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Stress fractures in the lower extremity
European Journal of Radiology 62 (2007) 16–26
Stress fractures in the lower extremity The importance of increasing awareness amongst radiologists Ferco H. Berger, Milko C. de Jonge, Mario Maas ∗ Academic Medical Center, University of Amsterdam, Department of Radiology, Meibergdreef 9, 1105 AZ Amsterdam-ZO, The Netherlands Received 15 January 2007; received in revised form 16 January 2007; accepted 17 January 2007
Abstract Stress fractures are fatigue injuries of bone usually caused by changes in training regimen in the population of military recruits and both professional and recreational athletes. Raised levels of sporting activity in today’s population and refined imaging technologies have caused a rise in reported incidence of stress fractures in the past decades, now making up more than 10% of cases in a typical sports medicine practice. Background information (including etiology, epidemiology, clinical presentation and treatment and prevention) as well as state of the art imaging of stress fractures will be discussed to increase awareness amongst radiologists, providing the tools to play an important role in diagnosis and prognosis of stress fractures. Specific fracture sites in the lower extremity will be addressed, covering the far majority of stress fracture incidence. Proper communication between treating physician, physical therapist and radiologist is needed to obtain a high index of suspicion for this easily overlooked entity. Radiographs are not reliable for detection of stress fractures and radiologist should not falsely be comforted by them, which could result in delayed diagnosis and possibly permanent consequences for the patient. Although radiographs are mandatory to rule out differentials, they should be followed through when negative, preferably by magnetic resonance imaging (MRI), as this technique has proven to be superior to bone scintigraphy. CT can be beneficial in a limited number of patients, but should not be used routinely. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Magnetic resonance imaging; Radiographs; Stress fractures; Lower extremity
1. Introduction Using the term stress fracture may be confusing, as it has different meanings in contemporary literature. Most authors use it to indicate fatigue fractures, where others use it in its proper meaning, indicating a group of fractures made up of fatigue fractures and insufficiency fractures (including pathologic fractures). In this article it is used as a substitute for fatigue fractures. Stress fractures belong to the wide spectrum of overuse injuries. Due to their strenuous training activities, military recruits and competitive athletes are primarily affected and have been subject of most articles written about stress fractures. However, the increase in participation of recreational athletes in major sports events (i.e. marathon running), often pushing their limits, have led to an increase of stress fractures in this population as well. Increased incidence has subsequently increased under-
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standing of stress fracture mechanism and behavior, resulting in recognition of low and high risk sub categories. In 1855, the Prussian military physician Breithaupt was the first to describe the stress fractures in the metatarsals of soldiers, now commonly referred to as a march fracture, depicting clinical setting and symptoms [1]. Forty years later, only 2 years after the discovery of roentgen and its clinical application, Stechow reported on radiographic identification of metatarsal stress fractures [2]. The diagnosis remained a solely military one until Pirker reported on the first stress fracture diagnosed in an athlete, a transverse femoral shaft fracture, in 1934 [3]. Devas was the first to report a large series of stress fractures in athletes in 1956 [4]. Since then, stress fractures have been increasingly reported upon in medical literature in both clinical and research settings. This paper intends to increase radiologists’ awareness of stress fractures and to give a compact overview of background on stress fractures. The clinical picture and symptoms of stress fractures will be described and special attention will be given to the imaging options available for early diagnosis of the
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condition, as this has significant implications for treatment and outcome, which are also briefly discussed. Although stress fractures can occur in almost any bone, 95% of stress fractures occur in the lower extremity. Therefore, stress fractures of the lower extremity are the focus of this paper. 2. Clinical picture 2.1. Etiology The risk of stress fractures is influenced by many factors, being divided into intrinsic (gender, age, race, fitness and muscle strength) and extrinsic factors (training regimen, footwear, training surface and type of sport), biomechanical factors (bone mineral density and bone geometry), anatomic factors (foot morphology, leg length discrepancy and knee alignment), hormonal factors (delayed menarche, menstrual disturbance and contraception) and nutritional factors (low calcium and vitamin D intake, eating disorders and the female athlete triad) [5,6]. Unraveling the multifactorial cause of stress fractures is difficult, but training regimen plays a major role. Especially high weekly running mileage and abrupt or rapid changes in duration, frequency or intensity of training increase the risk of stress fractures [6]. Proper communication between treating physician, physical therapist and radiologist in which training history is an important aspect is essential to create the high index of suspicion needed to detect this easily overlooked entity. The precise pathogenesis of stress fractures is not clear; there are several theories to explain their causative mechanism, which are shortly mentioned. In response to changing mechanical (cyclic) loading, Harvesian remodeling [7] of bone takes place by initial osteoclastic activity causing resorption of lamellar bone, followed by replacement with osteonal, stronger bone by osteoblasts [8]. Remodeling especially takes place at the site of microcracks [9] present in normal bone, stimulating bone turn-over, creating need for understanding microcrack initiation and propagation. Microcrack density (the number of microcracks in a certain volume) increases with number of loading cycles and stress level [10], however microcrack density has not been shown to cause bone failure directly. A study of Sobelman showed the opposite; higher microcrack density correlates with longer fatigue life [11]. The reason for bone failure therefore may be related to microcrack propagation. When microcracks encounter microscopic boundaries (osteons or cement lines), crack length seems to play an important role in microcrack propagation. Longer cracks seem to be able to continue to grow, whereas shorter microcracks stop growing [10], enlighting the possible role of microscopic structure of bone (osteon density). Yet another explanation can be found in the remodeling process. New bone formation by osteoblasts begins 10–14 days after the onset of remodeling, leading to temporarily weakened bone by the formation of hollow Haversian canals. To counterbalance this temporary weakness, the periosteum is strengthened by inflammation. However, the periosteum does not mature until about 20 days, thus creating a period in remodeling in which the cortex is at risk of accelerated break-down if continued stress is applied [8].
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Muscles play a role by helping to reduce tensile forces on bone, which are mostly equipped to withstand compression forces. When muscles get fatigued, tensile forces on bone will increase, rendering bone fatigue more likely. Muscles play a role in another way when training changes are considered. Muscle strength increases more rapidly than bone strength when a new stress is applied, thus creating a mechanical imbalance with excess force on bone [12]. To summarize, multiple factors seem to cause bone to be relatively weak when training regimens are intensified, osteoblastic activity lagging behind osteoclastic activity. Adequate levels of rest should probably be incorporated in training regimens to allow for bone strengthening, thereby adapting to new stresses applied. 2.2. Epidemiology Bone stress injury accounts for at least 10% of cases in a typical sports medicine practice, with prevalence in athletes and recruits reported to range from 0.2% to as high as 49%. In running-sports population, prevalence ranges from 10% to 31% [12,13] and 17% are bilateral [12]. Incidence varies with age, mean age reported from 19 to 30 years. Children are increasingly affected due to growing participation in rigorous training programs, but are still a minority. Incidence in women is consistently reported higher than in men, ranging from 1.5 to 3.5 times higher in athletes to 3–12 times higher in recruits. Besides difference in incidence, women also show a different distribution of bones affected. Stress fractures of the metatarsals and the pelvis are more common, and the fibula is affected less. The tibia is the most affected bone in both sexes [5]. 2.3. Clinical presentation Patients typically present with an insidious onset of pain over the affected region without having experienced any form of trauma. This may falsely lead the physician away from including a (stress) fracture in the differential diagnosis. First, pain is experienced during the provoking activity and relieved by rest. Continuing activity at the same level, pain continues after the activity and will later cause the athlete to cease sport activity. Finally, pain is also experienced at rest. Superficial location of the affected bone will cause pain on palpation or distal percussion, and redness or swelling may be appreciated. Painful range of motion at physical examination might be found in deeper locations around the pelvis/femur. Patients may show an antalgic gait, but usually no evidence of muscle atrophy, weakness, deformity or limited range of motion is present. 3. Imaging Radiologists play a central role in detecting stress fractures and ruling out differentials by using state of the art imaging techniques. Radiographs are notoriously unreliable at an early stage, but are mandatory to rule out differentials like tumor, infection or frank fracture. However, if radiographs are negative more advanced techniques should be applied, timely diagnosis
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being essential for treatment and prognosis. Accurate estimates of return to competition time is another benefit of imaging, likely to increase compliance of the athlete.
