Stress Fracture

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Basics

Description

  • Stress fractures are overuse injuries caused by cumulative microdamage from repetitive bone loading.
  • Stress fractures occur in different situations:
    • Fatigue fracture: abnormal repetitive stress applied to normal bone (e.g., young college athletes or new military recruits with increased physical activity demands and inadequate conditioning). Common sites include tibia, fibula, metatarsals, femoral neck, and navicular.
    • Insufficiency fracture: normal stress applied to structurally abnormal bone (e.g., femoral neck fracture in osteopenic bone, metabolic bone disease). Common sites include spine, sacrum, femoral neck, and medial femoral condyle.
    • Combination fracture: abnormal stress applied to abnormal bone (e.g., female long-distance runners with premature osteoporosis from female athletic triad)
  • Weight-bearing bones of the lower extremity are most commonly affected at the following sites:
    • Tibia/fibula
    • Metatarsal bones
    • Navicular
    • Femoral neck
    • Pars interarticularis
  • Less commonly affected sites:
    • Pelvis
    • Calcaneus
    • Ribs
    • Ulna
  • High-risk stress fractures occur in zones of tension or areas with poor blood supply and are more likely to result in fracture displacement and/or nonunion. High-risk sites include the following:
    • Tension side of femoral neck
    • Anterior tibial diaphysis
    • Sesamoids
    • Pars interarticularis of lumbar spine (L4, L5)
    • 5th metatarsal at metaphyseal–diaphyseal junction
    • Proximal 2nd metatarsal
    • Medial malleolus
    • Tarsal navicular
    • Patella
    • Talar neck
  • Synonym(s): march fracture; fatigue fracture

Epidemiology

Incidence
  • Greatest incidence in 15- to 27 year olds
  • Females have higher incidence as compared to males (attributed to female athlete triad) (1).
  • Accounts for up to 20% of visits to sports medicine and orthopedic clinics
  • Across all sports, the most commonly injured body sites are the lower leg, foot, and lower back/lumbar spine/pelvis.

Prevalence
  • Occurs in <1% of general population
  • Affects up to 6.9% of male and 21.0% of female military members
  • Affects 1–3% of college athletes
  • Affects 9–21% of track and field athletes annually

Etiology and Pathophysiology

  • Bone is dynamic and constantly remodeling in response to applied physiologic stress.
  • Repetitive loading or overuse causes microfractures that fail to heal due to imbalance between bone resorption and bone formation.
  • If microdamage accumulates in excess of reparation, bony fatigue leads to stress fracture.

Risk Factors

  • Intrinsic
    • Females are at 2.3 times higher risk than males
    • Female athlete triad (low energy availability with or without disordered eating, menstrual dysfunction, and low bone mineral density)
    • Small tibial width
    • Females with disrupted menstrual cycles are 2 to 4 times more likely to sustain stress injury (1)[C].
    • History of previous stress fracture—increases risk of future stress fracture by 5 times
    • History of osteoporosis, osteomalacia, rheumatoid arthritis, prolonged corticosteroid therapy
    • Body composition—increased risk of stress fractures with BMI <19
    • Skeletal malalignment: pes cavus/planus, leg length discrepancies, excessive forefoot varus, tarsal coalitions, prominent posterior calcaneal process, tight heel cords
    • Biomechanical factors such as increased vertical loading rate (e.g., heel-to-toe running instead of forefoot striking)
  • Extrinsic
    • Type of exercise—both male and female athletes who participate in running, track and field, cross country, and gymnastics are at highest risk
    • Training regimen—running >32 km/week increases risk by 2 times in all athletes and by 3 times in female athletes
    • Training for more than 5 hr/day
    • Nutritional/dietary habits—inadequate caloric intake or history of a diagnosed eating disorder
    • Low vitamin D of <40 ng/mL (<100 mmol/L)
    • Rapid increase in mileage, running pace, or training volume
    • Inappropriate footwear (Quality and type of footwear should fit with sport and foot/arch shape.)
    • Running surface (hard training surface)
    • Inadequate recovery or rest and training with fatigued muscle
    • Hormonal contraception: Medroxyprogesterone (DMPA) use within the last 2 years is slightly more likely to be associated with a stress fracture in comparison with use of oral contraception or no hormonal contraception. There is no evidence that use of oral contraceptives is related to stress fracture risk.

General Prevention

  • Avoid abrupt increases in physical activity (no more than 10% increase in load per week).
  • Reduce intensity and duration of activity if new-onset pain.
  • Proper footwear (Athletes should have a gait analysis prior to training.)
  • Increasing dynamic physical activity (jumping; plyometric training) increases bone density and resistance to mechanical stress.
  • Decrease vertical loading rate either by switching to forefoot strike running or (if continuing with heel-to-toe strike) by using a heel pad insert.
  • Shock-absorbing foot inserts may help.
  • Increased calcium and vitamin D intake may reduce stress fractures.
  • Adequate potassium intake from consumption of fruits and vegetables has been shown to have a beneficial effect on bone mineral density, independent of calcium.
  • Vitamin D supplementation (800 IU/day) in combination with calcium (2,000 mg/day) is effective in reducing fracture risk.

