Stress fracture

1. STRESS FRACTURE

2. FATIGUE FRACTURE
Fracture occurs through an otherwise normal bone that is
subjected to repeated episodes of stress, less severe than that
necessary to produce an acute #.
Results from summation of stresses any one of which by itself
would have been harmless.
Overuse injuries.

3. By repetitive submaximal forces that exceed the adaptive
ability of the bone.
Common in athletes & military recruits.
1% incidence in athletes, 20% in runners.
Females prone [female athlete triad]
late adolescence and early adulthood
Increasing incidence in elderly.

4. Weight bearing lower limb bone prone
Tibia – [50%] most common
Tarsals & metatarsals
Specific anatomic sites
- shaft of humerus  cricket/ throwing sp.
- ribs  golf & rowing
- spine  pars # gymnastics
- pubic rami  inferior in children, both in
adults
- lower extremities  running activities.

5. -Femoral neck  any age
-Femoral shaft  lower third
-Patella  children & young athletes
-Tibial shaft pro 3
rd
in children, mid 3
rd
in athletes, distal 3
rd

in elderly.
-Fibula high shaft – jumpers, distal 3
rd
in runners.
-Calcaneum  adults / compression stress/ anterior to
tuberosity.
-Metatarsals  march # / 2
nd
MT neck.
-Great toe sesamoids.

6. PATHOGENESIS
Excessive, repetitive, submaximal loads on bones that cause
an imbalance between bone resorption and formation.
An abrupt increase in the duration, intensity, or frequency of
physical activity without adequate periods of rest may lead to
an escalation in osteoclast activity.
During periods of intense exercise, bone formation lags
behind bone resorption.

7. When bone subjected to hyper physiological loads, its
ultimate strength decreases  susceptible to microfractures
Continuous loading  microcracks coalesce to stress #.
ETIOLOGY – multifactorial
Depends on type of bone composition, vascular supply,
surrounding muscle attachments, systemic factors, athletic
type.
Role of muscle – M . Fatigue, concentrating forces to
localised area.

8. Intrinsic factors
Hormonal imbalances
- female, estrogen deficiency.
- male athletes – testosterone- inhibits IL-6 – osteoclast
production - activity.
Nutritional deficiencies
Sleep deprivation
Collagen abnormalities
Metabolic bone disorders

9. Stages in development
1.Crack initiation
2.Crack propagation
3.Rapid failure of bone.
Bone can repair itself quickly, pathological strain is
removed before the third stage.

10. Clinical features
History of unaccustomed & repeated activity.
Sequence – pain after exercise, pain during ex, pain without
ex.
Load related pain – early symptom
 general health, medications, diet, and menstrual history in
women
Increase in training volume or intensity, a change in
technique or surface, or an alteration of footwear

11. H/O previous stress fractures or other painful sites, and the
presence of eating disorders,
Limb biomechanics - leg length discrepancy, or muscle
imbalance, excessive subtalar pronation.
Focal bone pain with palpation and stressing – Hall mark.
Local swelling- callus –late presentations
Location of pain – medially / femoral shaft
Inaccessible sites – femoral neck - movts

12. Imaging modalities
Confirm the diagnosis, more information for differential
evaluation.
X- RAY
Normal – 1
st
2-3 wks after the onset of symptoms
Periosteal response – 3 months after onset of symptoms.
Periosteal bone formation, horizontal or oblique linear
patterns of sclerosis, endosteal callus, and a frank fracture
line.

13. Gray cortex  ovoid lucency with in a thickened area of
cortical hyperostosis  radiolucent line with extension
partially or completely across the cortex
cancellous bone  a fracture lucency oriented perpendicular
to the trabeculae.
X ray more useful in fibula & metatarsals.

14. Scintigraphy
Sensitive method
Confirming clinically suspected stress fractures.
Acute stress fractures are depicted as discrete, localized,
areas of increased uptake on all three phases of a Tc-99m
Soft-tissue injuries are characterized by increased uptake
only in the first two phases.
Lacks specificity.

15. Indications for bone scan
suspected lesions in the spine or Pelvis
identifying multiple stress fractures,
distinguishing bipartite bones from stress fractures.
- positive images in phase III persists – many months, should
not be used to monitor healing and dictate return to activity.

16. CT scan
Navicular bone
Diaphyseal bone with longitudinal # lines
Pars & sacral stress # .

17. SPECT scanning
suspected pars interarticularis and sacral stress fractures

18. MRI
More specific
Avoids radiation exposure
Less time
More expensive
Grading the stage of certain stress fractures and, therefore,
predicting the time to recovery
femoral neck stress fracture in an athlete.

