Complications of fractures
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Complications of fractures



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Complications of fractures Complications of fractures Presentation Transcript

  • Subhanjan Das
  • IntroductionThese are the associated pathologies other than the loss of bone continuity which either co exist or originate due to the fracture. early diagnosis and aggressive treatment is necessary to minimize disabilities.
  • ClassificationI.IMMEDIATEA.Systemichypovolaemic ShockB.Localinjury to1. major vessels2. Muscles and tendons3. Joints4. viscera
  • II.EARLYA.Systemic1. Hypovolaemic shock2. ARDS3. Fat embolism4. DVT & pulmonary embolism5. Aseptic traumatic fever6. Septicaemia7. Crush syndromeB. Local1. Infection2. Compartment syndrome
  • III. LATE COMPLICATIONSA. Related to imperfect union1. Delayed union2. Non union3. Mal union4. Cross unionB.Others1. Avascular necrosis2. Shortening3. Joint stiffness4. Sudeck’s dystrophy5. Osteomyelitis6. Ischemic contracture7. Myositis ossificans8. OA
  • Hypovolaemic shock Commonest cause of death in fractures of major bonesLike pelvis or femur
  • cause External or internal haemorrhage. External: compound fractures injuring major vessels of the LIMB Internal: injury to body cavities- chest or pelvis Internal is more difficult to diagnose. # pelvis (1.5-2 litres) # femur (1-1.5 litres) produces major haemorrhage.
  • Prevention Early stopping of bleeding Avoiding shifting of the patients For # pelvis- temporary stabilization with external fixator Emergency angiography and embolisation of bleeding vessels for deeper vessels.
  • Management Starts even before the cause is established Two large bore iv cannulas put Infuse 2000 ml of crystalloids (ringer lactate) followed by colloid (haemaccel) and blood if needed Cut down if peripheral vasoconstriction is present Localise the site of lesion- if in body cavities, perform chest aspiration or diagnostic peritonial lewage. Sometimes a simple x ray is enough. Chest bleeding-ICDT Abdominal bleeding- laperotomy
  • ARDS Respiratory distress following a trauma Cause- not definite. Hypothesized to be by release of Inflammatory cells and proteinaceous fluid that accumulate in the alveolar spaces leading to a decrease in diffusing capacity and hypoxemia. The microvasculature in dysrupted. Onset- 24 hours after injury
  •  Features: Tachypnea Laboured breathing X- ray- diffusedpulmonary infiltrates Arterial Po2 below 50
  • management 100% O2 and assisted ventilation It takes upto 7 days to get the chest clear If not detected early death occurs by multiorgan failure or cardiorespiratory failure.
  • Fat EmbolismIt is a life threatening complication of fracture where fat globules occlude the small blood vessels.Embolism is the process of occlusion of blood vessel by any material which is brought to the site from elsewhere by bloodstream.
  • PathogenesisInjury to large bones (e.g. femur) release fat globule from bone marrow to blood stream. Alternatively fat can also be released from the adipose tissue.The fat globules obstruct capillary vasculature of the lungs.Also, fat is converted to free fatty acid, which induces toxic vasculitis followed by thrombosis which obstruct the microvasculature.
  • Clinical featuresCOMMON PULMONARY TYPEPatechial rash of anterior Tachypnoea neck, anterior axillary Tachycardia fold or conjunctiva Respiratory failureCEREBRAL TYPEDrowsinessRestlessnessDisorientationComa
  • DiagnosisRetinal artery emboliUrine: fat globulesCXR: pulmonary infiltration/Snow storm appearanceClinical features
  • management Respitarory support Heparinisation i.v. low mol wt dextran Corticosteroid Dextrose and alcohol infusion to emulsify fat.
  • Deep Vein ThrombosisIt is a common complication originating from altered Pathology: hemodynamics in lower limb and spinal injuries.
  • pathologyVirchows triad trauma1. decreased flow rate of the blood2. damage to the blood immobilisation vessel wall3. hypercoagulability Venous stasis thrombosis
  • Clinical featuresElderly and obese patients are at risk.Leg swellingLocal redness, warmthCalf tendernessPain in passive dorsiflexion (Homan sign)Venography shows DVT
  •  Sequale1. The venous thrombosis can get dislodged and produce embolism elsewhere. If it is pulmonary embolism the condition is life threatening. Embolism usually occurs within 4-5 days after injury.2. A late complication of DVT is the post-phlebitic syndrome, which can manifest itself as edema, pain or discomfort and skin problems.
  • Other causes Risk factor: Surgerycompression of the veins hospitalization physical trauma immobilization cancer orthopedic casts infections economy class syndromeinflammatory diseases smoking stroke Obesity heart failure age nephrotic syndrome certain drugs (such as estrogen or erythropoietin) thrombophilia pregnancy postnatal period.
