; 1983.
Styf JR, Korner LM. Microcapillary infusion technique for measurement of intramuscular pressure during exercise. Clin Orthop Relat Res. 1986;207:253–62.
Tzortziou V, Maffulli N, Padhiar N. Diagnosis and management of chronic exertional compartment syndrome (CECS) in the United Kingdom. Clin J Sport Med. 2006;16(3):209–13.
Waterman BR, Laughlin M, Kilcoyne K, Cameron KL, Owens BD. Surgical treatment of chronic exertional compartment syndrome of the leg. J Bone Joint Surg. 2013;95:592–6.
Pedowitz RA, Hargesn AR. Acute and chronic compartment syndromes. In: Garret WE, Speer KP, Kirendall DT, editors. Principles and practice of orthopaedic sports medicine. Philadelphia: Lippincott Williams & Wilkins; 2001. pp. 87–97.
Waterman BR, Liu J, Newcomb R, Schoenfeld AJ, Orr JD, Belmont PJ. Risk factors for chronic exertional compartment syndrome in a physical active military population. Am J Sports Med. 2013;41(11):2545–9.
Brennan FH, Kane SF. Diagnosis, treatment options, and rehabilitation of chronic lower leg exertional compartment syndrome. Curr Sports Med Rep. 2003;2(5):247–50.
Glorioso J. Exertional leg pain. In: O’Connor FG, Wilder RP, Nirschl R, editors. Textbook of running medicine. New York: McGraw-Hill; 2000. pp. 188–9.
Kirby RL, McDermott AG. Arch Phys Med Rehabil. Arch Phys Med Rehabil. 1983;54(7):296–9.
Tsintzas D, Ghosh S, Maffulli N, King JB, Padhiar N. The effect of ankle position on intracompartmental pressures of the leg. Acta Orthop. 43(1):42–8.
Diebal AR, Gregory R, Alitz C, Gerber JP. Effects of forefoot running on chronical exertional compartment syndrome: a case series. Int J Sports Phys Ther. 2011;6(4):312–21.
Fallat L, Grimm DJ, Saracco JA. Sprained ankle syndrome: prevalence and analysis of 639 acute injuries. J Foot Ankle Surg. 1998;37(4):280–5.
Ferran NA, Maffulli N. Epidemiology of sprains of the lateral ankle ligament complex. Foot Ankle Clin. 2006;11(3):659–62.
Waterman BR, Belmont PJ Jr, Cameron KL, et al. Epidemiology of ankle sprain at the United States military academy. Am J Sports Med. 2010;38(4):797–803.
Cordova ML, Sefton JM, Hubbard TJ. Mechanical joint laxity associated with chronic ankle instability: a systematic review. Sports Health. 2010;2(6):452–9.
Bridgman SA, Clement D, Downing A, et al. Population based epidemiology of ankle sprains attending accident and emergency units in the West Midlands of England, and a survey of UK ew. Sports Health. 2010;2(6):452–9.
Soboroff SH, Pappius EM, Komaroff AL. Benefits, risks, and costs of alternative approaches to the evaluation and treatment of severe ankle sprain. Clin Orthop Relat Res. 1984. 183:160-8. practice for severe ankle sprains. Emerg Med J. 2003;20(6):508–10.
Holmer P, Sondergaard L, Konradsen L, et al. Epidemiology of sprains in the lateral ankle and foot. Foot Ankle Int. 1994;15(2):72–4.
Waterman BR, Owens BD, Davey S, et al. The epidemiology of ankle sprain in the United States. J Bone Joint Surg Am. 2010;92(13):2279–84.
Lillywhite LP. Analysis of extrinsic factor associated with 379 injuries occurring during 34,236 military parachute descents. JR Army Med Corps (London). 1991;137:115–21.
Knapik JJ, Spiess A, Swedler DI, Grier TL, Darakjy SS, Jones BH. Systematic review of the parachute ankle brace: injury risk reduction and cost effectiveness. Am J Prev Med. 2010;38(1):182–8.
Luippold RS, Sulsky SI, Amoroso PJ. Effectiveness of an external ankle brace in reducing parachuting-related ankle injuries. Inj Prev. 2011;17(1):58–61.
Williams JG. Aetiologic classification of sports injuries. Br J Sports Med. 1971;4:228–30.