Table 1 Grade
MRI feature
3.1. Radiography Conventional radiographs have a sensitivity of 15–35% on initial examination, which increases to 30–70% during follow up because of more overt bone reaction [14]. Detection of changes is more difficult in regions covered by more soft tissue. In cortical (osteonal) bone, stress fractures may be appreciated in various ways. Endosteal or periosteal callus may be visible without a fracture line, circumferential periosteal reaction with fracture line through one cortex may be visualized or even frank fracture may be present. In cancellous bone, stress fractures are even less well visible but may be appreciated by hardly noticeable flake like patches of new bone formation some 2–3 weeks after the onset of pain. After formation of a wider, cloudlike area of mineralized bone, the stress fracture evolves into a focal linear area of sclerosis, oriented perpendicular to the trabeculae. Calcaneal stress fractures are examples of these cancellous bone stress fractures. Even though sensitivity of the conventional radiograph is very low, this examination is mandatory as a first imaging study to rule out differentials as infection, malignancy or overt fracture. With a high index of suspicion, the radiologist should initiate further studies in the case of a negative examination, in no case accepting an unremarkable film as the final answer. 3.2. State of the art imaging Although triple phase technetium-99m biphosphate bone scintigraphy has been the standard of reference in past decades, recent years have brought about a growing consensus of MRI being a superior imaging tool [15]. One study comparing MRI, bone scintigraphy and radiography of stress fractures in the pelvis and the lower extremity reports a specificity of 86% combined with a sensitivity of 100%, accuracy of 95%, positive predictive value of 93% and negative predictive value of 100% [16]. More studies have shown MRI to be at least as sensitive as scintigraphy [17–24], at the same time having significantly higher specificity. MRI has promising features to give a reliable estimate of treatment time by dividing stress fractures into four grades depending on the appearance of a basic set of three MRI sequences (short tau inversion recovery (STIR) images, T1 weighted and T2 weighted images) [22,25] (Table 1). Grade 1 stress fractures show mild to moderate periosteal edema on STIR images but no marrow abnormalities. Grade 2 shows moderate to severe periosteal edema on STIR images with added marrow edema on T2 weighted images. Grade 3 ads marrow edema on T1 weighted images and in grade 4 stress fractures a fracture line is clearly visible. Time of conservative treatment increases with grade as is shown in Table 1. This grading system can be used in symptomatic as well as asymptomatic individuals, facilitating comparison between different
1 2 3 4
Positive STIR 1 + positive T2W 2 + positive T1W 3 + definite fracture line a b
Treatment by relative rest Fredericson et al.a
Arendt and Griffithsb
2–3 weeks 4–6 weeks 6–9 weeks 6 weeks cast + 6 weeks rest
3 weeks 3–6 weeks 12–16 weeks >16 weeks
[22]. [25].
studies. However, therapy consequences should be restricted to symptomatic individuals only, since reports show stress fracture findings in asymptomatic individuals continuing training at the same level do not progress to grade 4 fractures [13,26]. In certain cases computer tomography (CT) may be of added value in the work-up of stress fracture diagnosis. However, even though technical advances have provided sub millimeter isotropic voxel imaging with high resolution reconstructions in any plane, multidetector CT still has low sensitivity for detecting stress fractures compared to bone scintigraphy (and thus MRI) [27]. Adding the disadvantage of radiation dose, CT should not routinely be used as an initial investigation. If performing MRI is not possible (e.g. in claustrophobic patients or patients with pacemaker implants) or sites of interest are not well visualized with MRI (e.g. sacrum, pelvis or spine), CT could be a useful alternative. More importantly, if MRI is equivocal on a grade 4 stress fracture or more information is needed for surgical planning, CT in our experience proves to be useful. In addition, CT may be helpful if differentials like malignancy, osteomyelitis/Brodie’s abscess or osteoid osteoma have not confidently been ruled out. Whether newer scanners with 64 or more detector rows will change the position of CT in the work-up of stress fracture diagnosis will have to be investigated by future studies. In these studies, attention has to be given to the possible capability of early stress fracture diagnosis with CT by detection of focal osteopenia, possibly a precursor of stress fractures [27]. Some reports have stated ultrasound to be of value when used for superficially located stress fractures, like in metatarsals and the fibula, but no large trials have been undertaken [28–30]. Typical findings described are periosteal elevation with small fluid collection, soft tissue edema, hypervascularity and increased posterior shadowing. 4. Treatment and prevention Relative rest, meaning cessation of the offending activity, will be adequate therapy in lower grade low risk stress fractures, while immobilization by bed rest or use of crutches may be necessary in higher grades. However, high risk stress fractures at certain anatomic locations will not heal without surgery or are likely to evolve to delayed union, non-union or displaced complete fractures. Important examples of these high risk
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stress fractures are tension sided femoral neck, patella, anterior tibial diaphysis, medial malleolus, tarsal, fifth metatarsal and great toe sesamoid stress fractures. Stress fractures of these bones should be treated more aggressively [31]. Use of nonsteroidal anti-inflammatory drug (NSAID) should be avoided or be kept as short as possible. Although no definite evidence in humans exists, animal studies have shown NSAID use to delay fracture healing and cause non-union [32,33]. Compliance is critical and alternative exercise programs to prevent detraining may help the injured athlete. A pain-free period of 2–3 weeks with full weight bearing allows the athlete to gradually resume sporting activity well below former levels. As rule of thumb, activity should not be increased more then 10% a week and recurrence of pain mandates 2 weeks of modified activity [5].
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Stress fractures are best prevented with gradual changes of training regimen, be it intensity, type of exercise or materials used (surface and shoes). A paper by Fredericson et al. discusses the effect of playing ball sports in childhood and adolescence, which significantly lowers future risk of stress fracture development [34]. This may be caused by denser bone formation due to constant microdamage to the bone during these sports, number of years played directly being related with decrease in stress fracture risk. An experimental study in rats shows that exercise programs aimed at modifying bone structure may be a feasible prevention strategy for stress fractures [35]. Prophylactic treatment with biphosphonates (risedronate), commonly used in treating osteoporosis, did not show reduction of stress fracture incidence in a military training population at high risk of stress fractures [36].
Fig. 1. 29 year old male, unsupervised recreational athlete training for marathon, running 10 miles a week. Insidious onset of right groin pain since one month, not relieved by rest. MRI with coronal STIR sequence (a) and coronal T1-weighted sequence (b), showing edema (arrow heads) and overt fracture line (arrows), making this a grade 4 stress fracture. X-ray performed the same day (c), showing hardly discernable sclerotic line at the stress fracture site (arrow). Follow-up MRI at one month of relative rest shows remarkable decrease of edema and no discernable fracture line on T1-weighted (d) and STIR sequences (e).
