Updated: Nov 7, 2007
Stress fractures are a common problem in various populations, including runners and military trainees.1,2,3 These fractures can occur with as little as 2-3 weeks of training, be very mild, and cause only minimal changes to the bone, which eventually heals, or they may progress to a complete fracture that requires surgical fixation. Although rare, poor outcomes may occur in the form of nonunions or avascular necrosis. Certain stress fractures have a higher risk of poor outcome, including anterior tibial and femoral neck stress fractures (FNSFs).
(See also the eMedicine articles Femoral Head Avascular Necrosis [in the Sports Medicine section], Avascular Necrosis, Femoral Head and Stress Fracture [in the Radiology section], and Stress Fracture [in the Physical Medicine and Rehabilitation section], as well as Risk Factors for Bone tress Injuries: A Follow-up Study of 102,515 Person-Years and Total Hip Arthroplasty in the Older Population on Medscape.)
FNSFs are some of the most difficult injuries to diagnose. The pain associated with such an injury may be poorly localized in the hip and may be referred to the thigh or back. Physical examination findings are not very specific for this injury, and diagnostic radiographs in the form of x-ray films, bone scans, and/or magnetic resonance images (MRIs) are often necessary.4 Failure to diagnose FSNFs may lead to catastrophic consequences, including avascular necrosis of the femoral head and the need for a hip replacement in otherwise healthy young individuals.5,6,7 A high index of suspicion in the appropriate risk populations is the key to diagnosing and treating FNSFs.
(See also the eMedicine article Femoral Neck Stress and Insufficiency Fractures.)
For excellent patient education resources, visit eMedicine's Foot, Ankle, Knee, and Hip Center; Breaks, Fractures, and Dislocations Center; and Sports Injury Center. Also, see eMedicine's patient education articles Broken Leg and Total Hip Replacement.
Stress fractures may develop in up to 15% of runners and military trainees.3 Of those patients who develop stress fractures, about 5-10% of the fractures are in the femoral neck.8 Stress fractures on the compression side (the inferior aspect) of the femoral neck are more common than stress fractures on the tension side (the superior aspect).
The femoral neck lies between the femoral head and femoral shaft, demarcated by the greater and lesser trochanters. Weight-bearing forces from the trunk cause a compressive force on the inferior aspect of the femoral neck, whereas the superior aspect is subject to tensile forces.6,9 The blood supply to the femoral head runs through the femoral neck; thus, an FNSF may disrupt the blood supply to the femoral head and cause avascular necrosis of the femoral head.6
The load of the runner's body weight is transmitted down the lower extremities through the bones and may exceed 3-5 times the body weight in the femoral neck during running. Muscles help to absorb forces and distribute load, especially the gluteus medius. The weight of the trunk and upper extremities applies compressive forces to the inferior aspect of the femoral neck. Conversely, tensile forces act upon the superior aspect of the femoral neck. These forces become important in the prognosis and management of the stress fracture. A sudden reduction in weight and lower muscle mass combined with daily training was associated with an increased risk of FNSF in US Naval Academy plebes.3
| Femoral Head Avascular Necrosis | Iliopsoas Tendinitis |
| Femoral Neck Fracture | Osteitis Pubis |
| Groin Injury | Piriformis Syndrome |
| Hip Dislocation | Sacroiliac Joint Injury |
| Hip Fracture | Slipped Capital Femoral Epiphysis |
| Hip Pointer | Snapping Hip Syndrome |
| Hip Tendonitis and Bursitis |
Avascular Necrosis, Femoral Head
Bone tumors
Degenerative arthritis
Hip capsulitis and synovitis
Inflammatory arthropathy
Legg-Calve-Perthes Disease (in the Radiology section) (See also Legg-Calve-Perthes Disease [in the Emergency Medicine section] and Legg-Calve-Perthes Disease [in the Orthopedic Surgery section].)
Rectus femoris tendonitis
Referred pain from a herniated disk in the lower back
Septic hip
Slipped Capital Femoral Epiphysis (in children)
Trochanteric Bursitis
Follow the acute treatment principles of protection, rest, ice, compression, elevation, medication, and modalities (PRICEMM). This treatment regimen is most appropriate for compression (as opposed to tension) fractures. Patient compliance is important.
If the stress fracture is on the compression side of the femoral neck and if the fracture is not displaced, patients usually do well with conservative management (non-weight bearing on crutches), with a gradual progression to touchdown weight bearing, partial weight bearing, then to no crutches in 4-6 weeks, depending upon the clinical response.
