STRESS FRACTURE

FATIGUE
FRACTURE
1. Fracture occurs through an otherwise normal bone
that is subjected to repeated episodes of stress,
less severe than that necessary to produce an
acute # .
2. Results from summation of stresses any one of
which by itself would have been harmless.
3. Overuse injuries.
By repetitivesubmaximal 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.
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.
- Femoral neck  any age
- Femoral shaft  lower third
- Patella  children & young athletes
- Tibial shaft pro 3rdin children, mid 3rdin athletes,
distal 3rd in elderly.
- Fibula high shaft – jumpers, distal 3rdin runners.
- Calcaneum  adults / compression stress/
anterior to tuberosity.
- Metatarsals  march # / 2ndMT neck.
- Great toe sesamoids.
 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.
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.
 Intrinsic
factorsimbalances
Hormonal

- female, estrogen deficiency.

- male athletes – testosterone- inhibits IL-6 –
osteoclast production - activity.
Nutritional deficiencies
Sleep deprivation
Collagen abnormalities
Metabolic bone disorders
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.
 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
 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.
Focalbone pain with palpation and stressing –
Hall mark.
Local swelling- callus –late presentations
Location of pain – medially / femoral shaft
Inaccessible sites – femoral neck - movts
 Imaging
Confirm the diagnosis, more information for
modalities
differential evaluation.
X- RAY
Normal – 1st 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.
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.
CT
scan
Navicular bone

Diaphyseal bone with longitudinal #

lines
Pars & sacral stress # .
 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
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.
 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 #
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
Differential diagnosis
Stress reaction
periostitis, infection,
avulsion injuries, muscle strain,
bursitis, neoplasm,
Exertional
compartment syndrome, and nerve
entrapment.
 PREVENTI
ON errors - most frequent culprit and
Training
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.
Femaleathletes – alerted , eating disorders,
hormonal abnormalities.
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
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
 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.
More problematic – anterior cortex of middle 3rdof
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.
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.
 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.
 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.
 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.
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.
 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.