Stress fracture


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Stress fracture

  2. 2. FATIGUE FRACTUREFracture 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.
  3. 3. 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 adulthoodIncreasing incidence in elderly.
  4. 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 inadults- lower extremities  running activities.
  5. 5. - 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.
  6. 6. PATHOGENESISExcessive, 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.
  7. 7. When bone subjected to hyper physiological loads, itsultimate 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, athletictype.Role of muscle – M . Fatigue, concentrating forces tolocalised area.
  8. 8. Intrinsic factorsHormonal imbalances- female, estrogen deficiency.- male athletes – testosterone- inhibits IL-6 – osteoclastproduction - activity.Nutritional deficienciesSleep deprivationCollagen abnormalitiesMetabolic bone disorders
  9. 9. Stages in development1. Crack initiation2. Crack propagation3. Rapid failure of bone. Bone can repair itself quickly, pathological strain isremoved before the third stage.
  10. 10. Clinical featuresHistory 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 inwomenIncrease in training volume or intensity, a change intechnique or surface, or an alteration of footwear
  11. 11. 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 presentationsLocation of pain – medially / femoral shaftInaccessible sites – femoral neck - movts
  12. 12. Imaging modalitiesConfirm the diagnosis, more information for differentialevaluation.X- RAYNormal – 1st2-3 wks after the onset of symptomsPeriosteal response – 3 months after onset of symptoms.Periosteal bone formation, horizontal or oblique linearpatterns of sclerosis, endosteal callus, and a frank fractureline.
  13. 13. Gray cortex  ovoid lucency with in a thickened area ofcortical hyperostosis  radiolucent line with extensionpartially or completely across the cortexcancellous bone  a fracture lucency oriented perpendicularto the trabeculae.X ray more useful in fibula & metatarsals.
  14. 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 uptakeonly in the first two phases.Lacks specificity.
  15. 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, shouldnot be used to monitor healing and dictate return to activity.
  16. 16. CT scanNavicular boneDiaphyseal bone with longitudinal # linesPars & sacral stress # .
  17. 17. SPECT scanningsuspected pars interarticularis and sacral stress fractures
  18. 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. 19. Radiological grading
  20. 20. Treatment OverviewFundamental 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
  21. 21. 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.
  22. 22. HIGH RISK STRESS #predilection for progressing to complete fracture, delayedunion, 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 #
  23. 23. 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
  24. 24. Differential diagnosisStress reactionperiostitis, infection,avulsion injuries, muscle strain,bursitis, neoplasm,Exertional compartment syndrome, and nerve entrapment.
  25. 25. PREVENTIONTraining errors - most frequent culprit and should becorrected.Assessment of the type and condition of the runningshoesViscoelastic insoles, may help reduce the incidence oflower-extremity stress fractures.Education – parents, coaches, military personnel –periodic rest.Female athletes – alerted , eating disorders, hormonalabnormalities.
  26. 26. 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
  27. 27. Distraction or tension stress # - starts in superior cortexHigh chance of displacement & progressionGrade 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
  28. 28. 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 ofactivities.
  29. 29. More problematic – anterior cortex of middle 3rdof shaft.X ray – subtle, high incidence of suspicionBoth 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.
  30. 30. V –shaped defect in the anterior cortexCallus formation – absentDreaded black line.Anterior tibial stress fractures with an established transversecortical lucency have limited healing potential even withactivity modificationReamed intramedullary nailing predictably leads to healing ofthe stress fracture in a shorter time course.
  31. 31. Medial MalleolusRepetitive 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.
  32. 32. 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 invertedCT, 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.
  33. 33. Fifth metatarsalproximal 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 canalpropensity for delayed union or nonunion and have ahigh risk of refracture after nonoperative treatment.
  34. 34. 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 boneEstabilised NonU – grafting.functional metatarsal brace should be used for atleast 1month after surgery – reinjury.
  35. 35. Great toe sesamoidspredominance at the medial sesamoidRepeated dorsiflexion of the great toe during running andjumpingweight-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 preventdorsiflexionSesamoidectomy.