Beynnon BD, Murphy DF, Alosa DM. Predictive factors for lateral ankle sprains: a literature review. J Athl Train. 2002;37(4):376–80.
Cameron KL. Time for a paradigm shift in conceptualizing risk factors in sports injury research. J Ath Train. 2010;45(1):58–60.
Gwinn DE, Wilckens JH, McDevitt ER, et al. The relative incidence of anterior cruciate ligament injury in men and women at the United States Naval Academy. Am J Sports Med. 2000;28(1):98–102.
Beynnon BD, Renstrom PA, Alosa DM, et al. Ankle ligament injury risk factors: a prospective study of college athletes. J Orthop Res. 2001;19(2):213–20.
Hosea TM, Carey CC, Harrer MF. The gender issue: epidemiology of ankle injuries in athletes who participate in basketball. Clin Orthop. 2000;372:45–49.
Frank C, Amiel D, Woo SL, Akeson W. Normal ligament properties and ligament healing. Clin Orthop 1985;196:15–25.
Ekstrand J, Gillquist J. Soccer injuries and their mechanisms: a prospective study. Med Sci Sports Exerc. 1983;15(3):267–70.
McKay GD, Goldie PA, Payne WR, Oakes BW. Ankle injuries in basketball: injury rate and risk factors. Br J Sports Med. 2001;35(2):103–8.
Milgrom C, Shlamkovitch N, Finestone A, et al. Risk factors for lateral ankle sprain: a prospective study among military recruits. Foot Ankle. 1991;12(1):26–30.
Malliaropoulos N, Ntessalen M, Papacostas E, et al. Reinjury after acute lateral ankle sprains in elite track and field athletes. Am J Sports Med. 2009;37(9):1755–61.
Tyler TF, McHugh MP, Mirabella MR, et al. Risk factors for noncontact ankle sprains in high school football players: the role of previous ankle sprains and body mass index. Am J Sports Med. 2006;34(3):471–5.
Sitler MR, Ryan J, Wheeler B, McBride J. The efficacy of a semirigid ankle stabilizer to reduce acute ankle injuries in basketball: a randomized clinical study at West Point. Am J Sports Med. 1994;22(4):454–61.
Freeman MA, Dean MR, Hanham IW. The etiology and prevention of functional instability of the foot. J Bone Joint Surg Br. 1965;47(4):678–85.
Leanderson J, Eriksson E, Nilsson C, Wykman A. Proprioception in classical ballet dancers. A prospective study of the influence of an ankle sprain on proprioception in the ankle joint. Am J Sports Med. 1996;24(3):370–4.
Leanderson J, Wykman A, Eriksson E. Ankle sprain and postural sway in basketball players. Knee Surg Sports Traumatol Arthrosc. 1993;1(3–4):203–5.
Perrin PP, Bene MC, Perrin CA, Durupt D. Ankle trauma significantly impairs posture control. a study in basketball players and controls. Int J Sports Med. 1997;18(5):387–92.
McGuine TA, Greene JJ, Best T, Leverson G. Balance as a predictor of ankle injuries in high school basketball players. Clin Sports Med. 2000;10(4):239–44.
Trojian TH, McKeag DB. Single leg balance test to identify risk of ankle sprains. Br J Sports Med. 2006;40(7):610–3.
Stecco C, Macchi V, Porzionato A, et al. The ankle retinacula: morphological evidence of the proprioceptive role of the fascial system. Cells Tissues Organs. 2010;192(3):200–10.
Riemann BL. Is there a link between chronic ankle instability and postural instability? J Athl Train. 2002;37(4):386–93.
McKeon PO, Hertel J. Systematic review of postural control and lateral ankle instability, part II. Is balance training clinically effective? J Athl Train. 2008;43(3):305–15.
Mohammadi F, Roozdar A. Effects of fatigue due to contraction of evertor muscles on the ankle joint position sense in male soccer players. Am J Sports Med. 2010;38(4):824–8.
Fong DT, Hong Y, Chan LK, et al. A systematic review on ankle injury and ankle sprain in sports. Sports Med. 2007;37(1):73–94.
Arnason A, Gudmundsson A, Dahl HA, et al. Soccer injuries in Iceland. Scand J Med Sci Sports. 1996;6(1):40–5.