  • diagnosisD-dimersdoppler ultrasoundvenographyClinical features
  • treatmentProphylaxis Management Active/ passive calf pump Complete rest with elevation and toe movement thrombolysis Elevation Anticoagulant therapy Deep breathing exercise graduated compression Elastic TED stockings stockings ( Early internal fixation to thromboembolic deterrent provide early mobility. stockings) or intermittent pneumatic compression devices. Respiratory support in case of pulmonary embolism
  • Crush syndromeIt is renal failure following Clinical features extensive crushing injury (appear within 2-3 days of injury) of muscles. Signs of deficient renal function:Pathogenesis: Oliguria (Scanty urine)Crushing of muscles causes Apathy entry of myoglobin into Restlessness circulation. Myoglobin precipitates in renal Delirium tubules causing acute Cardiac arrhythmia & failure tubular necrosis, Hypothermia metabolic acidosis & Shock hperkalemia
  • TreatmentProphylaxis TreatmentApplication of tourniquet Treated as acute renal and gradual release to failure. slowly allow the myoglobin to reach the kidneys
  • Compartment syndrome An increased pressure within enclosedosteofascial space that reduces capillary per-fusion below level necessary for tissueviability; the underlying mechanism is: - increased volume within space - decreased space for contents - combination of both
  • Etiology Trauma withbleeding/swelling Bleeding disorders Burns Tight wraps Traction Surgical positioning Pneumatic antishockgarment Reprefusion swelling Casting & Wraps
  • Pathophysiology: Increased compartment pressureleads to increased venous pressurewhich decreases A-V gradient resultingin muscle and nerve ischemia.
  • Compartments Most common  Forearm  Leg Other compartments  Hand  Finger  Gluteal  Thigh  Foot
  • Diagnosis History Clinical exam: the Ps Compartment pressures Laboratory tests  CPK  Urine myoglobin
  • Clinical features The six ‘Ps’:  Pressure: palpation of compartment and its tension or firmness Pain: Exaggerated with passive stretch of the involved muscles in compartment Earliest symptom but inconsistent  Paresthesia:Peripheral nerve tissue is more sensitive than muscle to ischemia  Will progress to anesthesia if pressure not relieved  Paralysis: late finding  Pallor  Pulselessness
  • Treatment Lower leg to level of the heart Remove cast Split all dressings down to skin Fasciotomy if continued clinical findings and/or elevated compartment pressure
  • Forearm
  • Leg Anatomy
  • Leg Single Incision Technique
  • Leg Two Incision Technique
  • Hand Compartments
  • Foot Compartments
  • Delayed/ Non unionWhen a fracture takes more than the usual time to unite it is said to have gone in delayed union.When the process of healing stops before completion the fracture is said to have gone for non union. To diagnose non union the fracture has to be minimum six months old.
  • causesI. Related to patient Old age Associated systemic illness: ex. MalignancyII. Related to fracture Distraction at fracture site Muscle pulling the fragments: ex. # patella Gravity: ex. # shaft of humerus Soft tissue interposition: ex. # shaft of humerus Bone loss during fracture: ex. # tibia open type Infection from open fracture: ex. # tibia Damage to blood supply of # fragment: ex. # scaphoid Pathological fracture: ex. # osteomyelitic tibia
  • III causes related to treatment: Inadequate reduction: # shaft of long bones Inadequate immobilisation:# shaft of long bones Distraction (excessive) during treatment::# shaft of femur.
  • types1. Atrophic: no or minimal callus formation2. Hypertrophic: callus is present but it does not bridge the fracture site.
  • Common sitesNeck of femurScaphoidLower third of tibiaLower third of ulnaLateral condyle of humerus
  • Clinical features Pain Deformity Abnormal mobility RefractureRadiological findingsDelayed union: inadequate callus, visible fracture lineNon union: ends are rounded, smooth sclerotic. Medullary cavity may be obliterated. visible fracture line.
  • Treatment: Delayed union1. Most commonly prolonged conservative management2. Surgical intervention: bone grafting with or without internal fixation.
  • Treatment: non unionDepends upon site and resulting disability. Following are the options.1. Bone grafting: commonest.2. Excision of fragments: when it can be done with minimal loss of function. A prosthesis may be used to replace the lost part, eg. In # neck of femur the head can be replaced with an austin moore prosthesis.3. Illizarov menthod4. No treatment: when there is no disability, eg. # scaphoid.
  • Mal union When a fracture does not unite in proper position it is said to have malunited.Causes:1. Improper reduction2. Unchecked muscle pull3. Excessive communication
  • ConsequencesDeformityShortening of limbLimitation of movements
  • treatment1. osteoclasis: refracture, done in children to correct mild to moderate angular deformities under GA.2. Redoing the fracture surgically: most common. ORIF is generally done along with bone grafting.3. Corrective osteotomy: performed at a site away from the fracture. Eg. Supracondyle # of humerus.4. Excision of protruding bone.
  •  No treatment may be necessary if remodelling occurs.