Complications of fracture repair Flashcards
Factors to be considered when dealing with fracture complications
Immobilisation
Biology (blood supply, bone viability, periosteum integrity, marrow cells)
Infection
Others (severity of the trauma, defect size, patient related factors)
Direct bone healing
Absolute stability (<2% interfragmentary strain)
No gap or very small gap (<1mm)
Will not result in callus formation
Indirect bone healing
Relative stability (10% interfragmentary strain)
Can occur with larger gaps
Will result in callus formation
How to calculate strain
Strain = deltal L / L
= Gap movement / fracture gap
Delayed union
A fracture that has not healed in the time normally expected for that fracture type to heal
Non-union
Fracture healing stops and union will not occur without surgical intervention
(non-progression for 3mo after fracture should have healed)
Clinical signs of a delayed or non-union
Painful motion at the fracture site
Pseudoarthritis
Progressive deformity
Disuse of the limb
Muscle atrophy
Joint stiffness
Causes of delayed and non-union
Inadequate immobilisation
Inadequate reduction
Loss of blood supply
Infection
Loss of bone from trauma
What is the commonest cause of delayed or non-union?
Inadequate immobilisation of the fracture
Radiological appearance of delayed union
A radiolucent gap between fracture fragments, with a feathery or chewed up appearance of the fracture ends and moderate callus
Radiographic appearance of non-union
No radiological evidence of healing - no callus, ends of bone segment are rounded and the marrow cavity is sealed with dense (sclerotic) trabecular bone.
Bone ends can be enlarged (elephant foot) or narrowed (atrophic).
Two main groups of non-unions
Biologically acitve/viable non-unions
Biologically inactive/non-viable non-unions
Types of biologically active or viable non-unions
Hypertrophic (elephant foot)
Slightly hypertrophic type (horses foot)
Oligotrophic type
Types of biologically inactive or non-viable non-unions
The dystrophic type (torsion wedge)
The necrotic type (necrotic segment)
The defect type (big gap)
The atrophic type
Causes of hypertrophic non-union (biologically active)
Usually a complication of IM pinning of humeral and femoral shaft fractures - caused by rotation at fracture site
Can be a complication of loose cerclage wires or sequestra
A well-developed elephant-foot shaped callus develops which does not bridge the fracture gap
Biology of a hypertrophic non-union
The gap contains cartilage and fibrous tissue
There is sclerosis of the bone ends and later the medullary cavity becomes sealed.
Treatment of hypertrophic non-union
Rigid immobilisation preferably with a compression plate or anti-rotational ESF.
Cartilage and fibrous tissue between bone ends rapidly ossifies so it is not as necessary to freshen the ends or use a bone graft
Remove loose implants or sequestra - necrotic bone is yellowish white in appearance
Following debridement flatten out the ends so they can be compressed
Slightly hypertrophic non-union (horses foot)
Instability following plate fixation
Minimal callus formation
Oligotrophic non-union
No callus formation and the fragments are usually widely separated and joined by fibrous tissue only e.g. avulsion fractures
May benefit from adjusting the biological or mechanical environment
Dystrophic non-union (torsion wedge)
Seen as a complication of comminuted fractures where a poorly revascularised fragment or fragments impedes fracture healing
Necrotic non-union
Seen in commoinuted or infected fractures where non-viable fragments or sequestra at the fracture site impede healing
Defect non-union
A major defect in the bone caused by removal of fragments or sequestra which is too big to be bridged by the normal healing process.
Often seen after severe soft tissue injury or a loss of vascularity in the area - often become atrophic.
Treatment of viable non-union
Remove loose implants
Rigid immobilisation - preferably with a compression plate or with anti-rotational ESF
Biomechanical stimmuli (e.g. shockwave therapy) can stimulate bone healing
Don’t need ends freshening or bone grafts
Treatment of non-viable non-unions
Harder
Fracture site debridement - remove loose implants, sequestra, or unhealthy callus
Exposing viable bone ends - cut back 2-3mm creating two flat surfaces
Compression with DC plate
Opening medullary cavity
Bone graft
Stem cell therapy
Biomechanical stimuli
Malunion
Defined as a fracture that has healed or is healing in an abnormal position - usually caused by improper immobilisation or reduction during healing
Classifications of malunions
Overriding
Angular
Rotational
Translational
What disease can axial and rotational deviations (malunions) predispose to?
DJD
Osteomyelitis
Any inflammatory condition of the bone which involves the haversian systems, volkmanns, cortex, and generally the marrow and periosteum
Osteitis
Inflammation of the bone only
Discospondylitis
Inflammation of the disc only
Epiphysitis
Inflammation of the epiphysis only
Source of infection of osteomyelitis
Iatrogenic
Haematogenous
Extension
Open fracture/external trauma
Nosocomial
What % of osteomyelitis cases are iatrogenic?
70%
What can cause osteomyelitis by haematogenous spread?
Spread from another infective focus in the body e.g. endocarditis
Osteomyelitits from an open fracture/external trauma
Any trauma causing a pathway from the outside of the body to the bone.
Extraneous sources can include bites, foreign bodies, and even following radiation of neoplasms
Primary bacterial contamination occurs in about 1/3 of open fractures and necrotic tissue left in the wound serves as a nidus for bacterial multiplication
Secondary bacterial infection occurs after 6-8hrs
Nosocomial infections
Infections acquired by patients during the course of hospitalisation
Pre-disposing factors to osteomyelitits (14)
Vascular compromise
Iatrogenic contamination
Dead space haematoma at fracture site
Destructive fixation devices (IM pins)
Immunosuppression (corticosteroids)
Systemic problems
Break in sterility
Length of surgery
Remote infections
Old age
Length of hospitalisation
Antimicrobial therapy
Surgical drains, urinary catheters, IV cannulas
Diagnostic procedures
Causative organisms of osteomyelitis
Bacteria - commonest
- Staph aureus
- Streps
- Coliforms
- Proteus
- Pasteurella
- Pseudomonas
- Corynebacterium
- Fusiformis necrophorus
- Nocardia
Tuberculosis - rare
Mycoses
- Cryptococcus
- Aspergillus
History of acute osteomyelitis
Recent fracture repair of arthroplasty
Clinical signs of acute osteomyelitis
Severe pain, swelling, pyrexia, lameness, tenderness and possibly a sub-periosteal abscess.
Discharge at the surgical wound may be visible
Radiographic appearance of acute osteomyelitis
No bony changes identifiable on radiographs
Treatment of acute osteomyelitis
Loose implant needs to be revised
Antibiotics (broad spec)
Bacterial culture and sensitivity
Min antibiotic course - 6wks
If not responding - surgical debridement and antibiotic implantation (beads)
History of chronic osteomyelitis
Months or even years after surgery
Clinical signs of chronic osteomyelitis
Systemic signs are rare
Less severe lameness
Radiographic appearance of chronic osteomyelitis
Evident radiographic changes
Periosteal reaction (new bone in unhealthy formation)
Focal bone lucencies and osteopaenia
Wide spread bone lysis in more chronic cases
Sequestra develop
Sclerosis of surrounding bone
Implant lossening if present
Treatment of chronic osteomyelitis
Surgical debridement and lavage and/or implant removal/revision surgery
Surgical drain or wound left to heal by second intention
Regular bacterial swab for C&S
Antibiotic loaded beads or bone cement
