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Complication of fracture

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  • Type I open fracture can be managed with non-operative approach and closed reduction.
  • may lead to irreversible damage of the life supporting organs.Thirst, rapid shallow breathing, the lips and skin are pale and the extremities feel cold,if the compansation fails….. impaired renal function test and decreased urinary output.
  • Dopamine (1-20g/kg/min)Dobutamine (1-20g/kg/min)Adrenaline (1-20g/min)Noradrenaline (1-20g/min)
  • DIVC
  • It’s a re-perfusion injury seen after the release of crushing pressure, there will be release of muscular breakdown products(myoglobin,k+,p) which have nephrotoxic effect on the kidneyFirst describe by Eric Bywaters
  • It’s a re-perfusion injury seen after the release of crushing pressure, there will be release of muscular breakdown products(myoglobin,k+,p) which have nephrotoxic effect on the kidneyFirst describe by Eric Bywaters
  • Petechial haemorrhage
  • 4C – Colour – blue-black purpleConsistency – MushyContractibility – unableCut – not capable to bleedDeep, penetrating wound in muscular tissue should be explored, ALL DEAD TISSUE SHOULD BE COMPLETELY EXCISED, if there is doubt about tissue viability, the wound should be left opened
  • Neuropraxia = misspellingNeurapraxia = neuro + a [no] + praxia [action]Axonotmesis = axon + tmesis [cut]Neurotmesis = Nerve + tmesis [cut]

Complication of fracture Complication of fracture Presentation Transcript

  • FRACTURES
    AnandkumarBalakrishna
    Wong Poh Sean
    MohdHanafiRamlee
  • CONTENT
    DEFINITION
    PRINCIPLE MANAGEMENT
    COMPLICATIONS
  • DEFINITION
  • CAUSES
    Sudden trauma
    direct(fracture of the ulna caused by blow on the arm)
    indirect(spiral fractures of the tibia and fibula due to torsion of the leg, vertebral compression fractures, avulsion fractures)
    Stress or fatigue-repetitive stress(athletes, dancers, army recruits)
    Pathological(osteoporosis, Paget’s disease, bone tumour)
  • TYPES OF FRACTURES
  • COMPLETE FRACTURES
  • INCOMPLETE FRACTURE
  • FRACTURES DISPLACEMENT
    After a complete fracture the fragments usually displaced:
    partly by the force of injury
    partly by gravity
    partly by the pull of muscles attached to them.
    4 types:
    Translation/Shift
    Alignment/Angulation
    Rotation/Twist
    Altered length
  • SIDEWAYS
    OVERLAP
    IMPACTION
  • HOW FRACTURES HEAL?
    Healing by callus
    Healing without callus
  • Healing by callus
    Callus is the response to movement at the fracture site to stabilize the fragments as rapidly as possible.
    Steps:
  • Healing without callus
    For fracture that is absolutely immobile:
    impacted fracture in cancellous bone.
    fracture rigidly immobilized by internal fixation
    New bone formation occurs directly between fragments.
    Gaps between the fracture surfaces are invaded by new capillaries & bone forming cells growing in from edges.
    For very narrow crevices(<200um), osteogenesis produces lamellar bone(mature).
    For wider gaps, osteogenesis begins with woven bone (immature) first which is then remodelled to lamellar bone (mature bone).
  • RATE OF REPAIR DEPENDS UPON:
  • CAUSES OF DELAYED UNION OR NON-UNION OF THE FRACTURES
  • FRACTURES- PRINCIPLE OF TREATMENT
  • Management of Closed Fracture
  • First aid management
    Airway, Breathing and Circulation
    Splint the fracture
    Look for other associated injuries
    Check distal circulation – is distal circulation satisfactory?
    Check neurology – are the nerve intact?
    AMPLE history- Allergies, Medications, Past medical history, Last meal, Events
    Radiographs – 2 views, 2sides, 2 joints, 2 times.
