High Risk Stress Fractures Pathogen Es is Evaluation Treatment

20 ........................................................COMP THER. 2006;32(1)

STEVEN R. MURRAY,1 MICHAEL T. REEDER,2

BRIAN E. UDERMANN,3

AND ROBERT W. PETTITT4

1Department of Kinesiology, Mesa State College,Grand Junction, CO; 2Western Orthopedicsand Sports Medicine, Grand Junction, CO;3Department of Exercise and Sport Science,University of Wisconsin, LaCrosse, WI;and 4Department of Kinesiology, California StateUniversity, Fresno, CA

O R I G I N A L A R T I C L E

High-risk stress fractures require precise assessmentand treatment because of their propensity for delayedunion, nonunion, or complete fracture and theirresulting disabling complications. Proper diagnosisnecessitates a thorough clinical evaluation, centeringon the patient’s diet and history, particularly thetraining regimen. For a definitive diagnosis, plainradiography, ultrasound, bone scintigraphy, magneticresonance imagery (MRI), and computed tomography(CT) are helpful, and each plays a specific role. High-risk stress fractures typically require aggressive treat-ment such as nonweight-bearing immobilizationcoupled with therapy and often surgery.

High-Risk Stress FracturesPathogenesis, Evaluation, and Treatment

CORRESPONDENCE Steven R. Murray, DA, Department of Kinesiology, Mesa State College, 1100North Avenue, Grand Junction, CO 81501. E-mail: [email protected]

The authors have stated that they do not have a significant financial interest orother relationship with any product manufacturer or provider of services dis-cussed in this article. The authors do not discuss the use of off-label products,which includes unlabeled, unapproved, or investigative products or devices.

Submitted for publication: January 11, 2006. Accepted: January 16, 2006.

Comprehensive Therapy, vol. 32, no. 1, Spring 2006© Copyright 2006 by ASCMSAll rights of any nature whatsoever reserved.0098-8243/06/32:20–25/$30.00 (Online) ISSN 1559–1190

INTRODUCTIONStress fractures are common overuse injuries traditionallyafflicting athletes and military personnel. They first weredescribed as “march fractures” in 1855 by Breithaupt, aPrussian military physician, who observed that militaryrecruits often displayed the signs and symptoms ofmetatarsal fractures after marching long distances (1).Some 100 years later, stress fractures were first noted inathletes (2). Today, however, stress fractures no longer areassociated primarily with athletes and military recruits, asmany laypersons exercise regularly and inevitably placethemselves at a higher risk for developing them. In fact,some 10% of all athletic injuries are stress fractures (3),affecting roughly 1% of the overall athletic population (4).

With stress fractures becoming more commonplace, itis crucial for health care providers to have a high indexof suspicion for them during patient evaluation. More-over, the propensity of high-risk stress fractures to resultin debilitating complications and, in some cases, even toresult in catastrophic bone failure, makes proper assess-ment and treatment imperative. In this article, we reviewthe pathogenesis, evaluation, and treatment of high-riskstress fractures.

PATHOGENESISThe pathogenesis of stress fractures is cyclic, repetitive,

submaximal loading of the bone. Bone tissue is dynamic,

05_Murray 4/5/06 5:14 PM Page 20

COMP THER. 2006;32(1)...............................................................21

and it adapts to the stresses placed on it by remodeling.When bone is stressed it will strain or change shape viaelastic or plastic deformation (5). The determining factorfor how bone handles physical stress is the intensity of theload, specifically if the load reaches a specific “criticallevel” (6). If the critical-level stress is repeated oftenenough, bone damage occurs to the point where microfrac-tures develop. Eventually, bone resorption outpaces boneformation during remodeling, and the bone becomes morefragile and highly susceptible to stress fractures (7).Repetitive and excessive submaximal loads overload thebone tissue and create numerous microfractures, especiallywhen the duration, intensity, or frequency of physicalactivity are rapidly increased. If this damage is not abatedthrough adequate rest, it ultimately exceeds the reparativeability of the skeletal system, and the microfracturesproliferate and eventually coalesce into a stress fracture.