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5. Specific fracture sites 5.1. Femur/femoral neck (tension side = high risk, compression side = low risk) Stress fractures of the femur can occur throughout the bone, but most commonly affect the femoral neck, one of the contributing factors being fatigue of the gluteus medius muscle resulting in diminished shock absorbance [37]. In addition to the general risk factors mentioned earlier, coxa vara seem to predispose for femoral neck fractures [38]. The complications of femoral neck fractures make this entity more important than its incidence, possible devastating results for the athlete ensue if complaints are ignored, being delayed union, non-union, fragment dislocation or a vascular femoral head necrosis. In 2004 Provencher et al. proposed a modification of a classification system described by Fullerton and Snowdy in 1988, before the advent of MRI [39]. On the basis of three cases of atypical tension sided femoral neck stress fractures that healed by conservative treatment, they included this category to prevent all tension sided femoral neck stress fractures from being operated on, as advised by the previous classification. Femoral neck stress fractures thus can be classified into four groups: compression (inferior aspect) (Fig. 1), tensile (mid to distal superior aspect), displaced (Fig. 2) and atypical tensile (proximal superior aspect near femoral head) [40]. Conservative treatment is adequate for compression type stress fractures involving less than 50% of neck width and atypical tensile type, surgery is advised for all remaining types. Five to 7 year follow up of 25 patients treated for femoral neck fractures (17 operative) showed 68% was still feeling bothered or even disabled [41]. 5.2. Patella (transverse = high risk, longitudinal = low risk) Stress fractures of the patella can be transverse in direction or longitudinal, the former being caused by traction forces the latter by compression against the femoral condyles [5]. Transverse stress fractures have increased risk of becoming frank fractures and should be treated by non-weight bearing cast immobilization with the knee extended for 4 weeks. Displaced patellar stress fractures require surgical treatment. 5.3. Tibia (anterior midshaft or medial malleolus = high risk, posteromedial aspect = low risk) The tibia is reportedly the most affected bone in the body, representing 20–75% of all stress fractures [31]. Compression sided tibial stress fractures affecting the posteromedial cortex are the most frequently encountered and will mostly heal with relative rest. The longitudinal stress fracture is more uncommon, difficult to differentiate from shin splints without MRI, and will also heal with relative rest. Less often encountered but more complicated tension sided stress fractures occur at the anterior cortex, showing a transverse lucent line with bordering sclerosis on lateral radiographs or MRI (Fig. 3). Caused by jumping and leaping activities, these fractures are prone to delayed and non-union and the radio-
Fig. 2. 41 year old female with insidious onset of pain in the left groin, no recollection of trauma. Initial exams were negative. Follow up at 4 months (a) and 16 months (b) show very slow healing of a mildly dislocated stress fracture of the neck of the left femur (arrows).
graphic appearance has therefore been connotated the dreaded black line [31,42]. These should be treated aggressively with surgery if conservative treatment fails, using an intramedullary tibial nail or anterior tension band plating, which according to one report shortens return to competition time [43,44]. Two even more infrequently encountered tibial stress fractures are at the medial or lateral tibial plateau and the medial malleolus. The former tends to occur in older patients than is usual for other stress fractures and if radiographs are positive,
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Fig. 3. 26 year old male professional ballet dancer, with progressive bilateral complaints of anterior tibia during jumping exercises since 8 weeks. Conventional lateral radiographs of both tibiae showing multiple wedge shaped fractures of the anterior cortex of the mid-tibia, the so called ‘dreaded black lines’, indicating high risk tension sided stress fractures (arrows).
they show a linear transverse region of sclerosis 2–3 mm wide, close to the level of the epiphyseal scar. MRI will show bone marrow edema, periosteal edema and possibly a hypointense fracture line [42] (Fig. 4). Medial malleolus stress fractures tend to occur in running and jumping [5,42]. Usually ankle effusion is present together with tenderness over the medial malleolus. The fracture extends vertically or obliquely upwards from the junction of the medial malleolus and the tibial plafond (Fig. 5). Non-displaced fractures can be treated with immobilization while displaced fractures require open reduction and internal fixation. 5.4. Fibula (low risk) Stress fractures in the fibula usually occur in the distal third, the so called ‘runners fracture’, but are also described proximally [5,45]. Compression, torsion and muscle contraction are thought to cause these fractures. Patients report lateral leg pain over the affected area, often exacerbated by exercise and relieved by rest, sometimes show swelling and redness and an antalgic gait is
common. Pressing the fibula against the tibia provokes pain, occasionally callus might be palpated. The fibula not being a weight bearing bone, these stress fractures tend to heal well by relative rest, but healing will be delayed when offending activity is not stopped. 5.5. Tarsal bones (talus and tarsal navicular = high risk, calcaneus = low risk) Of the tarsal bones the calcaneus is the most affected causing insidious onset heel pain that is aggravated by running or jumping and causes tenderness and pain with posterosuperior compression on examination. Radiographs only show changes after 2–3 weeks by a sclerotic line perpendicular to the trabecular lines, paralleling the posterior cortex on lateral images, changes at onset will only be shown with MRI or scintigraphy. Relative rest for 6 weeks with sometimes use of crutches for pain relieve will usually have a good response [5,45]. Talar stress fractures until recently were only mentioned in literature by case reports, indicating its rarity, partially explained
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Fig. 4. 42 year old male, suffering from progressive pain in the left knee during running, recently having become a recreational athlete. Grade 3 stress fracture of the medial tibia plateau, classically seen in older patients than usual, with increased signal on STIR sequence (a), lowered signal on both T2-weighted (b) and T1-weighted images (c) and sclerosis visible on axial CT (d) and coronal MPR (e) (arrows). No discrete fracture line visible, ruling out grade 4 stress fracture.
by its difficult detection by radiography. However, Sormaala et al. recently have published a MRI based study consisting of 51 consecutive recruits suffering from this entity in an 8year period, describing incidence and anatomic distribution [46]. An incidence of 4.4 (3.2–5.5)/10,000 person-years for military
recruits is reported. In 10% stress fractures were bilateral, in 67% located in the talar head, 25% in the body and the remaining 8% in the posterior talus. Talar head stress fractures were associated with tarsal navicular stress fractures in 60%, 18% was grade 4 showing a fracture line. At all anatomical locations, low grade
Fig. 5. 26 year old male professional soccer player with known medial malleolus stress fracture, anteromedial impingement and loose body of the left ankle. Radiograph (a) showing medial malleolus stress fracture at 12 months follow up, originating at classical anatomic landmark (junction of tibial plafond and medial malleolus lines, arrows). MRI and CT performed at the same day; Axial PD-weighted image showing hypointense fracture line (b) (arrow) and CT showing fracture line with bordering sclerosis (c) (arrow).
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Fig. 6. 45 year old female with insidious onset forefoot pain. At presentation, a conventional radiograph is negative (a). At 16 days periosteal reaction (arrowhead) as well as an overt fracture line (arrow) are visible at the distal shaft of the second metatarsal (b). At 7 weeks, prominent callus formation shows healing progress of stress fracture (c).
stress fractures dominated. In only 21% the talus was the single bone affected, but all recruits were successfully treated with 2–4 weeks of reduced exercise. The tarsal navicular stress fracture is of special attention because its high risk of delayed healing, delayed or non-union and even displaced complete fractures, caused by poor vascularization at the most often affected middle third of the bone. In addition, the anatomic position of the bone makes diagnosis with radiographs especially difficult, delaying diagnosis. Invariably, these fractures are linear and within the sagittal plane [12].
Stress fractures at this site are caused by explosive athletic activities involving sprinting, jumping and hurdling and patients will report medial dorsal midfoot pain, especially when jumping [5]. Extensive training on artificial turf surface may be another cause [12] as are associated foot anomalies. Palpation of the navicular bone will cause pain and patients may limp. Incomplete fractures affecting one cortex can be treated with non-weight bearing cast immobilization for 6–8 weeks followed by another 6 weeks of weight bearing cast, while complete and sclerotic fractures mandate surgery.
Fig. 7. Young male, professional athlete with pain of left forefoot during training for some weeks, especially at second metatarsal. Swelling of soft tissues and painful palpation. If relative rest applied, complaints are relieved after 3–4 days. Conventional radiograph showing mild periosteal reaction of the proximal 1/3rd of the second metatarsal (a) (arrows). Same day MRI shows markedly elevated signal intensity on axial T2-wieghted sequence with fat-saturation (arrowheads) and possible fracture line (b) (arrow). Corresponding low signal intensity on axial PD-weighted images (c) (arrowheads).