Chomiak J, Junge A, Peterson L, Dvorak J. Severe injuries in football players: influencing factors. Am J Sports Med. 2000;28(5 Suppl):S58–68.
Kujala UM, Taimela S, Antti-Poika I, et al. Acute injuries in soccer, ice hockey, volleyball, basketball, judo, and karate: analysis of national registry data. BMJ. 1995;311(7018):1465–8.
Sullivan JA, Gross RH, Grana WA, et al. Evaluation of injuries in youth soccer. Am J Sports Med. 1980;8(5):325–7.
Chomiak J, Junge A, Peterson L, Dvorak J. Severe injuries in football players: influencing factors. Am J Sports Med. 2000;28(5 Suppl):S58–68.
Peterson L, Junge A, Chomiak J, et al. Incidence of football injuries and complaints in different age groups and skill-level groups. Am J Sports Med. 2000;28(5 Suppl):S51–7.
Arnason A, Gudmundsson A, Dahl HA, et al. Soccer injuries in Iceland. Scand J Med Sci Sports. 1996;6(1):40–5.
Dvorak J, Junge A, Chomiak J, et al. Risk factor analysis for injuries in football players: possibilities for a prevention program. Am J Sports Med. 2000;28(5 Suppl):S69–74.
Ekstrand J, Gillquist J, Moller M, et al. Incidence of soccer injuries and their relation to training and team success. Am J Sports Med. 1983;11(2):63–7.
Olsen OE, Myklebust G, Engebretsen L, et al. Exercises to prevent lower limb injuries in youth sports: clustered randomized controlled trial. BMJ. 2005;330(7489):449.
Frey C, Feder KS, Sleight J. Prophylactic ankle brace use in high school volleyball players. A prospective study. Foot Ankle Int. 2010;31(4):296–300.
Saxena A, Eakin C. Articular talar injuries in athletes: results of microfracture and autogenous bone graft. Am J Sports Med. 2007;35(10):1680–7.
Leontaritis N, Hinojosa L, Panchbhavi VK. Arthroscopically detected intra-articular lesions associated with acute ankle fractures. J Bone Joint Surg. 2009;91(2):333–9.
Berndt AL, Harty M. Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg Am. 2004;86(6):1336.
Stone JW. Osteochondral lesions of the talar dome. J Am Acad Orthop Surg. 1996;4(2):63–72.
Orr JD, Dawson LK, Garcia EJ, Kirk KL. Incidence of osteochondral lesions of the talus in the United States military. Foot Ankle Int. 2011;32(10):948–54.
O’Loughlin PF, Heyworth BE, Kennedy JG. Current concepts in the diagnosis and treatment of osteochondral lesions of the ankle. Am J Sports Med. 2010;38(2):392–404.
DiGiovanni BF, Fraga CJ, Cohen BE, Shereff MJ. Associated injuries found in chronic lateral ankle instability. Foot Ankle Int. 2000;21(10):809–15.
Komenda GA, Ferkel RD. Arthroscopic findings associated with the unstable ankle. Foot Ankle Int. 1999;20(11):708–13.
Schafer D, Hintermann B. Arthroscopic assessment of the chronic unstable ankle joint. Knee Surg Sports Traumatol Arthrosc. 1996;4(1):48–52.
Taga I, Shino K, Inoue M, Nakata K, Maeda A. Articular cartilage lesions in ankles with lateral ligament injury: an arthroscopic study. Am J Sports Med. 1993;21:120–7.
Chew KT, Tay E, Wong YS. Osteochondral lesions of the talus. Ann Acad Med Singapore. 2008;37(1):63–8.
Bosien WR, Staples OS, Russell SW. Residual disability following acute ankle sprains. J Bone Joint Surg. 1955;1(37):1237–43.
Shearer C, Loomer R, Clement D. Nonoperatively managed stage 5 osteochondral talar lesions. Foot Ankle Int. 2002;23(7):651–4.
Tol JL, Strujis PA, Bossuyt PM, Verhagen RA, van Dijk CN. Treatment strategies in osteochondral defects of the talar dome a systematic review. Foot Ankle Int. 2000;21(2):119026.
Philbin TM, Landis GS, Smith B. Peroneal tendon injuries. J Am Acad Orhrop Surg. 2009;17(5):306–17.