Running is reported to be the predominant cause ofstress fractures, but other factors contribute to theirdevelopment such as bone composition, vascular supply,hormonal imbalances, nutritional status, and physicaltraining (6)—particularly training surface (8), trainingtechniques (9), and inappropriate footwear (8). Poor con-ditioning (8,10), muscular fatigue (4), and biomechanicalabnormalities (11), especially leg-length discrepancies(12), play a concomitant role in the development ofstress fractures, but three specific mechanical events leadto stress fractures: (a) the applied load is increased, (b)the number of repetitions is increased, or (c) the load isapplied to a smaller surface area (6,13). Regardless ofthe specific mechanical event that overstresses the boneor the other associated factors involved, the developmentof a stress fracture is the direct result of the bone’sinability to compensate for the repeated stresses.

No one sport or skeletal area has been shown to bethe lone domain of stress fractures (see Table 1 [6]),but stress fractures typically occur in the lower extrem-ities, especially the tibia (14). Runners have the highestincidence rate at 20% (4), but many types of athletesdevelop stress fractures. Women tend to be more pronethan men to developing stress fractures (8,15), with theincidence rate reported to be as much as 10–12 timeshigher (16,17). This increase in the fracture rate isbelieved to be related to women’s lower bone mineraldensity (18,19). The incidence rate is even higher forwomen with menstrual irregularities (17–20), andhypoestrogenic osteoporosis, as a result of the femaleathlete triad—osteoporosis, amenorrhea, and disor-dered eating—has been purported to explain whywomen have such a high incidence rate (6). Contro-versy does exist in the literature, and some authors

report that both sexes are at equal risk for developingstress fractures (18,21).

EVALUATIONMost stress fractures are straightforward and are classi-

fied as low risk. Typically, the patient experiences aninsidious onset of localized pain after a marked increasein the duration or intensity of exercise, usually running.For certain superficial stress fractures, pain is elicited andperiosteal thickening can be felt via palpation. Limb bio-mechanics should be assessed to ascertain concomitantrisk factors such as inflexibility, muscle imbalances, andlimb-length discrepancies as well as arch problems (22).

Some stress fractures, however, are high risk. They man-ifest with vague pain, are typically difficult to diagnosespeedily, and can lead to a prolonged recovery because of

TABLE 1Stress Fracture Sites and Commonly

Related Sports

Site of stressfracture Commonly related sports

Acromion WeightliftingFemur Running, ballet, jumping sportsFibula Distance running, aerobics,

ballet Humerus/olecranon Throwing sports, racquet sports Medial malleolus Jumping sports, distance

running Metatarsals Distance running, marching,

ballet, jumping sports Patella Hurdling, jumping sports,

running Pars interarticularis Gymnastics, diving, ballet,

volleyball, cricket,fast bowling

Ribs Throwing sports, rowing Sacrum Distance running Sesamoids of Distance running, ballet,

the foot jumping sports Tarsal bones Distance running, ballet,

sprinting, marching,jumping sports

Tibia Distance running, jumpingshots, ballet

Ulna Racquet sports, fast-pitchsoftball, gymnastics

05_Murray 4/5/06 5:14 PM Page 21

COMP THER. 2006;32(1)...............................................................22

complications with bone union (4). These stress fractures,which may require surgical treatment, occur in the femoralneck, patella, anterior cortex of the tibia, medial malleolus,talus, tarsal navicular bones, fifth metatarsal, and great toesesamoid bones (Table 2).

As a general rule, the classification of a stress fractureas either low or high risk depends on its location andpotential for serious sequelae (12,20). Most importantly,if high-risk stress fractures are not diagnosed and treatedproperly, severe complications could arise with cata-strophic consequences; therefore, an early and accuratediagnosis is essential, and a meticulous clinical evalua-tion with a high index of suspicion is warranted.