19. Radiological grading

20. Treatment Overview
Fundamental principle of initial management is REST to
allow the bone remodeling process to equilibrate.
identifying and correcting any predisposing factors.
Hormone replacement therapy.
Training errors - identified and corrected

21. Low risk stress #
Diagnosed on the basis of a thorough history, physical
examination, and radiographs.
A rest period of 1 to 6 weeks of limited weight bearing
progressing to full weight bearing  phase of low-impact
activities  high impact activities.

22. HIGH RISK STRESS #
predilection for progressing to complete fracture, delayed
union, or nonunion
more aggressive treatment approach
fractures include those in the femoral neck (tension side),
patella, anterior cortex of the tibia, medial malleolus, talus,
tarsal navicular, fifth metatarsal, and great toe sesamoids.
Due to high complication rate treated as acute #

24. HR # of the lower leg and foot - aggressive nonoperative
protocol consisting of non-weight-bearing cast
immobilization.
Exception to this rule is the tension-side femoral neck stress
fracture,which requires internal fixation

25. Differential diagnosis
Stress reaction
periostitis, infection,
avulsion injuries, muscle strain,
bursitis, neoplasm,
Exertional compartment syndrome, and nerve entrapment.

26. PREVENTION
Training errors - most frequent culprit and should be
corrected.
Assessment of the type and condition of the running
shoes
Viscoelastic insoles, may help reduce the incidence of
lower-extremity stress fractures.
Education – parents, coaches, military personnel –
periodic rest.
Female athletes – alerted , eating disorders, hormonal
abnormalities.

27. Femoral neck #
High complication rate
Due to hip musculature fatigued due to prolonged activity &
subsequent loss of shock absorbing effect.
Coxa vara & osteopenia
Pain at extremes of rotation.
More common is compression type –benign

28. Distraction or tension stress # - starts in superior cortex
High chance of displacement & progression
Grade 3 or grade 4 tension-side femoral neck stress fractures
should be stabilized with multiple screw fixation to promote
healing and prevent displacement.
avoid lateral entry points below the midportion of the level
of the lesser trochanter

29. Tibial fractures
Most common site [20-75%]
Posteromedial cortex [compression side] most common.
Transverse # common
Longitudinal # ,atypical presentation, MRI
Conservative Rx.
Pneumatic brace – supplemental use – early return of
activities.

30. More problematic – anterior cortex of middle 3
rd
of shaft.
X ray – subtle, high incidence of suspicion
Both constant tension from posterior muscle forces and
hypovascularity of the anterior aspect of the tibia predispose
this site to nonunion or delayed union.
Tension side # occurs in those performing repetitive
jumping & leaping activities.

31. V –shaped defect in the anterior cortex
Callus formation – absent
Dreaded black line.
Anterior tibial stress fractures with an established transverse
cortical lucency have limited healing potential even with
activity modification
Reamed intramedullary nailing predictably leads to healing of
the stress fracture in a shorter time course.

33. Medial Malleolus
Repetitive impingement of the talus on the medial malleolus
during ankle dorsiflexion and tibial rotation.
The fracture line is vertical or oblique and originates from
the junction of the tibial plafond and the medial malleolus.
Athletes desiring early return to competition, with a
complete fracture line – surgery.

34. Navicular #
sprinting and jumping sports.
Insidious onset vague medial arch pain
 In the sagittal plane in the relatively avascular central
third of the bone.
Anatomic AP view with foot inverted
CT, MRI.
Acute # - an initial 6-week period of non weight-
bearing cast immobilization.
Delayed diagnosis or delayed union, compression screw
stabilization
 Displaced fractures and established sclerotic nonunions
require ORIF and supplemental bone graft.

36. Fifth metatarsal
proximal diaphysis of the bone just distal to the
tuberosity and the ligamentous structures.
basketball players.
problematic site is in the proximal 1.5 cm of the
diaphysis, where cortical hypertrophy commonly occurs
in running and jumping athletes, rendering the zone
relatively avascular with a narrow medullary canal
propensity for delayed union or nonunion and have a
high risk of refracture after nonoperative treatment.

37. Acute #  non wt bearing cast immobilisation.
Intermediate delayed union  intramedullary compression
screw placement after the medullary canal at the fracture site
has been adequately drilled to remove fibrous tissue and
sclerotic bone
Estabilised NonU – grafting.
functional metatarsal brace should be used for atleast 1
month after surgery – reinjury.

38. Great toe sesamoids
predominance at the medial sesamoid
Repeated dorsiflexion of the great toe during running and
jumping
weight-bearing anteroposterior and lateral views as well as
an axial view centered on the sesamoids.
Acute stress # Rx with 6 weeks of non-weightbearing cast
that extends to the distal tip of the toe to prevent
dorsiflexion
Sesamoidectomy.