Tension-side fracture treatment is somewhat controversial, with some physicians advocating surgical pinning (even for nondisplaced fractures) and others advocating conservative treatment such as for compression-side fractures. In a compliant patient who will maintain non-weight bearing on crutches, a trial of conservative treatment with non-weight bearing on crutches is recommended for both types of fractures unless displacement is present, in which case, urgent referral for operative evaluation and fixation is indicated.
Treatment of the tension-side stress fracture is based on the completeness of the fracture (ie, unicortical vs bicortical), which, in turn is, based on a classification scheme. In general, bicortical tension-side fractures are treated surgically.
Surgical intervention is dependent upon the type of fracture. Compression-side fractures can be treated with conservative therapy. Nondisplaced tension-side treatment is controversial, with some physicians advocating prophylactic surgical fixation and others advocating a trial of conservative therapy in compliant patients. Urgently refer the patient for orthopedic evaluation for surgical fixation in cases with displaced fractures.
Regardless of the presence or absence of fracture displacement, tension-side stress fractures of the femoral neck should be managed in coordination with an orthopedic specialist.
Review the patient's diet; ensure adequate calcium and vitamin D intake, and supplement as needed. Consider oral contraceptives for amenorrheic women; such agents may aid in the recovery of bone mass in these women. Athletes with eating disorders may need psychologic and nutritional support.
As the patient’s pain decreases, gradually increase activity from non-weight bearing to touchdown weight bearing, then to partial weight bearing, and eventually, discontinuation of the crutches. This process usually takes 4-6 weeks. Coordinate the patient's rehabilitation with the orthopedic specialists for those individuals who have hips with surgical pinning. After the patient is able to walk 1.5 miles without pain (usually in 8-12 wk, but sometimes longer), begin a gradual return to a running program. Usually, it takes approximately 2.5 months to be able to run 3 miles pain free. If pain returns during the rehabilitation period, decrease the patient's activity until walking is pain free again.
Non–weight-bearing training can also play a role in the patient's rehabilitation. Activities such as running in water with an appropriate floatation vest can be helpful. Upper-extremity resistance exercises and aerobic training can also be used.
A very mild pain may return briefly when the patient first attempts to run. If the pain is more than a very mild intensity, the stress fracture may not have healed completely yet and needs additional rest. If the patient's pain is severe, obtain another x-ray to check for displacement. Avascular necrosis, nonunion, malunion, and eventual hip replacement may result from complications of an FNSF that is not diagnosed in time or that is rehabilitated too quickly.
If the patient's pain persists for longer than 2 weeks — despite true compliance with non–weight-bearing status on a tension-side, nondisplaced stress fracture — consider surgical fixation, if the procedure has not already been performed.
Consult an orthopedic specialist if the patient's rehabilitation for an FSNF is not progressing adequately.
Ensure the patient has an adequate calcium and vitamin D intake. If an eating disorder is present, monitor the patient's treatment and help the patient recover proper dietary and weight-management habits.
Monitor the patient's activity to ensure that the same training errors that initially resulted in the stress fracture are not committed again. Gradual increases in mileage (£ 10%/wk) are generally accepted as safe and effective. Likewise, the intensity of the patient's workouts should increase gradually, not dramatically.
If the same type of pain reappears despite therapy, the patient should return to the clinician to check for a recurrent stress fracture.
If the femoral neck was surgically fixed, consult the orthopedic specialist regarding when (if ever) the pins should be removed.
Obtain an orthopedic consultation if the patient's recovery is not progressing adequately.
The patient should continue calcium supplementation, if necessary. Monitor for recurrence of an eating disorder, if appropriate.
The goals of pharmacotherapy are to reduce morbidity and to prevent complications in patients with FNSFs.
Calcium supplementation may be necessary for patients with FNSFs. The average daily recommendations for children aged 9-18 years is 1300 mg of calcium daily. Individuals aged 19-50 years and postmenopausal women should have a daily calcium intake of 1000 mg of calcium. Middle-aged women and males 50 years and older should receive 1200 mg of calcium daily. Vitamin D supplementation may also be necessary.
Used for the supplementation of calcium. Give the amount that is needed to supplement an individual's diet to reach the recommended daily amounts.
500 mg PO qd
Not established
May decrease the effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; IV administration antagonizes the effects of verapamil; large intakes of dietary fiber may decrease calcium absorption and levels
Renal calculi, hypercalcemia, hypophosphatemia, renal or cardiac disease, patients with digitalis toxicity
A - Fetal risk not revealed in controlled studies in humans
Caution in digitalized patients and in the presence of respiratory failure or acidosis
Moderates nerve and muscle performance by regulating the action potential excitation threshold. Give the amount that is needed to supplement an individual's diet to reach the recommended daily amounts.