To properly evaluate and treat high-risk stress frac-tures, identifying the causative factors and modifying oreliminating them to prevent recurrence is paramount.With stress fractures being multifactorial, evaluating thepatient’s training history is essential, especially review-ing any recent, abrupt changes in training intensity and

duration, the running terrain employed, and the footwearworn. Additionally, if the bones of the lower extremityare affected, the patient’s gait should be analyzed forbiomechanical abnormalities. Special attention should begiven to the diet, bone density, and, in women, menstrualhistory. Training errors are the predominant cause ofstress fractures, but in female patients, diagnosis couldbe more complex, especially with respect to the femaleathlete triad; these factors should be assessed as well.

Initial plain radiographs are not overly helpful for diag-nosing stress fractures, as stress fractures generally do notbecome visible on x-rays for 2 to 3 wk (see Fig. 1 [13]).In fact, for most stress fractures, the definitive diagnosis isascertained through the response to simple rest (23). Twomonths of complete rest is generally all that is required formost stress fractures to heal completely. Most athletes,however, are unwilling to accept a 2-mo layoff from train-ing without visible confirmation of an injury, especiallydistance runners. Furthermore, advanced imaging may

TABLE 2High-Risk Stress Fractures, Signs and Symptoms, and Examination

Site Signs and symptoms Diagnostic evaluation Treatmenta

Femoral neck Usually insidious pain in the Usually requires bone ORIF for distraction-typegroin, buttock, or knee scan or MRI fractures

Patella Insidious pain; may Requires MRI ORIF for chronicrelate to ACL surgery or displaced fractures

Tibia (anterior) Anterior tibia pain “Dreaded black line” Consider intramedullary nailing on lateral plain films in elite athletes

Medial malleolus Medial ankle pain May be seen on plain ORIF in complete fractures films; may require MRIor bone scan

Talus Insidious ankle pain Usually requires MRI or CT Nonweight-bearingimmobilization unlessdisplaced

Tarsal navicular Insidious mid-foot pain Usually requires MRI or CT ORIF in complete fracturesFifth metatarsal Pain in mid- to proximal Often seen on plain film Consider ORIF in elite athletes

fifth metatarsalGreat toe sesamoids Tenderness directly over the May be seen on plain film; Conservative treatment initially;

plantar aspect of the MRI may help differentiate surgical evaluation first MTP joint acute from chronic in failures

stress fractureaSome controversy exists in the literature concerning proper treatments of high-risk stress fractures (7,24,25,28). We have listed treatments

for the most serious spectrum of fractures. Initial conservative treatment requires a minimum of 6–8 wk of nonweight-bearing immobilization.Surgery is often needed.

MRI, magnetic resonance imaging; ORIF, open reduction and internal fixation; ACL, anterior cruciate ligament; CT, computed tomography;MTP, metatarsophalangeal.

(Reproduced with permission from ref. 13. Copyright © 2005 The McGraw-Hill Companies. All rights reserved.)

05_Murray 4/5/06 5:14 PM Page 22

COMP THER. 2006;32(1)...............................................................23

provide indications for more specific treatment. MRIsand radionuclide bone scanning should be used. Thebone scan has been considered the “gold standard” and isextremely sensitive, detecting new bone formation asearly as 6–72 h after injury. MRI provides more anatomic

detail and can be helpful in the estimation of duration anddisability. A reasonable grading system of stress fracturesusing bone scan and MRI findings, correlating these withplain radiographs and/or CT, has been proposed (24).MRI and bone scanning may be used, but one is not aprecursor to the other. A recently published case studydemonstrates the importance of utilizing advanced imag-ing for evaluation purposes (13). In this study, identicaltwin female distance runners presented, 3 wk apart, pal-pable pain directly over their naviculars. Initial plain radi-ographs were normal (Fig. 1), but a bone scan (Fig. 2)and an MRI (Fig. 3) in the twins indicated navicularstress fractures. The use of the advanced imaging allowed

Fig. 1. Anteroposterior radiograph of the left foot of a 17-yr-oldfemale distance runner shows no evidence of a stress fracture,despite physical symptoms being present.

Fig. 2. Anterior and medial bone scan views of the feet of a17-yr-old female distance runner (the same patient seen inFig. 1) reveal diffuse uptake in the talonavicular area, mostmarked in the left navicular area.