Commonly Associated Conditions

  • Osteoporosis/osteopenia
  • Female athlete triad
  • Metabolic bone disorders

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Basics

Description

  • Stress fractures are overuse injuries caused by cumulative microdamage from repetitive bone loading.
  • Stress fractures occur in different situations:
    • Fatigue fracture: abnormal repetitive stress applied to normal bone (e.g., young college athletes or new military recruits with increased physical activity demands and inadequate conditioning). Common sites include tibia, fibula, metatarsals, femoral neck, and navicular.
    • Insufficiency fracture: normal stress applied to structurally abnormal bone (e.g., femoral neck fracture in osteopenic bone, metabolic bone disease). Common sites include spine, sacrum, femoral neck, and medial femoral condyle.
    • Combination fracture: abnormal stress applied to abnormal bone (e.g., female long-distance runners with premature osteoporosis from female athletic triad)
  • Weight-bearing bones of the lower extremity are most commonly affected at the following sites:
    • Tibia/fibula
    • Metatarsal bones
    • Navicular
    • Femoral neck
    • Pars interarticularis
  • Less commonly affected sites:
    • Pelvis
    • Calcaneus
    • Ribs
    • Ulna
  • High-risk stress fractures occur in zones of tension or areas with poor blood supply and are more likely to result in fracture displacement and/or nonunion. High-risk sites include the following:
    • Tension side of femoral neck
    • Anterior tibial diaphysis
    • Sesamoids
    • Pars interarticularis of lumbar spine (L4, L5)
    • 5th metatarsal at metaphyseal–diaphyseal junction
    • Proximal 2nd metatarsal
    • Medial malleolus
    • Tarsal navicular
    • Patella
    • Talar neck
  • Synonym(s): march fracture; fatigue fracture

Epidemiology

Incidence
  • Greatest incidence in 15- to 27 year olds
  • Females have higher incidence as compared to males (attributed to female athlete triad) (1).
  • Accounts for up to 20% of visits to sports medicine and orthopedic clinics
  • Across all sports, the most commonly injured body sites are the lower leg, foot, and lower back/lumbar spine/pelvis.

Prevalence
  • Occurs in <1% of general population
  • Affects up to 6.9% of male and 21.0% of female military members
  • Affects 1–3% of college athletes
  • Affects 9–21% of track and field athletes annually

Etiology and Pathophysiology

  • Bone is dynamic and constantly remodeling in response to applied physiologic stress.
  • Repetitive loading or overuse causes microfractures that fail to heal due to imbalance between bone resorption and bone formation.
  • If microdamage accumulates in excess of reparation, bony fatigue leads to stress fracture.

Risk Factors

  • Intrinsic
    • Females are at 2.3 times higher risk than males
    • Female athlete triad (low energy availability with or without disordered eating, menstrual dysfunction, and low bone mineral density)
    • Small tibial width
    • Females with disrupted menstrual cycles are 2 to 4 times more likely to sustain stress injury (1)[C].
    • History of previous stress fracture—increases risk of future stress fracture by 5 times
    • History of osteoporosis, osteomalacia, rheumatoid arthritis, prolonged corticosteroid therapy
    • Body composition—increased risk of stress fractures with BMI <19
    • Skeletal malalignment: pes cavus/planus, leg length discrepancies, excessive forefoot varus, tarsal coalitions, prominent posterior calcaneal process, tight heel cords
    • Biomechanical factors such as increased vertical loading rate (e.g., heel-to-toe running instead of forefoot striking)
  • Extrinsic
    • Type of exercise—both male and female athletes who participate in running, track and field, cross country, and gymnastics are at highest risk
    • Training regimen—running >32 km/week increases risk by 2 times in all athletes and by 3 times in female athletes
    • Training for more than 5 hr/day
    • Nutritional/dietary habits—inadequate caloric intake or history of a diagnosed eating disorder
    • Low vitamin D of <40 ng/mL (<100 mmol/L)
    • Rapid increase in mileage, running pace, or training volume
    • Inappropriate footwear (Quality and type of footwear should fit with sport and foot/arch shape.)
    • Running surface (hard training surface)
    • Inadequate recovery or rest and training with fatigued muscle
    • Hormonal contraception: Medroxyprogesterone (DMPA) use within the last 2 years is slightly more likely to be associated with a stress fracture in comparison with use of oral contraception or no hormonal contraception. There is no evidence that use of oral contraceptives is related to stress fracture risk.

General Prevention

  • Avoid abrupt increases in physical activity (no more than 10% increase in load per week).
  • Reduce intensity and duration of activity if new-onset pain.
  • Proper footwear (Athletes should have a gait analysis prior to training.)
  • Increasing dynamic physical activity (jumping; plyometric training) increases bone density and resistance to mechanical stress.
  • Decrease vertical loading rate either by switching to forefoot strike running or (if continuing with heel-to-toe strike) by using a heel pad insert.
  • Shock-absorbing foot inserts may help.
  • Increased calcium and vitamin D intake may reduce stress fractures.
  • Adequate potassium intake from consumption of fruits and vegetables has been shown to have a beneficial effect on bone mineral density, independent of calcium.
  • Vitamin D supplementation (800 IU/day) in combination with calcium (2,000 mg/day) is effective in reducing fracture risk.

Commonly Associated Conditions

  • Osteoporosis/osteopenia
  • Female athlete triad
  • Metabolic bone disorders

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