  • Principle Of Treatment
  • The Fracture Quartet
  • Outline
  • Reduce
    Aim for adequate apposition and normal alignment of the bone fragments
    The greater contact surface area between fragments, the more likely is healing to occur
  • However, there are some situations in which reduction is unnecessary:
    When there is little or no displacement
    When displacement does not matter (e.g. in some fractures of the clavicle)
    When reduction is unlikely to succeed (e.g. with compression fracture of the vertebrae)
  • Reduction
  • Closed Reduction
    Suitable for
    Minimally displaced fractures
    Most fractures in children
    Fractures that are likely to be stable after reduction
  • Most effective when the periosteum and muscles on one side of fracture remain intact
    Under anaesthesia and muscle relaxation, a threefold manoeuvre applied:
    Distal part of the limb is pulled in line of the bone
    Disengaged, repositioned
    Alignment is adjusted
  • Mechanical Traction
    Some fractures (example fracture of femoral shaft) are difficult to reduce by manipulation because of powerful muscle pull
    However, they can be reduced by sustained muscle mechanical traction; also serves to hold the fracture until it starts to unite
  • Open Reduction
    Operative reduction under direct vision
    Indications:
    When closed reduction fails
    When there is a large articular fragment that needs accurate positioning
    For avulsion fractures in which the fragments are held apart by muscle pull
    When an operation is needed for associated injuries
    When a fracture needs an internal fixation
  • Hold
  • HOLD
  • Sustained Traction
    • Traction is applied to limb distal to the fracture
    • To exert continuous pull along the long axis of the bone
  • Disadvantage and complications
    Patient kept on bed for long time
    Pressure ulcer
    General weakness
    Pulmonary infection
    Contracture
    Pin tract infection
    Thromboembolic event
    Methods
    Traction by gravity
    Balanced traction
    Fixed traction
  • Traction By Gravity
    Example:
    Fracture of humerus
    • Weight of arm to supply traction
    • Forearm is supported in a wrist sling
  • Balanced Traction
  • Thomas’s Splint
  • Fixed Traction
    Principle = balanced traction
    Useful for when patient has to be transported
    Thomas’s splint
  • Cast Splintage
    Methods:
    Plaster of Paris
    Fibreglass
    Especially for distal limb # and for most children #
    Disadvantage: joint encased in plaster cannot move and liable to stiffen
    Can be minimized:
    Delayed splintage (traction initially)
    Replace cast by functional brace after few weeks
  • Complications
  • Functional Bracing
  • INTERNAL FIXATION
  • Principle
  • Indication
  • Type of internal fixation
  • advantages
  • Implant failureMetal is subjected to fatigue
    • Metal is subjected to fatigue
    • So, undue stress should therefore be avoided until the fragment has united.
    • Pain at the site of fracture site is a danger signal.
  • Refracture
    • It is important not to remove the metal implant too soon
    • A year is minimum and 18 to 24 month is safer
    • For several weeks after the implant removal the bone is weak so full weight-bearing should be avoided
  • EXTERNAL FIXATION
  • Principle
  • Indication
  • (a)The patient was fixed with a plate and screw but did not unite (b) external fixation was applied
  • Advantages
  • Exercise
    Prevention of edema
    active exercise and elevation
    Active exercise also stimulates the circulation. Prevents soft-tissue adhesion and promotes fracture healing.
    Preserve the joint movement
    Restore muscle power
    Functional activity
  • Management of Open Fractures
    Abreakin skin and underlying soft tissues leading directly to communicating with the fracture
  • Open Fracture
  • First Aid & Management of the Whole Patient
  • 1. Emergency Management of Open Fracture
    A,B,C
    Splint the limb
    Sterile cover - prevent contamination
    Look for other associate injury
    Check distal circulation – is distal circulation satisfactory?
    Check neurology – are the nerve intact?
    AMPLE history- Allergies, Medications, Past medical history, Last meal, Events
    Radiographs – 2 view, 2sides, 2 joints, 2 times.
