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Subhanjan Das
Introduction
These 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.
Classification
I.IMMEDIATE
A.Systemic
hypovolaemic Shock
B.Local
injury to
1. major vessels
2. Muscles and tendons
3. Joints
4. viscera
II.EARLY
A.Systemic
1. Hypovolaemic shock
2. ARDS
3. Fat embolism
4. DVT & pulmonary embolism
5. Aseptic traumatic fever
6. Septicaemia
7. Crush syndrome
B. Local
1. Infection
2. Compartment syndrome
III. LATE COMPLICATIONS
A. Related to imperfect union
1. Delayed union
2. Non union
3. Mal union
4. Cross union
B.Others
1. Avascular necrosis
2. Shortening
3. Joint stiffness
4. Sudeck’s dystrophy
5. Osteomyelitis
6. Ischemic contracture
7. Myositis ossificans
8. OA
Hypovolaemic shock
 Commonest cause of death in fractures of major bones
Like 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- diffused
pulmonary 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 Embolism
It 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.
Pathogenesis
Injury 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 features

COMMON                       PULMONARY TYPE
Patechial rash of anterior   Tachypnoea
  neck, anterior axillary    Tachycardia
  fold or conjunctiva        Respiratory failure
CEREBRAL TYPE
Drowsiness
Restlessness
Disorientation
Coma
Diagnosis
Retinal artery emboli
Urine: fat globules
CXR: pulmonary infiltration/
Snow storm appearance
Clinical features
management
 Respitarory support
 Heparinisation
 i.v. low mol wt dextran
 Corticosteroid
 Dextrose and alcohol infusion to emulsify fat.
Deep Vein Thrombosis
It is a common complication
 originating from altered    Pathology:
 hemodynamics in lower
 limb and spinal injuries.
pathology
Virchow's triad                trauma
1. decreased flow rate of
    the blood
2. damage to the blood      immobilisation
    vessel wall
3. hypercoagulability
                            Venous stasis




                             thrombosis
Clinical features
Elderly and obese patients are at risk.
Leg swelling
Local redness, warmth
Calf tenderness
Pain in passive dorsiflexion (Homan sign)
Venography shows DVT
 Sequale
1. 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:
                           Surgery
compression of the veins    hospitalization
 physical trauma           immobilization
 cancer                    orthopedic casts
 infections                 economy class syndrome
inflammatory diseases       smoking
 stroke                    Obesity
 heart failure              age
 nephrotic syndrome        certain drugs (such as estrogen
                              or erythropoietin)
                            thrombophilia
                           pregnancy
                            postnatal period.
diagnosis
D-dimers
doppler ultrasound
venography
Clinical features
treatment
Prophylaxis                    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 syndrome
It 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
Treatment

Prophylaxis                 Treatment
Application 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 enclosed
osteofascial space that reduces capillary per-
fusion below level necessary for tissue
viability; the underlying mechanism is:
     - increased volume within space
     - decreased space for contents
     - combination of both
Etiology
 Trauma with
bleeding/swelling
 Bleeding disorders
 Burns
 Tight wraps
 Traction
 Surgical positioning
 Pneumatic antishock
garment
 Reprefusion swelling
 Casting & Wraps
Pathophysiology:
    Increased compartment pressure
leads to increased venous pressure
which decreases A-V gradient resulting
in 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 union
When 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.
causes
I.   Related to patient
    Old age
    Associated systemic illness: ex. Malignancy
II. 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.
types
1. Atrophic: no or minimal callus formation
2. Hypertrophic: callus is present but it does not bridge
   the fracture site.
Common sites
Neck of femur
Scaphoid
Lower third of tibia
Lower third of ulna
Lateral condyle of humerus
Clinical features
 Pain
 Deformity
 Abnormal mobility
 Refracture
Radiological findings
Delayed union: inadequate callus, visible fracture line
Non union: ends are rounded, smooth sclerotic.
 Medullary cavity may be obliterated. visible fracture
 line.
Treatment: Delayed union
1. Most commonly prolonged conservative
   management
2. Surgical intervention: bone grafting with or without
   internal fixation.
Treatment: non union
Depends 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 menthod
4. 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 reduction
2. Unchecked muscle pull
3. Excessive communication
Consequences
Deformity
Shortening of limb
Limitation of movements
treatment
1. 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.