200 mg PO qd
Not established
May decrease the effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; IV administration antagonizes the effects of verapamil; large intakes of dietary fiber may decrease calcium absorption and levels
Renal calculi, hypercalcemia, hypophosphatemia, renal or cardiac disease, patients with digitalis toxicity
A - Fetal risk not revealed in controlled studies in humans
Caution in digitalized patients and in the presence of respiratory failure or acidosis
NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. The mechanism of action of these agents is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions. Many NSAIDs are currently on the market. There is no evidence to support that one agent is more efficacious than another; however, individual response may differ.
The routine use of NSAIDs for treating stress fractures has been called into question because these drugs have been shown to slow bone formation and may mask the pain that serves as a guide for the timing of advancing rehabilitation.11 Therefore, administer NSAIDs sparingly for initial pain, if at all. Furthermore, with the other complications of NSAIDs (eg, gastrointestinal [GI] bleeding) and the known difficulties with COX-2 inhibitors, caution is advised.
DOC for patients with initial mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis. May slow bone healing, so use sparingly.
200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d
<6 months: Not established
6 months to 12 years: 4-10 mg/kg/dose PO tid/qid
>12 years: Administer as in adults
Coadministration with aspirin increases the risk of inducing serious NSAID-related side effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; patients with peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or a high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Category D in third trimester of pregnancy; caution patients with congestive heart failure, hypertension, and decreased renal and hepatic function; caution in the presence of coagulation abnormalities or during anticoagulant therapy
For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis. May slow bone healing, so use sparingly.
500 mg PO followed by 250 mg PO q6-8h; not to exceed 1.25 g/d
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
Coadministration with aspirin increases the risk of inducing serious NSAID-related side effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Category D in third trimester of pregnancy; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug
For relief of mild to moderate pain and inflammation.
Small dosages are initially indicated in small and elderly patients and in those with renal or liver disease. Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution, and closely observe patient for response. May slow bone healing, so use sparingly.
25-50 mg PO q6-8h prn; not to exceed 300 mg/d
<3 months: Not established
3 months to 12 years: 0.1-1 mg/kg PO q6-8h
>12 years: Administer as in adults
Coadministration with aspirin increases the risk of inducing serious NSAID-related side effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Category D in third trimester of pregnancy; caution in patients with congestive heart failure, hypertension, and decreased renal and hepatic function; caution in the presence of coagulation abnormalities or during anticoagulant therapy
Once the athlete has completed the walk/run rehabilitation program and is able to run 3 miles without pain, gradually increase the mileage (no more than 10% per wk) until the goal level is obtained. Gradual sport-specific drills and higher-intensity training should be accomplished over a few weeks.
Complications of FNSFs include recurrence of the stress fracture and avascular necrosis of the femoral head.
Prevention of FNSFs includes gradually increasing the intensity and duration of training; halting/decreasing training upon return of symptoms; and reevaluating the patient for stress fracture recurrence, adequate calcium intake, and further treatment of an eating disorder (if appropriate).
Compression-side fractures have an excellent prognosis. Usually, if the injury is diagnosed early and the patient does not return to training too rapidly, tension-side fractures also do well. However, up to 25% of patients may have residual hip pain, discomfort, and gait problems 5-7 years after treatment.
Displaced fractures have a guarded prognosis until after surgical fixation, and then the patients undergo evaluation for another 4-6 weeks. Even after surgical fixation, displaced FNSFs have a high prevalence of avascular necrosis, with one case series reporting a rate of 24%.6 The authors reported persistent pain and a poor outcome occurred in 19% of the 42 patients.
Shaffer RA, Rauh MJ, Brodine SK, Trone DW, Macera CA. Predictors of stress fracture susceptibility in young female recruits. Am J Sports Med. Jan 2006;34(1):108-15. [Medline]. [Full Text].
DeFranco MJ, Recht M, Schils J, Parker RD. Stress fractures of the femur in athletes. Clin Sports Med. Jan 2006;25(1):89-103, ix. [Medline].
Armstrong DW 3rd, Rue JP, Wilckens JH, Frassica FJ. Stress fracture injury in young military men and women. Bone. Sep 2004;35(3):806-16. [Medline].
Shin AY, Gillingham BL. Fatigue fractures of the femoral neck in athletes. J Am Acad Orthop Surg. Nov 1997;5(6):293-302. [Medline].
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. May 2003;17(5):334-7. [Medline].
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. Dec 2003;123(10):527-33. [Medline].