    Relieve pain
    Tetanus prophylaxis
    Antibiotics
    Washout / Irrigation
    Wound debridement
    fracture stabilisation
    80
  • Open Fractures Classification
  • Preoperative Assessment
  • Preoperative Assessment
  • Treatment- Outline
  • 1) Analgesic + Antibiotic + AntitetanusProphylaxis
  • Antibiotic
    • GustiloGrade I- first generation of cephalosporin for 72 hours
    • Gustilo Grade II- first generation cephalosporin for 72 hours + Gram negative coverage (gentamicin) for at least 72 hours
    • Gustilo Grade III- first generation cephalosporin +G –ve coverage for at least 72 hours
    • For soil contamination- penicillin is added for clostridial coverage
  • 2) Irrigation
  • 3) Debridement
  • Surgical Debridement
    Type II and type III require surgical debridement.
    Important aspect of wound management.
    Reduce bacteria, remove foreign bodies, remove devitalized tissue.
    Removal of dead tissue reduces bacterial burden and accelerate healing.
    89
  • 4) Wound Closure
  • Wound Closure
    Uncontaminated I & II can be sutured – provided without tension
    All other wounds left open, packed with moist sterile gauze, to be inspected 24-48 hours – primary delayed closure
    If wound cannot be closed without tension – skin grafting
  • 5) Fracture Stabilization
  • Stabilization of the fracture
    To reduce infection and assist recovery of soft tissue
    Depends on:
    degree of contamination
    length of time from injury to operation
    amount of soft tissue damage
    If <8 hours: up to IIIA treated as closed fractures:
    Splintage
    Intramedullary nailing
    Plating
    External fixation
    Others: External fixation
  • Aftercare
  • COMPLICATION OF FRACTURE
  • GENERAL
    BONE
    JOINT
    SOFT TISSUE
  • General Complications
    Shock
    Diffuse coagulopathy
    Respiratory dysfunction
    Crush syndrome
    Venous thrombosis & Pulmonary embolism
    Fat embolism
    Gas Gangrene
    Tetanus
  • General 1: Shock
    Altered physiologic status with generalized inadequate tissue perfusion relative to metabolic requirements.  irreversible damage to vital organs
  • 1500-3000ml
    500-1000ml
    1500-3000ml
    100-300ml
    1000-2000ml
    1000-2000ml
    VOLUME DISTRIBUTION
  • General 1: Shock
  • General 2: DIFFUSE COAGULOPATHY
  • General 3: RESPIRATORY DYSFUNCTION
  • General 4: Crush Syndrome[traumatic rhabdomyolitis]
    Serious medical condition characterized by major shock & renal failure following a crushing injury to skeletal muscles or tourniquet left too long
    Bywaters’ Syndrome
  • General 4: Crush Syndrome
  • General 5: Deep vein thrombosis and pulmonary embolism.
    Virchow’s triad factor  Clot formation in large vein  thrombus breaks off  Emboli
    Site: leg, thigh and pelvic vein.
    Risk factors:
  • General 5: Management Deep vein thrombosis and pulmonary embolism.
    Anticoagulation
    Ambulate patient
    Established thrombosis/embolism
    Limb elevation
    Heparinization
    Thrombolysis
    Oxygenation or ventilation
    PREVENTION
    Correct hypovolemia
    Calf muscle exercise
    Proper positioning
    Well fitting bandages & cast
    Limb elevation
    Graduated compression stockings
    Calf muscle stimulation
  • General 6: Fat Embolism
    Fat globules from marrow pushed into circulation by the force of trauma that causing embolic phenomena
  • General 6: Fat Embolism
  • General 6: Fat Embolism
    SKIN: Fat droplets  obstruct alveolar capillaries  thromboplastin release  consumption of coagulation fx & platelets  DIVC/Skin necrosis  Petechia
    LUNG: Fat droplets  obstruct alveolar capillaries  thromboplastin release  alter membrane permeability / lung surfactant  oedema  respiratiory failure [V/Q Mismatch]
    BRAIN: Fat droplets  obstruct capillaries  confusion  coma/fits  death
  • General 7: Gas Gangrene
    Rapid and extensive necrosis of the muscle accompanied by gas formation and systemic toxicity due to clostridium perfringens infection
  • General 7: Gas Gangrene
    Prevention: ALL DEAD TISSUE [4C] SHOULD BE COMPLETELY EXCISED,
  • General 8: Tetanus
    A condition after clostridium tetani infection that passes to anterior horn cells where it fixed and cant be neutralized later produces hyper-excitability and reflex muscle spasm
  • Early Complications
    Visceral Injury
    Vascular Injury
    Compartment Syndromes
    Nerve injury
    Haemarthrosis
    Infection
  • Early 1: Visceral injury
    Fractures around the trunk are often complicated by visceral injury.
