4. â Fractures takes longer than usual to unite, but
passes through the normal clinical and radiological
stages of healing without any departure from
normal
â Mx : Reassurance of the patient
6. DEFINITION ď Healing has not advanced at the
average rate for the location and type of
fracture for three months.
⢠Biological process of repair is continuous.
âAs compared to slow union, radiographs
may show abnormal bone changes.
âThere is, however, no sclerosis of the bone
ends.
8. Management
â The problem is to differentiate between delayed
union which is going to proceed with proper
encouragement to union, and delayed union
which is going to go on to non-union
â Disadvantage of delaying intervention :
irreversible stiffness in joints which are
immobilised with the fracture
11. DEFINITION ď A minimum of nine months has past
since the injury and the fracture shows no clinical
and radiological progressive signs of healing
continuously.
⢠Complete suspension of biological process of
repair.
â Radiological changes which indicate that this situation
will be permanent.
â i.e. the fracture will never unite unless there is some
fundamental alteration in the line of treatment.
12. Types of non-union
(muller and weber)
a. Hypervascular b. Avascular
⢠# ends are viable and capable of
biological reaction
⢠Rigid internal fixation is enough
⢠# ends are inert and incapable of
biological reaction.
⢠Rigid internal fixation with bone
grafting is required
1. Elephant foot non union 1. Torsion wedge non union
⢠It is seen in segmental #
2. Horse hoof non union 2. Comminuted non union
⢠It is seen in comminuted #
3. Oligotrophic non union 3. Defect non union
⢠Seen in open fractures.
4. Atrophic non union
⢠The ends are tapered thin and sclerotic
with excessive scar tissue in between
13. Septic
Non-union
with
underlying
osteomyelitis
Aseptic
Hypertrophic Non-union
(Pseudarthrosis)
Excessive callus formations
around the fracture gap â
d/t insufficient stability of
the internal fixator
âElephant Footâ
Bone ends appear sclerotic
and are flared out ď
diameter of the bone
fragments at the level of the
fracture is increased
Fracture line is clearly visible,
Gap being filled with cartilage and
fibrous tissue cells
Good blood supply
(eventhough increase in
bone density)
Atrophic Non-union
No callus formations
ď d/t impaired
healing process
No evidence of cellular activity
at the level of the fracture
Bone ends are narrow,
rounded and osteoporotic
Frequently Avascular
Types of Non-union
15. CAUSES OF NON-UNION
Injury
Distraction
at fracture
site
Soft tissue
loss
Bone loss
Soft tissue
interposition
Bone
Poor blood
supply
Hematoma
Infection
Pathological
lesion
Surgeon
Poor
splintage
Poor
fixation
Impatience
Patient
Age
Poor
medical
condition
Smoking
and
Alcohol
Drugs
NSAIDs
Fluoro-
quinolone
16. MANAGEMENT
1. Open reduction and bone grafting
2. Electrical stimulation
3. Rigid internal fixation by DCP/interlocking nail Âą
Bone grafting.
4. Ilizarovâs technique
17. Difference between
non-union and delayed union
NON UNION DELAYED UNION
⢠No bony tenderness
⢠No bony crepitus
⢠Frank painless abnormal
mobility at fracture site.
Clinical
Features
⢠Bony tenderness present
⢠No bony crepitus
⢠A little (painful) or no abnormal
mobility at fracture site
ďźVisible # line without bridging
callus.
ďźThe fragments are rounded
smooth and sclerotic.
ďź The medullary canal may be
obliterated.
X-Ray Visible # line with inadequate callus
bridging the fracture site.
It is absolute indication for surgery
(no role of conservative treatment).
Treatment Conservative â prolonged
immobilization for longer period
(sometimes it may need surgical
intervention)