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Fig. 8. 29 year old male, no recollection of trauma, active recreational soccer player presenting with increasing pain over lateral margin of foot, present even at rest. Fracture line of the fifth metatarsal, distal to the tuberosity, was found, consistent with Jones fracture (a) (arrow). Follow up at 2 weeks (b) and 6 weeks (c) hardly show any tendency of healing, a known complication of this tension sided type of stress fracture (arrows).
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5.6. Metatarsals and sesamoids (sesamoids and fifth metatarsal = high risk, second or third metatarsal = low risk) Metatarsal stress fractures were the first to be described, being recognized as early as the mid 1850’s in soldiers subjected to long marches and therefore named march fractures. They account for approximately 10% of fractures in athletes [47], being the most affected site after the tibia. The second and third metatarsal are most often affected, the fracture typically occurring at the neck or distal diaphysis with forces being highest here in running. The patients complain of forefoot pain,
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which increases during running or jumping and is relieved by rest. Examination reveals tenderness over the affected bone and callus may be palpated after some time. Radiographs are not very sensitive, but MRI is very accurate and even ultrasound can be used for early detection (Figs. 6 and 7). This location poses no problem for healing, athletes usually can start training after 4–6 weeks when no pain is experienced anymore. Transverse stress fractures of the base of the fifth metatarsal more than 1.5 cm distal to the tuberosity are called Jones fractures (Fig. 8). Patients suffer from pain at the lateral aspect of the foot, aggravated by inversion, and are tender on palpation. Delayed union, non-union and displacement are well known complications of this tension sided stress fracture, necessitating non-weight bearing cast as initial treatment as opposed to relative rest for second and third distal metatarsal shaft fractures. Recurrence and failure of conservative treatment will result in need of surgery, usually by percutaneous screw fixation. Early surgical intervention may benefit athletes with Jones fractures [31]. Recent reports indicate that fourth metatarsal base stress fractures are very similar in behavior, needing long treatment period as well [48]. Stress fractures of the great toe sesamoids affect the medial more often than the lateral [5,42] (Fig. 9) and can lead to chronic pain due to non-union. Radiographs are difficult to interpret due to the wide variety in anatomy, especially the bipartite sesamoid. Therefore, MRI should be performed to detect significant bone marrow edema. Six weeks of non-weight bearing short leg cast that extends to the tip of the toe to prevent dorsiflexion is the treatment of choice, but failure of treatment or recurrence mandate excision or bone grafting. 6. Conclusion Raised awareness of medical staff and increased athletic activity have increased the incidence of stress fractures, now making up about 15% of the general sports medicine practice. These fractures can affect essentially every bone in the body, but are most frequent in the lower extremity. Timely diagnosis is essential to prevent dramatic consequences for the athlete, yet this is not easy. Thorough knowledge of typical sport mechanics and a high index of suspicion is needed to accurately image a professional or recreational sportsman/woman. In our opinion, radiography should still be the first examination performed, because even if a stress fracture is not visualized, differentials may be ruled out. However, negative radiographs are unreliable at any stage and should be followed by state of the art MRI, encompassing STIR, T2-weighted and T1-weigthed series for high sensitivity and specificity and for accurate prognosis of rehabilitation time. CT proves to be useful for surgical planning and ruling out differentials, and may be used in regions of the body which are not easily imaged with MRI.
Fig. 9. 27 year old female professional ballet dancer, complaining of increasing painful sensation at the base of the great toe of the right foot. Coronal MPR of MDCT (marking of right foot), showing sclerosis (arrowhead) and subtle fracture line (arrow) of medial sesamoid bone of the first ray of the right foot (a). Axial T2-weighted sequence with fat saturation showing edema of medial sesamoid (arrowheads).
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[3] Pirker H. Bruch der Oberschenkeldiaphyse durch Muskelzug. Arch Klin Chir 1934;175:155–68. [4] Devas MB, Sweetnam R. Stress fractures of the fibula; a review of fifty cases in athletes. J Bone Joint Surg Br 1956;38-B:818–29. [5] Pecina MM, Bojanic I. Stress Fractures. In: Pecina MM, Bojanic I, editors. Overuse injuries of the musculoskeletal system. 2nd ed. Boca Raton: CRC Press; 2003. p. 315–49. [6] Pepper M, Akuthota V, McCarty EC. The pathophysiology of stress fractures. Clin Sports Med 2006;25:1–16, vii. [7] Frost H. Presence of microscopic cracks in vivo bone. Henry Ford Hosp Bull 1960;8:27–35. [8] Romani WA, Gieck JH, Perrin DH, Saliba EN, Kahler DM. Mechanisms and management of stress fractures in physically active persons. J Athl Train 2002;37:306–14. [9] Drapeau MS, Streeter MA. Modeling and remodeling responses to normal loading in the human lower limb. Am J Phys Anthropol 2006;129:403–9. [10] O’Brien FJ, Hardiman DA, Hazenberg JG, et al. The behaviour of microcracks in compact bone. Eur J Morphol 2005;42:71–9. [11] Sobelman OS, Gibeling JC, Stover SM, et al. Do microcracks decrease or increase fatigue resistance in cortical bone? J Biomech 2004;37:1295–303. [12] Spitz DJ, Newberg AH. Imaging of stress fractures in the athlete. Radiol Clin North Am 2002;40:313–31. [13] Kiuru MJ, Niva M, Reponen A, Pihlajamaki HK. Bone stress injuries in asymptomatic elite recruits: a clinical and magnetic resonance imaging study. Am J Sports Med 2005;33:272–6. [14] Lassus J, Tulikoura I, Konttinen YT, Salo J, Santavirta S. Bone stress injuries of the lower extremity: a review. Acta Orthop Scand 2002;73:359–68. [15] Sofka CM. Imaging of stress fractures. Clin Sports Med 2006;25:53–62, viii. [16] Kiuru MJ, Pihlajamaki HK, Hietanen HJ, Ahovuo JA. MR imaging, bone scintigraphy, and radiography in bone stress injuries of the pelvis and the lower extremity. Acta Radiol 2002;43:207–12. [17] Anderson MW, Greenspan A. Stress fractures. Radiology 1996;199:1–12. [18] Gaeta M, Minutoli F, Scribano E, et al. CT and MR imaging findings in athletes with early tibial stress injuries: comparison with bone scintigraphy findings and emphasis on cortical abnormalities. Radiology 2005;235:553–61. [19] Slocum KA, Gorman JD, Puckett ML, Jones SB. Resolution of abnormal MR signal intensity in patients with stress fractures of the femoral neck. AJR Am J Roentgenol 1997;168:1295–9. [20] Stafford SA, Rosenthal DI, Gebhardt MC, Brady TJ, Scott JA. MRI in stress fracture. AJR Am J Roentgenol 1986;147:553–6. [21] Yao L, Johnson C, Gentili A, Lee JK, Seeger LL. Stress injuries of bone: analysis of MR imaging staging criteria. Acad Radiol 1998;5:34–40. [22] Fredericson M, Bergman AG, Hoffman KL, Dillingham MS. Tibial stress reaction in runners. Correlation of clinical symptoms and scintigraphy with a new magnetic resonance imaging grading system. Am J Sports Med 1995;23:472–81. [23] Ishibashi Y, Okamura Y, Otsuka H, Nishizawa K, Sasaki T, Toh S. Comparison of scintigraphy and magnetic resonance imaging for stress injuries of bone. Clin J Sport Med 2002;12:79–84. [24] Fredericson M, Jang K, Bergman AG, Gold GE. Femoral diaphyseal stress fractures: results of a systematic bone scan and magnetic resonance imaging evaluation in 25 runners. Phys Ther Sport 2004;5:188–93. [25] Arendt EA, Griffiths HJ. The use of MR imaging in the assessment and clinical management of stress reactions of bone in high-performance athletes. Clin Sports Med 1997;16:291–306. [26] Bergman AG, Fredericson M, Ho C, Matheson GO. Asymptomatic tibial stress reactions: MRI detection and clinical follow-up in distance runners. AJR Am J Roentgenol 2004;183:635–8.