    E.g. Rib fractures  pneumothorax / spleen trauma / liver injuries.
    E.g. Pelvic injuries  bladder or urethral rupture / severe hematoma in the retro-peritoneum .
    Rx: Surgery of visceral injuries
  • Early 2: Vascular injury
    Commonly associated with high-energy open fractures. They are rare but well-recognized.
    Mechanism of injuries:
    The artery may be cut or torn.
    Compressed by the fragment of bone.
    normal appearance, with intimal detachment that lead to thrombus formation.
    segment of artery may be in spasm.
    It may cause
    Transient diminution of blood flow
    Profound ischaemia
    Tissue death and gangrene
  • Early 2: Vascular injury
    X-ray: suggest high-risk fracture.Angiogram should be performed to confirm diagnosis.
  • Early 2: Vascular injury
    muscle ischaemic is irrevesible after 6 hours.
    Remove all bandages and splint & assess circulation
    Skeletal stabilization – temporary external fixation.
    Definitive vascular repair.
    Vessel sutured
    endarterectomy
  • Early 3: Compartment Syndrome
    A condition in which increase in pressure within a closed fascial compartment leads to decreased tissue perfusion.
    Untreated, progresses to tissue ischaemia and eventual necrosis
  • Early 3: Compartment Syndrome
    Most common sites (in ↓ freq): leg (after tibial fracture) -> forearm -> thigh -> upper arm. Other sites: hand, foot, abdomen, gluteal and cervical regions.
    High risk injuries:
    # of elbow, forearm bones, and proximal 3rd of tibia (30-70% after tibial #)
    multiple fracture of the foot or hand
    crush injuries
    circumferential burns
  • Early 3: Compartment Syndrome [aetiology]
  • Early 3: Compartment
    Syndrome
    Vicious cycle
    ↑ fluid content
    Constriction of compartment
    ↑ INTRACOMPARTMENTAL PRESSURE
    Capillary basement membranes become leaky -> oedema
    Obstruct venous return
    Vascular congestion
    Muscle and nerve ischaemia
    Further ↑ intracompartmental pressure
    ↓ capillary perfusion
    Compromise arterial circulation
    -> PROGRESSIVE NECROSIS OF MUSCLES AND NERVES !!
  • A vicious circle that ends after 12 hours or less
    Necrosis of the nerve and muscle within the compartment
    Nerve
    -capable to regenerate
    Muscle
    -infarcted
    Never recover
    Replaced by inelastic fibrous tissue
    ( Volkmann’s ischaemic contracture)
  • Investigations of compartment sydromes
    Intra-compartment Pressure Measurement (ICP)
    Use of slit catheter; quick and easy
    Indications:
    Unconscious patient
    Those who are difficult to assess
    Concomitant neurovascular injury
    Equivocal symptoms
    Especially long bone # in lower limb
    Perform as soon as dx considered
    > 40mmHg – urgent Rx! (normal 0 – 10 mmHg)
  • Investigations of compartment syndromes
    Other Ix – limited value; +ve only when CS is advanced
    Plasma creatinine and CPK
    Urinanalysis – myoglobinuria
    Nerve conduction studies
    Ix to establish underlying cause or exclude differentials
    X-ray of affected extremity
    Doppler US/arteriograms – determine presence of pulses; exclude vascular injuries and DVT
    PT/APTT – exclude bleeding disorder
  • Management
    Prompt DECOMPRESSION of affected compartment
    Remove all bandages, casts and dressings
    Examination of whole limb
    Limb should be maintained at heart level
    Elevation may ↓ arterio-venous pressure gradient on which perfusion depends
    Ensure patient is normotensive.
