FATIGUE FRACTUREFracture occurs through an otherwise normal bone that issubjected to repeated episodes of stress, less severe than thatnecessary to produce an acute #.Results from summation of stresses any one of which by itselfwould have been harmless.Overuse injuries.
By repetitive submaximal forces that exceed the adaptiveability of the bone.Common in athletes & military recruits.1% incidence in athletes, 20% in runners.Females prone [female athlete triad]late adolescence and early adulthoodIncreasing incidence in elderly.
Weight bearing lower limb bone proneTibia – [50%] most commonTarsals & metatarsalsSpecific anatomic sites- shaft of humerus cricket/ throwing sp.- ribs golf & rowing- spine pars # gymnastics- pubic rami inferior in children, both inadults- 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 3rdin elderly.- Fibula high shaft – jumpers, distal 3rdin runners.- Calcaneum adults / compression stress/ anterior totuberosity.- Metatarsals march # / 2ndMT neck.- Great toe sesamoids.
PATHOGENESISExcessive, repetitive, submaximal loads on bones that causean imbalance between bone resorption and formation.An abrupt increase in the duration, intensity, or frequency ofphysical activity without adequate periods of rest may lead toan escalation in osteoclast activity.During periods of intense exercise, bone formation lagsbehind bone resorption.
When bone subjected to hyper physiological loads, itsultimate strength decreases susceptible to microfracturesContinuous loading microcracks coalesce to stress #.ETIOLOGY – multifactorialDepends on type of bone composition, vascular supply,surrounding muscle attachments, systemic factors, athletictype.Role of muscle – M . Fatigue, concentrating forces tolocalised area.
Stages in development1. Crack initiation2. Crack propagation3. Rapid failure of bone. Bone can repair itself quickly, pathological strain isremoved before the third stage.
Clinical featuresHistory of unaccustomed & repeated activity.Sequence – pain after exercise, pain during ex, pain withoutex.Load related pain – early symptom general health, medications, diet, and menstrual history inwomenIncrease in training volume or intensity, a change intechnique or surface, or an alteration of footwear
H/O previous stress fractures or other painful sites, and thepresence of eating disorders,Limb biomechanics - leg length discrepancy, or muscleimbalance, excessive subtalar pronation.Focal bone pain with palpation and stressing – Hall mark.Local swelling- callus –late presentationsLocation of pain – medially / femoral shaftInaccessible sites – femoral neck - movts
Imaging modalitiesConfirm the diagnosis, more information for differentialevaluation.X- RAYNormal – 1st2-3 wks after the onset of symptomsPeriosteal response – 3 months after onset of symptoms.Periosteal bone formation, horizontal or oblique linearpatterns of sclerosis, endosteal callus, and a frank fractureline.
Gray cortex ovoid lucency with in a thickened area ofcortical hyperostosis radiolucent line with extensionpartially or completely across the cortexcancellous bone a fracture lucency oriented perpendicularto the trabeculae.X ray more useful in fibula & metatarsals.
ScintigraphySensitive methodConfirming clinically suspected stress fractures.Acute stress fractures are depicted as discrete, localized,areas of increased uptake on all three phases of a Tc-99mSoft-tissue injuries are characterized by increased uptakeonly in the first two phases.Lacks specificity.
Indications for bone scansuspected lesions in the spine or Pelvisidentifying multiple stress fractures,distinguishing bipartite bones from stress fractures.- positive images in phase III persists – many months, shouldnot be used to monitor healing and dictate return to activity.
CT scanNavicular boneDiaphyseal bone with longitudinal # linesPars & sacral stress # .
SPECT scanningsuspected pars interarticularis and sacral stress fractures
MRIMore specificAvoids radiation exposureLess timeMore expensiveGrading the stage of certain stress fractures and, therefore,predicting the time to recoveryfemoral neck stress fracture in an athlete.
Treatment OverviewFundamental principle of initial management is REST toallow 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, physicalexamination, and radiographs.A rest period of 1 to 6 weeks of limited weight bearingprogressing to full weight bearing phase of low-impactactivities high impact activities.
HIGH RISK STRESS #predilection for progressing to complete fracture, delayedunion, or nonunionmore aggressive treatment approachfractures 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 nonoperativeprotocol consisting of non-weight-bearing castimmobilization.Exception to this rule is the tension-side femoral neck stressfracture,which requires internal fixation
PREVENTIONTraining errors - most frequent culprit and should becorrected.Assessment of the type and condition of the runningshoesViscoelastic insoles, may help reduce the incidence oflower-extremity stress fractures.Education – parents, coaches, military personnel –periodic rest.Female athletes – alerted , eating disorders, hormonalabnormalities.
Femoral neck #High complication rateDue to hip musculature fatigued due to prolonged activity &subsequent loss of shock absorbing effect.Coxa vara & osteopeniaPain at extremes of rotation.More common is compression type –benign
Distraction or tension stress # - starts in superior cortexHigh chance of displacement & progressionGrade 3 or grade 4 tension-side femoral neck stress fracturesshould be stabilized with multiple screw fixation to promotehealing and prevent displacement.avoid lateral entry points below the midportion of the levelof the lesser trochanter
Tibial fracturesMost common site [20-75%]Posteromedial cortex [compression side] most common.Transverse # commonLongitudinal # ,atypical presentation, MRIConservative Rx.Pneumatic brace – supplemental use – early return ofactivities.
More problematic – anterior cortex of middle 3rdof shaft.X ray – subtle, high incidence of suspicionBoth constant tension from posterior muscle forces andhypovascularity of the anterior aspect of the tibia predisposethis site to nonunion or delayed union.Tension side # occurs in those performing repetitivejumping & leaping activities.
V –shaped defect in the anterior cortexCallus formation – absentDreaded black line.Anterior tibial stress fractures with an established transversecortical lucency have limited healing potential even withactivity modificationReamed intramedullary nailing predictably leads to healing ofthe stress fracture in a shorter time course.
Medial MalleolusRepetitive impingement of the talus on the medial malleolusduring ankle dorsiflexion and tibial rotation.The fracture line is vertical or oblique and originates fromthe junction of the tibial plafond and the medial malleolus.Athletes desiring early return to competition, with acomplete fracture line – surgery.
Navicular #sprinting and jumping sports.Insidious onset vague medial arch pain In the sagittal plane in the relatively avascular centralthird of the bone.Anatomic AP view with foot invertedCT, MRI.Acute # - an initial 6-week period of non weight-bearing cast immobilization.Delayed diagnosis or delayed union, compression screwstabilization Displaced fractures and established sclerotic nonunionsrequire ORIF and supplemental bone graft.
Fifth metatarsalproximal diaphysis of the bone just distal to thetuberosity and the ligamentous structures.basketball players.problematic site is in the proximal 1.5 cm of thediaphysis, where cortical hypertrophy commonly occursin running and jumping athletes, rendering the zonerelatively avascular with a narrow medullary canalpropensity for delayed union or nonunion and have ahigh risk of refracture after nonoperative treatment.
Acute # non wt bearing cast immobilisation.Intermediate delayed union intramedullary compressionscrew placement after the medullary canal at the fracture sitehas been adequately drilled to remove fibrous tissue andsclerotic boneEstabilised NonU – grafting.functional metatarsal brace should be used for atleast 1month after surgery – reinjury.
Great toe sesamoidspredominance at the medial sesamoidRepeated dorsiflexion of the great toe during running andjumpingweight-bearing anteroposterior and lateral views as well asan axial view centered on the sesamoids.Acute stress # Rx with 6 weeks of non-weightbearing castthat extends to the distal tip of the toe to preventdorsiflexionSesamoidectomy.