Geller J, Lin S, Cordas D, Vieira P. Relationship of a low-lying muscle belly t otears of the peroneus brevis tendon. Am J Orthop. 2003;32(11):541–4.
Sobel M, Hashimoto J, Arnoczky SP, Bohne WH. The microvasculature of the seasmoid complex: its clinical significance. Foot Ankle. 1992;13(6):359–63.
Hyer CF, Dawson JM, Philbin TM, Berlet GC, Lee TH. The peroneal tubercle: description, classification, and relevance. Foot Ankle Int. 2005;26(11):947–50.
Manoli A, Graham B. The subtle cavus foot, “the underpronator.” Foot Ankle Int. 2005;26(3):256–63.
Injuries T. Basic science and clinical medicine. Edited by Maffulli N, Renstrom P, Vayne B. Leadbetter.
Hess GW. Achilles tendon rupture: a review of etiology, population, anatomy, risk factors, and injury prevention. Foot Ankle Spec. 2010;3(1):29–32.
Jarvinen TA, Kannus P, Maffulli N, Khan KM. Achilles tendon disorders: etiology and epidemiology. Foot Ankle Clin. 2005;10(2):255–66.
Wong J, Barrass V, Maffulli N. Quantitative review of operative and nonoperative management of achilles tendon ruptures. Am J Sports Med. 2002;30(4):565–75.
Raikin SM, Garras DN, Krapchev PV. Achilles tendon injures in a United States population. Foot Ankle Int. 2013;34(4):475–80.
Davis JM, Mason KT, Clark DA. Achilles tendon ruptures stratified by age, race, and cause of injury among active duty US military members. Mil Med. 1999;164(12):872–3.
Maffulli N, Tallon C, Wong J, Peng Lim K, Bleakney R. No adverse effect on early weight bearing following open repair of acute tears of the Achilles tendon. J Sports Med Phy Fit. 2003;43(3):367–79.
Clark SC, Jones MW, Choudhury RR, Smith E. Bilateral patellar tendon rupture secondary to repeated local steroid injections. J Accid Emerg Med. 1995;12(4):300–1.
Newnham DM, Douglas JG, Legge JS, Friend JA. Achilles tendon rupture: an underrated complication of corticosteroid treatment. Thorax. 1991;46(11):853–4.
Stinner DJ, Orr JD, Hsu JR. Fluoroquinolone-associated bilateral patellar tendon rupture: a case report and review of the literature. Mil Med. 2010;175(6):457–9.
Wise BL, Peloquin C, Choi H, Lane NE, Zhang Y. Impact of age, sex, obesity, and steroid use on quinolone-associated tendon disorders. Am J Med. 2012;125(12):1228–38.
Owens B, Mountcastle S, White D. Racial differences in tendon rupture incidence. Int J Sports Med. 2007;28(7):617–20.
Kvist M. Achilles tendon injuries in athletes. Sports Med. 1994;18:173–201.
Mafi N, Lorentzon R, Alfredson H. Superior short-term results with eccentric calf muscle training compared to concentric training in a randomized prospective multicenter study on patients with chronic Achilles tendinosis. Knee Surg Sports Traumatol Arthrosc. 2001;9(1):42–7.
Silbernagel KG, Thomee R, Thomee P, Karlsson J. Eccentric overload training for patients with chronic Achilles tendon pain—a randomized controlled study with reliability testing of the evaluation methods. Scan J Med Sports Sci. 2001;11(4):197–206.
Jonsson P, Alfredson H, Sunding K, Fahlstrom M, Cook J. New regimen for eccentric calf-muscle training in patients with chronic insertional achilles tendinopathy: results of a pilot study. Br J Sports Med. 2008;42(9):746–9.
Singh D, Angel J, Bentley G, Trevino SG. Fortnightly review. Plantar fasciitis. BMJ. 1997;315(7101):172–5.
Gill LH. Plantar fasciitis: diagnosis and conservative management. J Am Orthop Surg. 1997;5(2):109–17.
Crawford F, Atkins D, Edwards J. Interventions for treating plantar heel pain. Cochrane Database Syst Rev. 2000;3:CD000416.
Schepsis AA, Leach RE, Gorzyca J. Plantar fasciitis. Etiology, treatment, surgical results, and review of the literature. Clin Orthop Relat Res. 1991;266:185–96.