    Hypotension ↓ tissue perfusion, aggravate the tissue injury.
  • Management
    Measure intra-compartment pressure
    If > 40mmHg
    Immediate open fasciotomy
    If < 40mmHg
    Close observation and re-examine over next hour
    If condition improve, repeated clinical evaluation until danger has passed
    Don’t wait for the obvious sings of ischemia to appear. If you suspect
    An impending compartment syndrome, start treatment straightaway
  • Fasciotomy
    Opening all 4 compartments
    Divide skin and deep fascia for the whole length of compartment
    Wound left open
    Inspect 5 days later
    If muscle necrosis, do debridement
    If healthy tissue, for delayed closure or skin grafting
  • Complications
    Volkmann’s ischaemiccontracture
    Motor/sensory deficits
    Kidney failure from rhabdomyolysis (if very severe)
    Infection – fasciotomy converts closed # to open #
    Loss of limb
    Delay in bone union
    Prognosis
    excellent to poor, depending on how quickly CS is treated and whether complications develop
  • Early 4: Nerve Injury
    It’s more common than arterial injuries.
    The most commonly injured nerve is the radial nerve [in its groove or in the lower third of the upper arm especially in oblique fracture of the humerus]
    Common with humerus, elbow and knee fractures
    Most nerve injuries are due to tension neuropraxia.
  • Early 4: Nerve Injury
    Damaged by laceration, traction, pressure or prolonged ischaemia
  • Early 4: Nerve Injury
    Investigations
    Electromyography
    Nerve conduction study
    May help to establish level and severity of lesion
    Clinical features
    Numbness and weakness
    Skin smooth and shiny but feels dry
    Muscle wasting and weakness
    Sensation blunted
    Tinel’s sign +ve
  • Early 4: Nerve Injury
  • Early 5: Haemarthrosis
    Bleeding into a joint spaces.
    Occurs if a joint is involved in the fracture.
    Presentation:
    swollen tense joint; the patient resists any attempt to moving it
    treatment:
    blood aspiration before dealing with the fracture; to prevent the development of synovial adhesions.
  • Early 6: INFECTION
    Closed fractures – hardly ever
    Open fractures – may become infected
    Post traumatic wound – may lead to chronic osteomyelitis
  • Late Complications
    Delayed Union
    Non-union
    Mal-union
    Avascular Necrosis
    Osteoarthritis
    Joint Stiffness
  • Late 1: DELAYED UNION
    Union of the upper limbs - 4-6 weeks
    Union of the lower limbs - 8-12 weeks(rough guide)
    Any prolong time taken is considered delayed
  • Late 1: DELAYED UNION
    Factors are either biological or biomechanical
    Biological :
    Poor blood supply
    Tear of periosteum, interruption of intramedullary circulation
    Necrosis of surface# and healing process will take longer
    Severe soft tissue damage
    Most important factor
    Longer time for bone healing due less inflammatory cell supply
    Infection: bone lysis, tissue necrosis and pus
    Periosteal stripping
    Less blood circulation to bone
  • Mechanical
    Over-rigid fixation-fixation devise
    Imperfect splintage
    Excessive traction creates a gap#(delay ossification in the callus)
    Late 1: DELAYED UNION
  • Clinical features:
    Tenderness persist
    Acute pain if bone is subjected to stress*
    ( * ask pt to walk, move affected limb)
    X RAYS -visible line# and very little callus
    formation/periosteal reaction
    - bone ends are not sclerosed/ atrophic
    (it will eventually unite)
    Late1: DELAYED UNION
  • Tx: conservative and operative
    Eliminate possible causes of delay
    Promote healing
    Immobilization should be sufficient to prevent movement at # site(cast / internal fixation)