[27] Groves AM, Cheow HK, Balan KK, Housden BA, Bearcroft PW, Dixon AK. 16-Detector multislice CT in the detection of stress fractures: a comparison with skeletal scintigraphy. Clin Radiol 2005;60:1100–5. [28] Howard CB, Lieberman N, Mozes G, Nyska M. Stress fracture detected sonographically. AJR Am J Roentgenol 1992;159:1350–1. [29] Banal F, Etchepare F, Rouhier B, et al. Ultrasound ability in early diagnosis of stress fracture of metatarsal bone. Ann Rheum Dis 2006;65: 977–8. [30] Bodner G, Stockl B, Fierlinger A, Schocke M, Bernathova M. Sonographic findings in stress fractures of the lower limb: preliminary findings. Eur Radiol 2005;15:356–9. [31] Kaeding CC, Yu JR, Wright R, Amendola A, Spindler KP. Management and return to play of stress fractures. Clin J Sport Med 2005;15:442–7. [32] Mehallo CJ, Drezner JA, Bytomski JR. Practical management: nonsteroidal antiinflammatory drug (NSAID) use in athletic injuries. Clin J Sport Med 2006;16:170–4. [33] Wheeler P, Batt ME. Do non-steroidal anti-inflammatory drugs adversely affect stress fracture healing? A short review. Br J Sports Med 2005;39:65–9. [34] Fredericson M, Ngo J, Cobb K. Effects of ball sports on future risk of stress fracture in runners. Clin J Sport Med 2005;15:136–41. [35] Warden SJ, Hurst JA, Sanders MS, Turner CH, Burr DB, Li J. Bone adaptation to a mechanical loading program significantly increases skeletal fatigue resistance. J Bone Miner Res 2005;20:809–16. [36] Milgrom C, Finestone A, Novack V, et al. The effect of prophylactic treatment with risedronate on stress fracture incidence among infantry recruits. Bone 2004;35:418–24. [37] Lee CH, Huang GS, Chao KH, Jean JL, Wu SS. Surgical treatment of displaced stress fractures of the femoral neck in military recruits: a report of 42 cases. Arch Orthop Trauma Surg 2003;123:527–33. [38] Carpintero P, Leon F, Zafra M, Serrano-Trenas JA, Roman M. Stress fractures of the femoral neck and coxa vara. Arch Orthop Trauma Surg 2003;123:273–7. [39] Provencher MT, Baldwin AJ, Gorman JD, Gould MT, Shin AY. Atypical tensile-sided femoral neck stress fractures: the value of magnetic resonance imaging. Am J Sports Med 2004;32:1528–34. [40] Niva MH, Kiuru MJ, Haataja R, Pihlajamaki HK. Fatigue injuries of the femur. J Bone Joint Surg Br 2005;87:1385–90. [41] Weistroffer JK, Muldoon MP, Duncan DD, Fletcher EH, Padgett DE. Femoral neck stress fractures: outcome analysis at minimum five-year follow-up. J Orthop Trauma 2003;17:334–7. [42] Bergman AG, Fredericson M. MR imaging of stress reactions, muscle injuries, and other overuse injuries in runners. Magn Reson Imaging Clin N Am 1999;7:151–74, ix. [43] Borens O, Sen MK, Huang RC, et al. Anterior tension band plating for anterior tibial stress fractures in high-performance female athletes: a report of 4 cases. J Orthop Trauma 2006;20:425–30. [44] Varner KE, Younas SA, Lintner DM, Marymont JV. Chronic anterior midtibial stress fractures in athletes treated with reamed intramedullary nailing. Am J Sports Med 2005;33:1071–6. [45] Boden BP, Osbahr DC, Jimenez C. Low-risk stress fractures. Am J Sports Med 2001;29:100–11. [46] Sormaala MJ, Niva MH, Kiuru MJ, Mattila VM, Pihlajamaki HK. Bone stress injuries of the talus in military recruits. Bone 2006;39:199– 204. [47] 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;15:46–58. [48] Hetsroni I, Mann G, Dolev E, Morgenstern D, Nyska M. Base of fourth metatarsal stress fracture: tendency for prolonged healing. Clin J Sport Med 2005;15:186–8.
Stress fractures in the lower extremity The importance of increasing awareness amongst radiologists Ferco H. Berger, Milko C. de Jonge, Mario Maas ∗ Academic Medical Center, University of Amsterdam, Department of Radiology, Meibergdreef 9, 1105 AZ Amsterdam-ZO, The Netherlands Received 15 January 2007; received in revised form 16 January 2007; accepted 17 January 2007
Abstract Stress fractures are fatigue injuries of bone usually caused by changes in training regimen in the population of military recruits and both professional and recreational athletes. Raised levels of sporting activity in today’s population and refined imaging technologies have caused a rise in reported incidence of stress fractures in the past decades, now making up more than 10% of cases in a typical sports medicine practice. Background information (including etiology, epidemiology, clinical presentation and treatment and prevention) as well as state of the art imaging of stress fractures will be discussed to increase awareness amongst radiologists, providing the tools to play an important role in diagnosis and prognosis of stress fractures. Specific fracture sites in the lower extremity will be addressed, covering the far majority of stress fracture incidence. Proper communication between treating physician, physical therapist and radiologist is needed to obtain a high index of suspicion for this easily overlooked entity. Radiographs are not reliable for detection of stress fractures and radiologist should not falsely be comforted by them, which could result in delayed diagnosis and possibly permanent consequences for the patient. Although radiographs are mandatory to rule out differentials, they should be followed through when negative, preferably by magnetic resonance imaging (MRI), as this technique has proven to be superior to bone scintigraphy. CT can be beneficial in a limited number of patients, but should not be used routinely. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Magnetic resonance imaging; Radiographs; Stress fractures; Lower extremity
1. Introduction Using the term stress fracture may be confusing, as it has different meanings in contemporary literature. Most authors use it to indicate fatigue fractures, where others use it in its proper meaning, indicating a group of fractures made up of fatigue fractures and insufficiency fractures (including pathologic fractures). In this article it is used as a substitute for fatigue fractures. Stress fractures belong to the wide spectrum of overuse injuries. Due to their strenuous training activities, military recruits and competitive athletes are primarily affected and have been subject of most articles written about stress fractures. However, the increase in participation of recreational athletes in major sports events (i.e. marathon running), often pushing their limits, have led to an increase of stress fractures in this population as well. Increased incidence has subsequently increased under-
∗
Corresponding author. Tel.: +31 20 5668698; fax: +31 20 5669119. E-mail address: [email protected] (M. Maas).