Fig. 3. Anterior–posterior (A) and lateral (B) magnetic reso-nance imaging views indicate a nondispalced stress fracture(arrows) of the tarsal navicular bone in the right foot of theother twin, also a distance runner.

05_Murray 4/5/06 5:14 PM Page 23

COMP THER. 2006;32(1)...............................................................24

for a definitive diagnosis and led to the proper aggressivetreatment. Moreover, some authors recommend CT in theinitial evaluation to help determine whether surgical ornonsurgical treatment is warranted (24,25).

TREATMENTThe initial treatment for stress fractures is recognizing

and eliminating the predisposing risk factors. Generally,stress fractures originate from an increase in the inten-sity as well as the duration of physical activity—a “too-much-too-soon” scenario—but intrinsic factors such ashormonal imbalances and malnutrition can augmenttheir development. Women who are amenorrheic oroligomenorrheic often have lower bone mineral densitythat predisposes them to developing stress fractures(19,26,27). At a minimum, they should be encouraged todecrease their training volume and intensity so that normalmenstruation may return. In addition, encouraging oralcontraceptive use or estrogen replacement to bring aboutregular menses, to increase bone mineral density, may beappropriate (22), although controversial.

Stress fractures are classified as either low or high risk.Low-risk stress fractures generally are easy to recognizeand are treated with 6–8 wk of relative rest and cessationof the precipitating activity (6,7). The predisposing causeof the stress fractures must be eliminated (e.g., throughtraining adaptations, nutritional modifications, and/or theuse of orthoses) before the athlete resumes the precipitat-ing activity. Patients should be encouraged to maintainfitness through cross-training, but care must be taken toavoid additional stress to the affected area. Care alsomust must be taken to prevent the athlete from doing toomuch too soon. Initially, a relative rest period of up to 6 wkof nonweight-bearing activities (e.g., pool running) shouldbe employed. Low-impact activities such as swimmingand cycling should follow as pain allows. Eventually,when the patient can complete low-impact activities forextended periods pain free, a progression to high-impactactivities may follow. Generally, walking leads to joggingthen running, and the patient ultimately returns to sport-specific movements at full speed and intensity.

For high-risk stress fractures, treatment with relativerest followed by a gradual return to activity may result indelayed union and nonunion of the bone (28). Aggressivetreatment is warranted, and these types of stress fracturesoften require lengthy periods of nonweight bearing orsurgery. For example, Kaeding et al. suggest that if a nav-icular fracture is visible on CT, regardless of the presenceor absence of sclerotic margins, the treatment should beopen reduction internal fixation and 6–8 wk of postopera-tive immobilization (24). In addition, others advise that

before proceeding with aggressive rehabilitation andallowing the patient to return to activity, CT should beused to confirm healing (23). With stress fractures beingmultifactorial, educating patients about periodized train-ing, proper footwear, diet, and calcium supplementationis necessary. If poor biomechanics are suspected, fittingthe patient with orthoses is recommended.

CONCLUSIONStress fractures are commonplace today and are

caused by repetitive stresses that exceed the skeletal sys-tem’s reparative ability. Multiple factors predispose anindividual to developing stress fractures, but increasedtraining volume and intensity are the main causes. Fortu-nately, most stress fractures are recognized easily andtreated successfully with relative rest and cessation ofthe precipitating activity. Nevertheless, some stress frac-tures are considered high risk because of their potentialmorbidity and require aggressive treatment such as 6–8 wkof immobilization, therapy, and possibly surgery. Spe-cialized imaging is warranted for proper evaluation.

ACKNOWLEDGMENTSThe authors thank the Department of Radiology,

St Mary’s Hospital, Grand Junction, CO, for theirassistance.

REFERENCES1. Breithaupt MD. The pathology of the human foot [in German].

Medizin Zeitung 1855;24:169–175. 2. Devas MB. Stress fracture of the tibia in athletes or “shin soreness.”