    Not to neglect # loading so, encourage muscle exercise and weight bearing in the cast/brace
    Operation
    > 6 mths & no signs of callus formation
    Internal fixation and bone graffting
    (operation-least possible damage to the soft tissue)
    Late 1: DELAYED UNION
  • Late 2 : NON-UNION
    In a minority of cases, delayed union--non-union
    Factors contributing to non-union:-
    inadequate treatment of delayed union
    too large gap
    interposition of soft tissues between the fragments
    The growth has stopped and pain diminished- replaced by fibrous tissue - pseudoarthrosis
    Treatment :-
    conservative / operative
    atrophic non-union – fixation and grafting
    hypertrophic non-union – rigid fixation
  • Late 2: NON UNION
    bone ends are rounded off or exuberant
    Hypertrophic non union
    Bone ends are enlarged, osteogenesis is still active but not capable of bridging the gap
    ‘elephant feet’ on X ray
    Atrophic non union
    Cessation of osteogenesis
    No suggestion of new bone formation
  • Non-union
    X- ray
    A – Atrophic non- union
    B – Hypertrophic non- union
    A
    B
  • Late 2: Non union
    Tx:
    Mostly symptomless
    Conservative
    Removable splint
    For hypertrophic non-union, functional bracing-induce union
    Pulsed electromagnetic fields and low frequency pulsed u/s can also be used to stimulate union.
    Operative
    Hypertrophic--Rigid fixation (internal or external)
    Atrophic--Excision of fibrous tissue ,sclerotic tissue at bone end, bone grafts packed around the fracture
  • Late 3: MALUNION
    Factors:-
    failure to reduce the fracture
    failure to hold the reduction while healing proceed
    gradual collapse of comminuted / osteoporotic bone
  • MALUNION
  • Late 3: Mal-union
    X-ray are essential to check the position of the fracture while uniting. important- the first 3 weeks so it can be easily corrected
    Clinical features:
    Deformity usually obvious , but sometimes the true extent of malunion is apparent only on x-ray
    Rotational deformity can be missed in the femur, tibia, humerus or forearm unless is compared with it’s opposite fellow
  • Treatment
    Decision about the need for re-manipulation and correction-difficult
  • Late 4: AVASCULAR NECROSIS
    Certain region-known for their propensity to develop ischaemia and bone necrosis
    Head of femur
    Proximal part of scaphoid
    Lunate
    Body of talus
    (Actually this is an early complication however the clinical and radiological effects are not seen until weeks or even months)
    No clinical feature of avascular necrosis but if there is a failure to unite or bone collapse-pain
  • A
    B
    The cardinal X-ray feature – increased bone density in the weight-bearing part of the joint(new bone ingrowth in necrotic segment)
  • Treatment:-
    Avascular necrosis can be prevented by early reduction of susceptible fractures and dislocations.
    Arthroplasty - Old people with necrosis of the femoral head.
    Realignment osteotomy or arthrodesis - for younger people with necrosis of the femoral head
    Symptomatic treatment for scaphoid or talus
  • Late 5: OSTEOARTHRITIS
    A fracture-joint may damage the articular cartilage and give rise to post traumatic osteoarthritis within a period of months.
    Even if the cartilage heals, irregularity of the joint surface may cause localized stress and so predispose to secondary osteoarthritis years later
  • Late 6: JOINT STIFFNESS
    Commonly occur at the joints close to malunion or bone loss eg: knee, elbow, shoulder
    Causes of joint stiffness
    haemarthrosis -> lead to synovial adhesion
    oedema and fibrosis
    adhesion of the soft tissues
    Worsen by prolong immobilization
    Treatment
    prevented with exercise
    physiotherapy
  • THANK YOU!!!!