Hill JJ, Cutting PJ. Heel pain and body weight. Foot Ankle. 1989;9(5):254–6.
Riddle DL, Pulisic M, Pidcoe P, Johnson RE. Risk factors for plantar fasciitis: a matched case-control study. J Bone and Joint Surg. 2003;85(5):872–7.
Rano JA, Fallat LM, Savoy-Moore RT. Correlation of heel pain with body mass index and other characteristics of heel pain. J Foot Ankle Surg. 2001;40(6):351–6.
Irving DB, Cook JL, Menz HB. Factors associated with chronic plantar heel pain: a systematic review. J Sci Med Sport. 2006;9(1–2):11–22.
Butterworth PA, Landorf KB, Smith SE, Menz HB. The association between body mass index and musculoskeletal foot disorders: a systematic review. Obesity Rev. 2012;13(7):630–42.
Rome K, Webb P, Unsworth A, Haslock I. Heel pad stiffness in runners with plantar heel pain. Clin Biomech. 2001;16(10):901–5.
Scher DL, Belmont PJ, Bear R, Mountcastle SB, Orr JD, Owens BD. The incidence of plantar fasciitis in the United States military. J Bone Joint Surg. 2009;91(12):2867–72.
Matheson GO, Macintyre JG, Taunton JE, Clement DB, Lloyd-Smith R. Musculoskeletal injuries associated with physical activity in older adults. Med Sci Sports Exerc. 1989;21(4):379–85.
Prichasuk S. The heel pad in plantar heel pain. J Bone Joint Surg. 1994;76(1):140–2.
Wearing SC, Smeathers JE, Yates B, Sullivan PM, Urry SR, Dubois P. Sagittal movement of the medial longitudinal arch is unchanged in plantar fasciitis. Med Sci Sports Exerc. 2004; 36(10):1761–7.
Taunton JE, Ryan MB, Clement DB, McKenzie DC, Lloyd-Smith DR, Zumbo BD. A retrospective case-control analysis of 2002 running injuries. BJSM. 2002;36(2):95–101.
Lapidus PW, Guidotti FP. Painful heel: report of 323 patients with 364 painful heels. Clin Orthop Relat Res. 1965;39:176–86.
Sobel M, Pavlov H, Geppert MJ, Thompson FM, DiCarlo EF, Davis WH. Painful os peroneum syndrome: a spectrum of conditions responsible for plantar lateral foot pain. Foot Ankle Int. 1994;15(3):112–24.
Patel A, Digiovanni B. Association between plantar fasciitis and isolated contracture of the gastrocnemius. Foot Ankle Int. 2011;32(1):5–8.
Garrett TR, Neibert PJ. The effectiveness of a gastrocnemius-soleus stretching program as a therapeutic treatment of plantar fasciitis. J Sport Rehab. 2013;22(4):308–12.
DiGiovanni BF, Nawoczenski DA, Lintal ME, Moore EA, Murray JC, Wilding GE, Baumhauer JF. Tissue-specific plantar fascia-stretching exercise enhances outcomes in patients with chronic heel pain. A prospective, randomized study. J Bone Joint Surg Am. 2003;85:1270–7.
DiGiovanni BF, Nawoczenski DA, Malay DP, Graci PA, Williams TT, Wilding GE, Baumhauer JF. Plantar fascia-specific stretching exercise improves outcomes in patients with chronic plantar fasciitis. A prospective clinical trial with two-year follow-up. J Bone Joint Surg Am. 2006;88(8):1775–81.
Pfeffer G, Bacchetti P, Deland J, et al. Comparison of custom and prefabricated orthoses in the initial treatment of proximal plantar fasciitis. Foot Ankle Int. 1999;20(4):214–21.
Wolgin M, Cook C, Graham C, Mauldin D. Conservative treatment of plantar heel pain: long-term follow up. Foot Ankle Int. 1994;15(3):97–102.
Gross MT, Byers JM, Krafft JL, Lackey EJ, Melton KM. The impact of custom semirigid foot orthotics on pain and disability for individuals with plantar fasciitis. J Orthop Sports Phys Ther. 2002;32(4):149–57.
