1. Subhanjan Das

2. 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. 3. ClassificationI.IMMEDIATEA.Systemichypovolaemic ShockB.Localinjury to1. major vessels2. Muscles and tendons3. Joints4. viscera 4. II.EARLYA.Systemic1. Hypovolaemic shock2. ARDS3. Fat embolism4. DVT & pulmonary embolism5. Aseptic traumatic fever6. Septicaemia7. Crush syndromeB. Local1. Infection2. Compartment syndrome 5. III. LATE COMPLICATIONSA. Related to imperfect union1. Delayed union2. Non union3. Mal union4. Cross unionB.Others1. Avascular necrosis2. Shortening3. Joint stiffness4. Sudecks dystrophy5. Osteomyelitis6. Ischemic contracture7. Myositis ossificans8. OA 6. Hypovolaemic shock Commonest cause of death in fractures of major bonesLike pelvis or femur 7. cause External or internal haemorrhage. External: compound fractures injuring major vessels ofthe 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) producesmajor haemorrhage. 8. Prevention Early stopping of bleeding Avoiding shifting of the patients For # pelvis- temporary stabilization with externalfixator Emergency angiography and embolisation of bleedingvessels for deeper vessels. 9. Management Starts even before the cause is established Two large bore iv cannulas put Infuse 2000 ml of crystalloids (ringer lactate) followedby colloid (haemaccel) and blood if needed Cut down if peripheral vasoconstriction is present Localise the site of lesion- if in body cavities, performchest aspiration or diagnostic peritonial lewage.Sometimes a simple x ray is enough. Chest bleeding-ICDT Abdominal bleeding- laperotomy 10. ARDS Respiratory distress following a trauma Cause- not definite. Hypothesized to be by release ofInflammatory cells and proteinaceous fluid thataccumulate in the alveolar spaces leading to a decreasein diffusing capacity and hypoxemia. Themicrovasculature in dysrupted. Onset- 24 hours after injury 11. Features: Tachypnea Laboured breathing X- ray- diffusedpulmonary infiltrates Arterial Po2 below 50 12. management 100% O2 and assisted ventilation It takes upto 7 days to get the chest clear If not detected early death occurs by multiorganfailure or cardiorespiratory failure. 13. 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. 14. PathogenesisInjury to large bones (e.g. femur) release fat globulefrom bone marrow to blood stream. Alternatively fatcan also be released from the adipose tissue.The fat globules obstruct capillary vasculature of thelungs.Also, fat is converted to free fatty acid, which inducestoxic vasculitis followed by thrombosis which obstructthe microvasculature. 15. Clinical featuresCOMMON PULMONARY TYPEPatechial rash of anterior Tachypnoeaneck, anterior axillaryTachycardiafold or conjunctivaRespiratory failureCEREBRAL TYPEDrowsinessRestlessnessDisorientationComa 16. DiagnosisRetinal artery emboliUrine: fat globulesCXR: pulmonary infiltration/Snow storm appearanceClinical features 17. management Respitarory support Heparinisation i.v. low mol wt dextran Corticosteroid Dextrose and alcohol infusion to emulsify fat. 18. Deep Vein ThrombosisIt is a common complication originating from alteredPathology: hemodynamics in lower limb and spinal injuries. 19. pathologyVirchows triadtrauma1. decreased flow rate ofthe blood2. damage to the bloodimmobilisationvessel wall3. hypercoagulabilityVenous stasis thrombosis 20. Clinical featuresElderly and obese patients are at risk.Leg swellingLocal redness, warmthCalf tendernessPain in passive dorsiflexion (Homan sign)Venography shows DVT 21. 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. 22. Other causes Risk factor: Surgerycompression of the veinshospitalization physical trauma immobilization cancerorthopedic casts infections economy class syndromeinflammatory diseases smoking strokeObesity heart failureage nephrotic syndromecertain drugs (such as estrogenor erythropoietin)thrombophilia pregnancypostnatal period. 23. diagnosisD-dimersdoppler ultrasoundvenographyClinical features 24. treatmentProphylaxisManagement Active/ passive calf pumpComplete rest with elevationand toe movement thrombolysis ElevationAnticoagulant therapy Deep breathing exercisegraduated compression Elastic TED stockings stockings ( Early internal fixation tothromboembolic deterrentprovide early mobility. stockings) orintermittent pneumaticcompression devices. Respiratory support in caseof pulmonary embolism 25. 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 causesApathy entry of myoglobin intoRestlessness circulation. Myoglobin precipitates in renalDelirium tubules causing acuteCardiac arrhythmia & failure tubular necrosis,Hypothermia metabolic acidosis & Shock hperkalemia 26. TreatmentProphylaxis TreatmentApplication of tourniquet Treated as acute renaland gradual release tofailure.slowly allow themyoglobin to reach thekidneys 27. 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 28. Etiology Trauma withbleeding/swelling Bleeding disorders Burns Tight wraps Traction Surgical positioning Pneumatic antishockgarment Reprefusion swelling Casting & Wraps 29. Pathophysiology:Increased compartment pressureleads to increased venous pressurewhich decreases A-V gradient resultingin muscle and nerve ischemia. 30. Compartments Most common Forearm Leg Other compartments Hand Finger Gluteal Thigh Foot 31. Diagnosis History Clinical exam: the Ps Compartment pressures Laboratory tests CPK Urine myoglobin 32. Clinical features The six Ps: Pressure: palpation of compartment and its tension or firmness Pain: Exaggerated with passive stretch of the involvedmuscles 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 33. Treatment Lower leg to level of the heart Remove cast Split all dressings down to skin Fasciotomy if continued clinical findings and/orelevated compartment pressure 34. Forearm 35. Leg Anatomy 36. Leg Single Incision Technique 37. Leg Two Incision Technique 38. Hand Compartments 39. Foot Compartments 40. 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. 41. causesI. Related to patientOld ageAssociated systemic illness: ex. MalignancyII. Related to fracture Distraction at fracture siteMuscle pulling the fragments: ex. # patellaGravity: 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 42. III causes related to treatment: Inadequate reduction: # shaft of long bones Inadequate immobilisation:# shaft of long bones Distraction (excessive) during treatment::# shaft offemur. 43. types1. Atrophic: no or minimal callus formation2. Hypertrophic: callus is present but it does not bridge the fracture site. 44. Common sitesNeck of femurScaphoidLower third of tibiaLower third of ulnaLateral condyle of humerus 45. 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. 46. Treatment: Delayed union1. Most commonly prolonged conservative management2. Surgical intervention: bone grafting with or without internal fixation. 47. Treatment: non unionDepends upon site and resulting disability. Following arethe options.1. Bone grafting: commonest.2. Excision of fragments: when it can be done withminimal loss of function. A prosthesis may be usedto replace the lost part, eg. In # neck of femur thehead can be replaced with an austin mooreprosthesis.3. Illizarov menthod4. No treatment: when there is no disability, eg. #scaphoid. 48. Mal union When a fracture does not unite in proper position it issaid to have malunited.Causes:1. Improper reduction2. Unchecked muscle pull3. Excessive communication 49. ConsequencesDeformityShortening of limbLimitation of movements 50. 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. 51. No treatment may be necessary if remodelling occurs.