0720-048X/$ – see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ejrad.2007.01.014
standing of stress fracture mechanism and behavior, resulting in recognition of low and high risk sub categories. In 1855, the Prussian military physician Breithaupt was the first to describe the stress fractures in the metatarsals of soldiers, now commonly referred to as a march fracture, depicting clinical setting and symptoms [1]. Forty years later, only 2 years after the discovery of roentgen and its clinical application, Stechow reported on radiographic identification of metatarsal stress fractures [2]. The diagnosis remained a solely military one until Pirker reported on the first stress fracture diagnosed in an athlete, a transverse femoral shaft fracture, in 1934 [3]. Devas was the first to report a large series of stress fractures in athletes in 1956 [4]. Since then, stress fractures have been increasingly reported upon in medical literature in both clinical and research settings. This paper intends to increase radiologists’ awareness of stress fractures and to give a compact overview of background on stress fractures. The clinical picture and symptoms of stress fractures will be described and special attention will be given to the imaging options available for early diagnosis of the
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condition, as this has significant implications for treatment and outcome, which are also briefly discussed. Although stress fractures can occur in almost any bone, 95% of stress fractures occur in the lower extremity. Therefore, stress fractures of the lower extremity are the focus of this paper. 2. Clinical picture 2.1. Etiology The risk of stress fractures is influenced by many factors, being divided into intrinsic (gender, age, race, fitness and muscle strength) and extrinsic factors (training regimen, footwear, training surface and type of sport), biomechanical factors (bone mineral density and bone geometry), anatomic factors (foot morphology, leg length discrepancy and knee alignment), hormonal factors (delayed menarche, menstrual disturbance and contraception) and nutritional factors (low calcium and vitamin D intake, eating disorders and the female athlete triad) [5,6]. Unraveling the multifactorial cause of stress fractures is difficult, but training regimen plays a major role. Especially high weekly running mileage and abrupt or rapid changes in duration, frequency or intensity of training increase the risk of stress fractures [6]. Proper communication between treating physician, physical therapist and radiologist in which training history is an important aspect is essential to create the high index of suspicion needed to detect this easily overlooked entity. The precise pathogenesis of stress fractures is not clear; there are several theories to explain their causative mechanism, which are shortly mentioned. In response to changing mechanical (cyclic) loading, Harvesian remodeling [7] of bone takes place by initial osteoclastic activity causing resorption of lamellar bone, followed by replacement with osteonal, stronger bone by osteoblasts [8]. Remodeling especially takes place at the site of microcracks [9] present in normal bone, stimulating bone turn-over, creating need for understanding microcrack initiation and propagation. Microcrack density (the number of microcracks in a certain volume) increases with number of loading cycles and stress level [10], however microcrack density has not been shown to cause bone failure directly. A study of Sobelman showed the opposite; higher microcrack density correlates with longer fatigue life [11]. The reason for bone failure therefore may be related to microcrack propagation. When microcracks encounter microscopic boundaries (osteons or cement lines), crack length seems to play an important role in microcrack propagation. Longer cracks seem to be able to continue to grow, whereas shorter microcracks stop growing [10], enlighting the possible role of microscopic structure of bone (osteon density). Yet another explanation can be found in the remodeling process. New bone formation by osteoblasts begins 10–14 days after the onset of remodeling, leading to temporarily weakened bone by the formation of hollow Haversian canals. To counterbalance this temporary weakness, the periosteum is strengthened by inflammation. However, the periosteum does not mature until about 20 days, thus creating a period in remodeling in which the cortex is at risk of accelerated break-down if continued stress is applied [8].
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Muscles play a role by helping to reduce tensile forces on bone, which are mostly equipped to withstand compression forces. When muscles get fatigued, tensile forces on bone will increase, rendering bone fatigue more likely. Muscles play a role in another way when training changes are considered. Muscle strength increases more rapidly than bone strength when a new stress is applied, thus creating a mechanical imbalance with excess force on bone [12]. To summarize, multiple factors seem to cause bone to be relatively weak when training regimens are intensified, osteoblastic activity lagging behind osteoclastic activity. Adequate levels of rest should probably be incorporated in training regimens to allow for bone strengthening, thereby adapting to new stresses applied. 2.2. Epidemiology Bone stress injury accounts for at least 10% of cases in a typical sports medicine practice, with prevalence in athletes and recruits reported to range from 0.2% to as high as 49%. In running-sports population, prevalence ranges from 10% to 31% [12,13] and 17% are bilateral [12]. Incidence varies with age, mean age reported from 19 to 30 years. Children are increasingly affected due to growing participation in rigorous training programs, but are still a minority. Incidence in women is consistently reported higher than in men, ranging from 1.5 to 3.5 times higher in athletes to 3–12 times higher in recruits. Besides difference in incidence, women also show a different distribution of bones affected. Stress fractures of the metatarsals and the pelvis are more common, and the fibula is affected less. The tibia is the most affected bone in both sexes [5]. 2.3. Clinical presentation Patients typically present with an insidious onset of pain over the affected region without having experienced any form of trauma. This may falsely lead the physician away from including a (stress) fracture in the differential diagnosis. First, pain is experienced during the provoking activity and relieved by rest. Continuing activity at the same level, pain continues after the activity and will later cause the athlete to cease sport activity. Finally, pain is also experienced at rest. Superficial location of the affected bone will cause pain on palpation or distal percussion, and redness or swelling may be appreciated. Painful range of motion at physical examination might be found in deeper locations around the pelvis/femur. Patients may show an antalgic gait, but usually no evidence of muscle atrophy, weakness, deformity or limited range of motion is present. 3. Imaging Radiologists play a central role in detecting stress fractures and ruling out differentials by using state of the art imaging techniques. Radiographs are notoriously unreliable at an early stage, but are mandatory to rule out differentials like tumor, infection or frank fracture. However, if radiographs are negative more advanced techniques should be applied, timely diagnosis
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being essential for treatment and prognosis. Accurate estimates of return to competition time is another benefit of imaging, likely to increase compliance of the athlete.
Table 1 Grade
MRI feature
3.1. Radiography Conventional radiographs have a sensitivity of 15–35% on initial examination, which increases to 30–70% during follow up because of more overt bone reaction [14]. Detection of changes is more difficult in regions covered by more soft tissue. In cortical (osteonal) bone, stress fractures may be appreciated in various ways. Endosteal or periosteal callus may be visible without a fracture line, circumferential periosteal reaction with fracture line through one cortex may be visualized or even frank fracture may be present. In cancellous bone, stress fractures are even less well visible but may be appreciated by hardly noticeable flake like patches of new bone formation some 2–3 weeks after the onset of pain. After formation of a wider, cloudlike area of mineralized bone, the stress fracture evolves into a focal linear area of sclerosis, oriented perpendicular to the trabeculae. Calcaneal stress fractures are examples of these cancellous bone stress fractures. Even though sensitivity of the conventional radiograph is very low, this examination is mandatory as a first imaging study to rule out differentials as infection, malignancy or overt fracture. With a high index of suspicion, the radiologist should initiate further studies in the case of a negative examination, in no case accepting an unremarkable film as the final answer. 3.2. State of the art imaging Although triple phase technetium-99m biphosphate bone scintigraphy has been the standard of reference in past decades, recent years have brought about a growing consensus of MRI being a superior imaging tool [15]. One study comparing MRI, bone scintigraphy and radiography of stress fractures in the pelvis and the lower extremity reports a specificity of 86% combined with a sensitivity of 100%, accuracy of 95%, positive predictive value of 93% and negative predictive value of 100% [16]. More studies have shown MRI to be at least as sensitive as scintigraphy [17–24], at the same time having significantly higher specificity. MRI has promising features to give a reliable estimate of treatment time by dividing stress fractures into four grades depending on the appearance of a basic set of three MRI sequences (short tau inversion recovery (STIR) images, T1 weighted and T2 weighted images) [22,25] (Table 1). Grade 1 stress fractures show mild to moderate periosteal edema on STIR images but no marrow abnormalities. Grade 2 shows moderate to severe periosteal edema on STIR images with added marrow edema on T2 weighted images. Grade 3 ads marrow edema on T1 weighted images and in grade 4 stress fractures a fracture line is clearly visible. Time of conservative treatment increases with grade as is shown in Table 1. This grading system can be used in symptomatic as well as asymptomatic individuals, facilitating comparison between different
1 2 3 4
Positive STIR 1 + positive T2W 2 + positive T1W 3 + definite fracture line a b
Treatment by relative rest Fredericson et al.a
Arendt and Griffithsb
2–3 weeks 4–6 weeks 6–9 weeks 6 weeks cast + 6 weeks rest
3 weeks 3–6 weeks 12–16 weeks >16 weeks
[22]. [25].