Seligman DA, Dawson DR. Customized heel pads and soft orthotics to treat heel pain and plantar fasciitis. Arch Phys Med Rehab. 2003;84(10):15564–7.
Landorf KB, Keenan AM, Herbert RD. Effectiveness of foot orthoses to treat plantar fasciitis: a randomized trial. Arch Int Med. 2006;26(166):1305–10.
Tong KBJW, Ng EY. Preliminary investigation on the reduction of plantar loading pressure with different insole materials. Foot. 2010;20(1):1–6.
Vuori JP, Aro HT. Lisfranc joint injuries: trauma mechanisms and associated injuries. J Trauma. 1993;35(1):40–5.
Kalia V, Fishman EK, Carrino JA, Fayad LM. Epidemiology, imaging, and treatment of Lisfranc fracture-dislocations revisited. Skeletal Radiol. 2012;41(2):129–36.
Mantas JP, Burks RT. Lisfranc injuries in the athlete. Clin Sports Med. 1994;13(4):719–30.
Thompson MC, Mormino MA. Injury to the tarsometatarsal joint complex. J Am Acad Orthop Sur. 11:260–7.
DeOrio M, Erickson M, Usuelli FG, Easly M. Lisfranc injuries in sport. Foot Ankle Clin. 2009;14:169–86.
Meyer SA Callaghan JJ, Albright JP, Crowley ET, Powell JW. Midfoot sprains in collegiate football players. Am J Sports Med. 1994;22:392–401.
Curtis MJ, Myerson M, Szura B. Tarsometatarsal joint injuries in the athlete. Am J Sports Med. 1993;21:497–502.
Rhim B, Hung JC. Lisfranc injury and Jones fracture in sports. Clin Podiatr Med Surg. 2011;28(1):69–86.
Ekstrand J, Van Dijk CN. Fifth metatarsal fractures among male professional footballers: a potential career-ending disease. BJSM. 2013;47(12):754–8.
Raikin SM, Slenker N, Ratigan B. The association of a varus hindfoot and fracture of the fifth metatarsal metaphyseal-diaphyseal junction: the Jones fracture. Am J Sports Med. 2008;36(7):1367–72.
Weinfeld SB, Haddad SL, Myerson MS. Metatarsal stress fractures. Clin Sports Med. 1997;12(2):319–38.
Bernstein A, Stone JR. March fracture: a report of three hundred and seven cases and a new method of treatment. J Bone Joint Surg. 1944;26(4):743–50.
Fetzer GB, Wright RW. Metatarsal shaft fractures and fractures of the proximal fifth metatarsal. Clin Sports Med. 2006;25(1):139–50.
Greaney RB, Gerber FH, Laughlin RL, Kmet JP, Metz CD, Kilcheski TS, Rao BR, Silverman ED. Distribution and natural history of stress fractures in US Marine recruits. Radiology. 1983;146(2):339–46.
Boden BP, Osbahr DC, Jimenez C. Low-risk stress fractures. Am J Sports Med. 2001;29:100–11.
Sullivan D, Warren RF, Pavlov H, Kelman G. Stress fractures in 51 runners. Clin Orthop Relat Res. 1984;187:188–92.
Gross TS, Bunch RP. A mechanical model of metatarsal stress fracture during distance running. Am J Sports Med. 1989;17:669–74.
Milgrom C, Finestone A, Sharkey N, Hamel A, Mandes V, Burr D, Arndt A, Ekenman I. Metatarsal strais are sufficient to cause fatigue fracture during cyclic overloading. Foot Ankle Int. 2002;23(3):230–5.
Milgrom C, Simkin A, Eldad A, Nyska M, Finestone A. Using bone’s adaptation ability to lower the incidence of stress fractures. Am J Sports Med. 2000;28:245–51.
Drez D, Young JC, Johnston RD, Parker WD. Metatarsal stress fractures. Am J Sports Med. 1980;8:123–5.
Kadel NJ, Teitz CC, Kronmal RA. Stress fractures in ballet dancers. Am J Sports Med. 1992;20:445–49.
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Waterman, B., Dunn, J., Orr, J. (2016). Lower Leg, Ankle, and Foot Injuries. In: Cameron, K., Owens, B. (eds) Musculoskeletal Injuries in the Military. Springer, New York, NY. https://doi.org/10.1007/978-1-4939-2984-9_11
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