J Bone Joint Surg Am 1958;40B:227–236. 3. McBryde AM. Stress fractures in athletes. J Sports Med 1975;3:

212–217. 4. Boden BP, Osbahr DC. High-risk stress fractures: evaluation and

treatment. J Am Acad Orthop Surg 2000;8(6):344–353. 5. Rockwood CA, Green DP. Fractures in adults. J.B. Lippincott,

Philadelphia, 1991, pp.1–8. 6. Reeder MT, Dick BH, Atkins JK, et al. Stress fractures: current con-

cepts of diagnosis and treatment. Sports Med 1996;22(3):198–212. 7. Tuan K, Wu S, Sennett B. Stress fractures in athletes: risk factors,

diagnosis, and management. Orthopedics 2004;27(6):583–591. 8. Greaney RB, Gerber FH, Laughlin RL, et al. Distribution and natural

history of stress fractures in US Marine recruits. Radiology 1983;146:339–346.

9. Frederichson M, Bergman AG, Hoffman KL, et al. Tibial stress reac-tion in runners: correlation of clinical symptoms and scintography witha new MRI grading system. Am J Sports Med 1995;23(4):472–481.

10. Stanitski CL, McMaster JH, Scranton PE. On the nature of stressfractures. Am J Sports Med 1978;6(6):391–396.

11. Sullivan D, Warren RF, Pavlov H, et al. Stress fractures in 51 run-ners. Clin Orthop 1984;187:188–192.

12. Friberg O. Leg length asymmetry in stress fractures. A clinical andradiological study. J Sports Med Phys Fitness 1982;22:485–488.

13. Murray SR, Reeder M, Ward T, et al. Navicular stress fractures inidentical twin runners: high-risk fractures require structured treat-ment. Phys Sportsmed 2005;33(1):28–33.

05_Murray 4/5/06 5:14 PM Page 24

COMP THER. 2006;32(1)...............................................................25

14. Matheson GO, Clement DB , McKenzie DC, et al. Stress fractures inathletes: a study of 320 cases. Am J Spors Med 1987;15(1):46–58.

15. Pester S, Smith PC. Stress fractures in the lower extremities of sol-diers in basic training. Orthop Rev 1992;21(3):297–303.

16. Protzman RR, Griffis CG. Stress fractures in men and women under-going military training. J Bone Joint Surg Am 1977;59:825.

17. Hulkko A, Orava S. Stress fractures in athletes. Int J Sports Med1987;8(3):221–226.

18. Myburgh KH, Hutchins J, Fataar AB, et al. Low bone density is anetiologic factor for stress fracture sin athletes. Ann Intern Med.1990;113:754–759.

19. Bennell KL, Malcolm SA, Thomas SA, et al. The incidence anddistribution of stress fractures in competitive track and field athletes:A twelve-month prospective study. Am J Sports Med 1996;24:211–217.

20. Marcus R, Cann C, Madvig P, et al. Menstrual function and bonemass in elite women distance runners: endocrine and metabolic fea-tures. Ann Intern Med 1985;102(2):158–163.

21. Peter S, Smith PC. Stress fractures in the lower extremities of sol-diers in basic training. Orthop Rev 1992;21(3):297–303.

22. Boden BP, Osbahr DC, Jimenez C. Low-risk stress fractures. Am JSports Med 2001;29(1):100–111.

23. Noakes, TD. Lore of Running: Discover the Science and Spirit ofRunning. Leisure Press, Champaine, IL, 1991.

24. Kaeding CC, Spindler KP, Amendola A. Management of trouble-some stress fractures. Instr Course Lect 2004;53:455–469.

25. Saxena A, Fullem B, Hannaford D. Results of treatment of 22 navic-ular stress fractures and a new proposed radiographic classificationsystem. J Foot Ankle Surg 2000;39(2):96–103.

26. Myburge KH, Hutchins J, Fataar AB, et al. Low bone density is anetiologic factor for stress fractures in athletes. Ann Intern Med 1990;113:754–759.

27. Barrow, GW, Saha S. Menstrual irregularity and stress fractures in col-legiate female distance runners. Am J Sports Med 1988;16:209–216.

28. Bruckner P, Bradshaw C, Bennell K. Managing common stress frac-tures: let risk level guide treatment. Phys Sportsmed 1998;26(8):39–47.

05_Murray 4/5/06 5:14 PM Page 25