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Complications of fractures

  • 2. Introduction These 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. Classification I.IMMEDIATE A.Systemic hypovolaemic Shock B.Local injury to 1. major vessels 2. Muscles and tendons 3. Joints 4. viscera
  • 4. II.EARLY A.Systemic 1. Hypovolaemic shock 2. ARDS 3. Fat embolism 4. DVT & pulmonary embolism 5. Aseptic traumatic fever 6. Septicaemia 7. Crush syndrome B. Local 1. Infection 2. Compartment syndrome
  • 5. III. LATE COMPLICATIONS A. Related to imperfect union 1. Delayed union 2. Non union 3. Mal union 4. Cross union B.Others 1. Avascular necrosis 2. Shortening 3. Joint stiffness 4. Sudeck’s dystrophy 5. Osteomyelitis 6. Ischemic contracture 7. Myositis ossificans 8. OA
  • 6. Hypovolaemic shock  Commonest cause of death in fractures of major bones Like pelvis or femur
  • 7. 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.
  • 8. 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.
  • 9. 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
  • 10. 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
  • 11.  Features:  Tachypnea  Laboured breathing  X- ray- diffused pulmonary 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 multiorgan failure or cardiorespiratory failure.
  • 13. Fat Embolism It 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. Pathogenesis Injury 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.
  • 15. Clinical features COMMON PULMONARY TYPE Patechial rash of anterior Tachypnoea neck, anterior axillary Tachycardia fold or conjunctiva Respiratory failure CEREBRAL TYPE Drowsiness Restlessness Disorientation Coma
  • 16. Diagnosis Retinal artery emboli Urine: fat globules CXR: pulmonary infiltration/ Snow storm appearance Clinical features
  • 17. management  Respitarory support  Heparinisation  i.v. low mol wt dextran  Corticosteroid  Dextrose and alcohol infusion to emulsify fat.
  • 18. Deep Vein Thrombosis It is a common complication originating from altered Pathology: hemodynamics in lower limb and spinal injuries.
  • 19. pathology Virchow's triad trauma 1. decreased flow rate of the blood 2. damage to the blood immobilisation vessel wall 3. hypercoagulability Venous stasis thrombosis
  • 20. Clinical features Elderly and obese patients are at risk. Leg swelling Local redness, warmth Calf tenderness Pain in passive dorsiflexion (Homan sign) Venography shows DVT
  • 21.  Sequale 1. 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: Surgery compression of the veins hospitalization physical trauma immobilization cancer orthopedic casts infections economy class syndrome inflammatory diseases smoking stroke Obesity heart failure age nephrotic syndrome certain drugs (such as estrogen or erythropoietin) thrombophilia pregnancy postnatal period.
  • 24. treatment Prophylaxis 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
  • 25. Crush syndrome It 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
  • 26. Treatment Prophylaxis Treatment Application of tourniquet Treated as acute renal and gradual release to failure. slowly allow the myoglobin to reach the kidneys
  • 27. Compartment syndrome An increased pressure within enclosed osteofascial space that reduces capillary per- fusion below level necessary for tissue viability; the underlying mechanism is: - increased volume within space - decreased space for contents - combination of both
  • 28. Etiology  Trauma with bleeding/swelling  Bleeding disorders  Burns  Tight wraps  Traction  Surgical positioning  Pneumatic antishock garment  Reprefusion swelling  Casting & Wraps
  • 29. Pathophysiology: Increased compartment pressure leads to increased venous pressure which decreases A-V gradient resulting in 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 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
  • 33. 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
  • 36. Leg Single Incision Technique
  • 37. Leg Two Incision Technique
  • 40. Delayed/ Non union When 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. causes I. Related to patient  Old age  Associated systemic illness: ex. Malignancy II. 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
  • 42. III causes related to treatment:  Inadequate reduction: # shaft of long bones  Inadequate immobilisation:# shaft of long bones  Distraction (excessive) during treatment::# shaft of femur.
  • 43. types 1. Atrophic: no or minimal callus formation 2. Hypertrophic: callus is present but it does not bridge the fracture site.
  • 44. Common sites Neck of femur Scaphoid Lower third of tibia Lower third of ulna Lateral condyle of humerus
  • 45. Clinical features  Pain  Deformity  Abnormal mobility  Refracture Radiological findings Delayed union: inadequate callus, visible fracture line Non union: ends are rounded, smooth sclerotic. Medullary cavity may be obliterated. visible fracture line.
  • 46. Treatment: Delayed union 1. Most commonly prolonged conservative management 2. Surgical intervention: bone grafting with or without internal fixation.
  • 47. Treatment: non union Depends 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 menthod 4. No treatment: when there is no disability, eg. # scaphoid.
  • 48. Mal union  When a fracture does not unite in proper position it is said to have malunited. Causes: 1. Improper reduction 2. Unchecked muscle pull 3. Excessive communication
  • 50. treatment 1. 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.