studies. However, therapy consequences should be restricted to symptomatic individuals only, since reports show stress fracture findings in asymptomatic individuals continuing training at the same level do not progress to grade 4 fractures [13,26]. In certain cases computer tomography (CT) may be of added value in the work-up of stress fracture diagnosis. However, even though technical advances have provided sub millimeter isotropic voxel imaging with high resolution reconstructions in any plane, multidetector CT still has low sensitivity for detecting stress fractures compared to bone scintigraphy (and thus MRI) [27]. Adding the disadvantage of radiation dose, CT should not routinely be used as an initial investigation. If performing MRI is not possible (e.g. in claustrophobic patients or patients with pacemaker implants) or sites of interest are not well visualized with MRI (e.g. sacrum, pelvis or spine), CT could be a useful alternative. More importantly, if MRI is equivocal on a grade 4 stress fracture or more information is needed for surgical planning, CT in our experience proves to be useful. In addition, CT may be helpful if differentials like malignancy, osteomyelitis/Brodie’s abscess or osteoid osteoma have not confidently been ruled out. Whether newer scanners with 64 or more detector rows will change the position of CT in the work-up of stress fracture diagnosis will have to be investigated by future studies. In these studies, attention has to be given to the possible capability of early stress fracture diagnosis with CT by detection of focal osteopenia, possibly a precursor of stress fractures [27]. Some reports have stated ultrasound to be of value when used for superficially located stress fractures, like in metatarsals and the fibula, but no large trials have been undertaken [28–30]. Typical findings described are periosteal elevation with small fluid collection, soft tissue edema, hypervascularity and increased posterior shadowing. 4. Treatment and prevention Relative rest, meaning cessation of the offending activity, will be adequate therapy in lower grade low risk stress fractures, while immobilization by bed rest or use of crutches may be necessary in higher grades. However, high risk stress fractures at certain anatomic locations will not heal without surgery or are likely to evolve to delayed union, non-union or displaced complete fractures. Important examples of these high risk
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stress fractures are tension sided femoral neck, patella, anterior tibial diaphysis, medial malleolus, tarsal, fifth metatarsal and great toe sesamoid stress fractures. Stress fractures of these bones should be treated more aggressively [31]. Use of nonsteroidal anti-inflammatory drug (NSAID) should be avoided or be kept as short as possible. Although no definite evidence in humans exists, animal studies have shown NSAID use to delay fracture healing and cause non-union [32,33]. Compliance is critical and alternative exercise programs to prevent detraining may help the injured athlete. A pain-free period of 2–3 weeks with full weight bearing allows the athlete to gradually resume sporting activity well below former levels. As rule of thumb, activity should not be increased more then 10% a week and recurrence of pain mandates 2 weeks of modified activity [5].
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Stress fractures are best prevented with gradual changes of training regimen, be it intensity, type of exercise or materials used (surface and shoes). A paper by Fredericson et al. discusses the effect of playing ball sports in childhood and adolescence, which significantly lowers future risk of stress fracture development [34]. This may be caused by denser bone formation due to constant microdamage to the bone during these sports, number of years played directly being related with decrease in stress fracture risk. An experimental study in rats shows that exercise programs aimed at modifying bone structure may be a feasible prevention strategy for stress fractures [35]. Prophylactic treatment with biphosphonates (risedronate), commonly used in treating osteoporosis, did not show reduction of stress fracture incidence in a military training population at high risk of stress fractures [36].
Fig. 1. 29 year old male, unsupervised recreational athlete training for marathon, running 10 miles a week. Insidious onset of right groin pain since one month, not relieved by rest. MRI with coronal STIR sequence (a) and coronal T1-weighted sequence (b), showing edema (arrow heads) and overt fracture line (arrows), making this a grade 4 stress fracture. X-ray performed the same day (c), showing hardly discernable sclerotic line at the stress fracture site (arrow). Follow-up MRI at one month of relative rest shows remarkable decrease of edema and no discernable fracture line on T1-weighted (d) and STIR sequences (e).
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5. Specific fracture sites 5.1. Femur/femoral neck (tension side = high risk, compression side = low risk) Stress fractures of the femur can occur throughout the bone, but most commonly affect the femoral neck, one of the contributing factors being fatigue of the gluteus medius muscle resulting in diminished shock absorbance [37]. In addition to the general risk factors mentioned earlier, coxa vara seem to predispose for femoral neck fractures [38]. The complications of femoral neck fractures make this entity more important than its incidence, possible devastating results for the athlete ensue if complaints are ignored, being delayed union, non-union, fragment dislocation or a vascular femoral head necrosis. In 2004 Provencher et al. proposed a modification of a classification system described by Fullerton and Snowdy in 1988, before the advent of MRI [39]. On the basis of three cases of atypical tension sided femoral neck stress fractures that healed by conservative treatment, they included this category to prevent all tension sided femoral neck stress fractures from being operated on, as advised by the previous classification. Femoral neck stress fractures thus can be classified into four groups: compression (inferior aspect) (Fig. 1), tensile (mid to distal superior aspect), displaced (Fig. 2) and atypical tensile (proximal superior aspect near femoral head) [40]. Conservative treatment is adequate for compression type stress fractures involving less than 50% of neck width and atypical tensile type, surgery is advised for all remaining types. Five to 7 year follow up of 25 patients treated for femoral neck fractures (17 operative) showed 68% was still feeling bothered or even disabled [41]. 5.2. Patella (transverse = high risk, longitudinal = low risk) Stress fractures of the patella can be transverse in direction or longitudinal, the former being caused by traction forces the latter by compression against the femoral condyles [5]. Transverse stress fractures have increased risk of becoming frank fractures and should be treated by non-weight bearing cast immobilization with the knee extended for 4 weeks. Displaced patellar stress fractures require surgical treatment. 5.3. Tibia (anterior midshaft or medial malleolus = high risk, posteromedial aspect = low risk) The tibia is reportedly the most affected bone in the body, representing 20–75% of all stress fractures [31]. Compression sided tibial stress fractures affecting the posteromedial cortex are the most frequently encountered and will mostly heal with relative rest. The longitudinal stress fracture is more uncommon, difficult to differentiate from shin splints without MRI, and will also heal with relative rest. Less often encountered but more complicated tension sided stress fractures occur at the anterior cortex, showing a transverse lucent line with bordering sclerosis on lateral radiographs or MRI (Fig. 3). Caused by jumping and leaping activities, these fractures are prone to delayed and non-union and the radio-
Fig. 2. 41 year old female with insidious onset of pain in the left groin, no recollection of trauma. Initial exams were negative. Follow up at 4 months (a) and 16 months (b) show very slow healing of a mildly dislocated stress fracture of the neck of the left femur (arrows).
graphic appearance has therefore been connotated the dreaded black line [31,42]. These should be treated aggressively with surgery if conservative treatment fails, using an intramedullary tibial nail or anterior tension band plating, which according to one report shortens return to competition time [43,44]. Two even more infrequently encountered tibial stress fractures are at the medial or lateral tibial plateau and the medial malleolus. The former tends to occur in older patients than is usual for other stress fractures and if radiographs are positive,
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Fig. 3. 26 year old male professional ballet dancer, with progressive bilateral complaints of anterior tibia during jumping exercises since 8 weeks. Conventional lateral radiographs of both tibiae showing multiple wedge shaped fractures of the anterior cortex of the mid-tibia, the so called ‘dreaded black lines’, indicating high risk tension sided stress fractures (arrows).