[Best Evidence] Pihlajamäki HK, Ruohola JP, Kiuru MJ, Visuri TI. Displaced femoral neck fatigue fractures in military recruits. J Bone Joint Surg Am. Sep 2006;88(9):1989-97. [Medline].
Egol KA, Koval KJ, Kummer F, Frankel VH. Stress fractures of the femoral neck. Clin Orthop Relat Res. Mar 1998;348:72-8. [Medline].
Jones BH, Harris JM, Vinh TN, Rubin C. Exercise-induced stress fractures and stress reactions of bone: epidemiology, etiology, and classification. Exerc Sport Sci Rev. 1989;17(1):379-422. [Medline].
Carpintero P, Leon F, Zafra M, et al. Stress fractures of the femoral neck and coxa vara. Arch Orthop Trauma Surg. Jul 2003;123(6):273-7. [Medline].
Stovitz SD, Arendt EA. NSAIDs should not be used in treatment of stress fractures [letter]. Am Fam Physician. Oct 15 2004;70(8):1452, 1454. [Medline]. [Full Text].
Beck TJ, Ruff CB, Mourtada FA, et al. Dual-energy X-ray absorptiometry derived structural geometry for stress fracture prediction in male U.S. Marine Corps recruits. J Bone Miner Res. May 1996;11(5):645-53. [Medline].
Blomfeldt R, Törnkvist H, Eriksson K, et al. A randomised controlled trial comparing bipolar hemiarthroplasty with total hip replacement for displaced intracapsular fractures of the femoral neck in elderly patients. J Bone Joint Surg Br. Feb 2007;89(2):160-5. [Medline].
Kunesová M, Koudela K Jr, Koudela K Sr, Koudelová J. [Magnetic resonance imaging for examination of proximal femoral fractures: its contribution to clinical medicine] [Czech]. Acta Chir Orthop Traumatol Cech. Dec 2006;73(6):380-6. [Medline].
Lloyd T, Petit MA, Lin HM, Beck TJ. Lifestyle factors and the development of bone mass and bone strength in young women. J Pediatr. Jun 2004;144(6):776-82. [Medline].
Macaulay W, Yoon RS, Parsley B, Nellans KW, Teeny SM. Displaced femoral neck fractures: is there a standard of care?. Orthopedics. Sep 2007;30(9):748-9. [Medline].
Maitra RS, Johnson DL. Stress fractures. Clinical history and physical examination. Clin Sports Med. Apr 1997;16(2):259-74. [Medline].
Pihlajamäki HK, Ruohola JP, Weckström M, Kiuru MJ, Visuri TI. Long-term outcome of undisplaced fatigue fractures of the femoral neck in young male adults. J Bone Joint Surg Br. Dec 2006;88(12):1574-9. [Medline].
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. Sep 2004;32(6):1528-34. [Medline].
Raaymakers EL. Fractures of the femoral neck: a review and personal statement. Acta Chir Orthop Traumatol Cech. 2006;73(1):45-59. [Medline].
Shimizu T, Miyamoto K, Masuda K, et al. The clinical significance of impaction at the femoral neck fracture site in the elderly. Arch Orthop Trauma Surg. Sep 2007;127(7):515-21. [Medline].
Strömqvist B, Hansson LI, Ljung P, Ohlin P, Roos H. Pre-operative and postoperative scintimetry after femoral neck fracture. J Bone Joint Surg Br. Jan 1984;66(1):49-54. [Medline]. [Full Text].
Yih-Shiunn L, Chien-Rae H, Wen-Yun L. Surgical treatment of undisplaced femoral neck fractures in the elderly. Int Orthop. Oct 2007;31(5):677-82. [Medline].
stress fracture of the hip, hip pain, hip replacement, total hip replacement, femoral stress fracture, FNSFs
Scott D Flinn, MD, Medical Director, Directorate for Primary Care, Primary Care, Naval Medical Center San Diego
Scott D Flinn, MD is a member of the following medical societies: American Academy of Family Physicians and American Medical Society for Sports Medicine
Disclosure: Nothing to disclose.
Gerard A Malanga, MD, Associate Professor, Department of Physical Medicine and Rehabilitation, New Jersey Medical School; Director of Pain Management, University of Medicine and Dentistry at New Jersey, Overlook Hospital; Director of Sports Medicine, Mountainside Hospital
Gerard A Malanga, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Jon B Whitehurst, MD, Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner and Executive Board Member, Rockford Orthopedic Associates; Orthopedic Chairman, Rockford Memorial Hospital
Jon B Whitehurst, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.
Sherwin SW Ho, MD, Associate Professor, Department of Surgery, Section of Orthopedic Surgery and Rehabilitation Medicine, University of Chicago
Sherwin SW Ho, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.
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