they show a linear transverse region of sclerosis 2–3 mm wide, close to the level of the epiphyseal scar. MRI will show bone marrow edema, periosteal edema and possibly a hypointense fracture line [42] (Fig. 4). Medial malleolus stress fractures tend to occur in running and jumping [5,42]. Usually ankle effusion is present together with tenderness over the medial malleolus. The fracture extends vertically or obliquely upwards from the junction of the medial malleolus and the tibial plafond (Fig. 5). Non-displaced fractures can be treated with immobilization while displaced fractures require open reduction and internal fixation. 5.4. Fibula (low risk) Stress fractures in the fibula usually occur in the distal third, the so called ‘runners fracture’, but are also described proximally [5,45]. Compression, torsion and muscle contraction are thought to cause these fractures. Patients report lateral leg pain over the affected area, often exacerbated by exercise and relieved by rest, sometimes show swelling and redness and an antalgic gait is
common. Pressing the fibula against the tibia provokes pain, occasionally callus might be palpated. The fibula not being a weight bearing bone, these stress fractures tend to heal well by relative rest, but healing will be delayed when offending activity is not stopped. 5.5. Tarsal bones (talus and tarsal navicular = high risk, calcaneus = low risk) Of the tarsal bones the calcaneus is the most affected causing insidious onset heel pain that is aggravated by running or jumping and causes tenderness and pain with posterosuperior compression on examination. Radiographs only show changes after 2–3 weeks by a sclerotic line perpendicular to the trabecular lines, paralleling the posterior cortex on lateral images, changes at onset will only be shown with MRI or scintigraphy. Relative rest for 6 weeks with sometimes use of crutches for pain relieve will usually have a good response [5,45]. Talar stress fractures until recently were only mentioned in literature by case reports, indicating its rarity, partially explained
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Fig. 4. 42 year old male, suffering from progressive pain in the left knee during running, recently having become a recreational athlete. Grade 3 stress fracture of the medial tibia plateau, classically seen in older patients than usual, with increased signal on STIR sequence (a), lowered signal on both T2-weighted (b) and T1-weighted images (c) and sclerosis visible on axial CT (d) and coronal MPR (e) (arrows). No discrete fracture line visible, ruling out grade 4 stress fracture.
by its difficult detection by radiography. However, Sormaala et al. recently have published a MRI based study consisting of 51 consecutive recruits suffering from this entity in an 8year period, describing incidence and anatomic distribution [46]. An incidence of 4.4 (3.2–5.5)/10,000 person-years for military
recruits is reported. In 10% stress fractures were bilateral, in 67% located in the talar head, 25% in the body and the remaining 8% in the posterior talus. Talar head stress fractures were associated with tarsal navicular stress fractures in 60%, 18% was grade 4 showing a fracture line. At all anatomical locations, low grade
Fig. 5. 26 year old male professional soccer player with known medial malleolus stress fracture, anteromedial impingement and loose body of the left ankle. Radiograph (a) showing medial malleolus stress fracture at 12 months follow up, originating at classical anatomic landmark (junction of tibial plafond and medial malleolus lines, arrows). MRI and CT performed at the same day; Axial PD-weighted image showing hypointense fracture line (b) (arrow) and CT showing fracture line with bordering sclerosis (c) (arrow).
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Fig. 6. 45 year old female with insidious onset forefoot pain. At presentation, a conventional radiograph is negative (a). At 16 days periosteal reaction (arrowhead) as well as an overt fracture line (arrow) are visible at the distal shaft of the second metatarsal (b). At 7 weeks, prominent callus formation shows healing progress of stress fracture (c).
stress fractures dominated. In only 21% the talus was the single bone affected, but all recruits were successfully treated with 2–4 weeks of reduced exercise. The tarsal navicular stress fracture is of special attention because its high risk of delayed healing, delayed or non-union and even displaced complete fractures, caused by poor vascularization at the most often affected middle third of the bone. In addition, the anatomic position of the bone makes diagnosis with radiographs especially difficult, delaying diagnosis. Invariably, these fractures are linear and within the sagittal plane [12].
Stress fractures at this site are caused by explosive athletic activities involving sprinting, jumping and hurdling and patients will report medial dorsal midfoot pain, especially when jumping [5]. Extensive training on artificial turf surface may be another cause [12] as are associated foot anomalies. Palpation of the navicular bone will cause pain and patients may limp. Incomplete fractures affecting one cortex can be treated with non-weight bearing cast immobilization for 6–8 weeks followed by another 6 weeks of weight bearing cast, while complete and sclerotic fractures mandate surgery.
Fig. 7. Young male, professional athlete with pain of left forefoot during training for some weeks, especially at second metatarsal. Swelling of soft tissues and painful palpation. If relative rest applied, complaints are relieved after 3–4 days. Conventional radiograph showing mild periosteal reaction of the proximal 1/3rd of the second metatarsal (a) (arrows). Same day MRI shows markedly elevated signal intensity on axial T2-wieghted sequence with fat-saturation (arrowheads) and possible fracture line (b) (arrow). Corresponding low signal intensity on axial PD-weighted images (c) (arrowheads).
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Fig. 8. 29 year old male, no recollection of trauma, active recreational soccer player presenting with increasing pain over lateral margin of foot, present even at rest. Fracture line of the fifth metatarsal, distal to the tuberosity, was found, consistent with Jones fracture (a) (arrow). Follow up at 2 weeks (b) and 6 weeks (c) hardly show any tendency of healing, a known complication of this tension sided type of stress fracture (arrows).
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5.6. Metatarsals and sesamoids (sesamoids and fifth metatarsal = high risk, second or third metatarsal = low risk) Metatarsal stress fractures were the first to be described, being recognized as early as the mid 1850’s in soldiers subjected to long marches and therefore named march fractures. They account for approximately 10% of fractures in athletes [47], being the most affected site after the tibia. The second and third metatarsal are most often affected, the fracture typically occurring at the neck or distal diaphysis with forces being highest here in running. The patients complain of forefoot pain,
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which increases during running or jumping and is relieved by rest. Examination reveals tenderness over the affected bone and callus may be palpated after some time. Radiographs are not very sensitive, but MRI is very accurate and even ultrasound can be used for early detection (Figs. 6 and 7). This location poses no problem for healing, athletes usually can start training after 4–6 weeks when no pain is experienced anymore. Transverse stress fractures of the base of the fifth metatarsal more than 1.5 cm distal to the tuberosity are called Jones fractures (Fig. 8). Patients suffer from pain at the lateral aspect of the foot, aggravated by inversion, and are tender on palpation. Delayed union, non-union and displacement are well known complications of this tension sided stress fracture, necessitating non-weight bearing cast as initial treatment as opposed to relative rest for second and third distal metatarsal shaft fractures. Recurrence and failure of conservative treatment will result in need of surgery, usually by percutaneous screw fixation. Early surgical intervention may benefit athletes with Jones fractures [31]. Recent reports indicate that fourth metatarsal base stress fractures are very similar in behavior, needing long treatment period as well [48]. Stress fractures of the great toe sesamoids affect the medial more often than the lateral [5,42] (Fig. 9) and can lead to chronic pain due to non-union. Radiographs are difficult to interpret due to the wide variety in anatomy, especially the bipartite sesamoid. Therefore, MRI should be performed to detect significant bone marrow edema. Six weeks of non-weight bearing short leg cast that extends to the tip of the toe to prevent dorsiflexion is the treatment of choice, but failure of treatment or recurrence mandate excision or bone grafting. 6. Conclusion Raised awareness of medical staff and increased athletic activity have increased the incidence of stress fractures, now making up about 15% of the general sports medicine practice. These fractures can affect essentially every bone in the body, but are most frequent in the lower extremity. Timely diagnosis is essential to prevent dramatic consequences for the athlete, yet this is not easy. Thorough knowledge of typical sport mechanics and a high index of suspicion is needed to accurately image a professional or recreational sportsman/woman. In our opinion, radiography should still be the first examination performed, because even if a stress fracture is not visualized, differentials may be ruled out. However, negative radiographs are unreliable at any stage and should be followed by state of the art MRI, encompassing STIR, T2-weighted and T1-weigthed series for high sensitivity and specificity and for accurate prognosis of rehabilitation time. CT proves to be useful for surgical planning and ruling out differentials, and may be used in regions of the body which are not easily imaged with MRI.
Fig. 9. 27 year old female professional ballet dancer, complaining of increasing painful sensation at the base of the great toe of the right foot. Coronal MPR of MDCT (marking of right foot), showing sclerosis (arrowhead) and subtle fracture line (arrow) of medial sesamoid bone of the first ray of the right foot (a). Axial T2-weighted sequence with fat saturation showing edema of medial sesamoid (arrowheads).
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