COMPLICATIONS OF

FRACTURES AND ITS

MANAGEMENT

dr. BAMBANG WIDIWANTO, MS, SpOT

FK UMM

INTRODUCTION

Because bones are

surrounded by soft tissue,
the physical forces that
produce a fracture always
produce some degree of
soft tissue injury as well.
The associated soft tissue
injury may assume much
greater clinical significance
than the fracture itself.

INTRODUCTION

Radiographs:
Just provide such
graphic evidence of a
fracture.
Seldom provide
evidence of the extent of
the associated soft
tissue injury.
Therefore it must be
thought in term of the
fracture: What has
happened to the
surrounding soft tissue?

Urgent
Local visceral injury
Vascular injury
Nerve injury
Compartment
Syndrome
Haemarthrosis
Infection
Gas gangrene

LOCAL
Less Urgent
Fracture blisters
Plaster sores
Pressure sores
Nerve entrapment
Myositis Ossificans
Ligament injury
Tendon lesions
Joint stiffness
Algdystrophy

Late

Delayed union
Malunion
Non-union
Avascular necrosis
Muscle contracture
Joint instability
Osteoarthrosis

VISCERAL INJURY

Penetration of the lung

with life threatening
pneumothorax -following rib fractures.
Rupture of the bladder
or urethra in pelvic
fractures.
These injuries require
emergency treatment.

VASCULAR INJURY

The artery may be cut,

torn, compressed or
contused, either by the
initial injury or
subsequently by jagged
bone fregments.
The effects vary from
transient diminution of
blood flow to profound
ischaemia, tissue death
and peripheral gangrene.

Common vascular injuries

Injury

Vessel

First rib fracture

Shoulder dislocation
Humeral supracondylar fracture
Elbow dislocation
Pelvic fracture
Femoral supracondylar fracture
Knee dislocation
Proximal tibial

Subclavian
Axillary
Brachial
Brachial
Presacral and internal iliac
Femoral
Popliteal
Popliteal

Clinical feature Vascular injury

Paraesthesia or
numbness in the toes
or fingers.
The injured limb is
cold and pale, or
slightly cyanosed.
The pulse is weak or
absent

Treatment Vascular injury

Prompt reduction is necessary.

The circulation is then reassessed.
If there is no improvement the vessels
must be explored by operation (preferably
with the benefit of preoperative or
peroperative angiography).
A torn vessel can be sutured, or a
segment may be replaced by a vein graft.
If it is thrombosed, endarterectomy may
restore the blood flow.

NERVE INJURY

Complaints of
numbness or
paraesthesia in the
nerve distribution.

In close injury the nerve

is seldom severed, and
spontaneous recovery
should be awaited it
occurs in 90% of cases
within 4 months.

Common nerve injuries

Injury

Nerve

Shoulder dislocation
Humeral shaft fracture
Humeral supracondylar fracture
Elbow medial condyle
Monteggia fracture-dislocation
Hip dislocation
Knee dislocation

Axillary
Radial
Radial or median
Ulnar
Posterior interosseous
Sciatic
Peroneal

NERVE INJURY
If recovery has not
occurred by the
expected time, and if
nerve conduction
studies fail to show
evidence of recovery,
the nerve should be
explored.
Early exploration should
also be considered if
signs of a nerve injury
appear after
manipulation of the
fracture. ( Siegel and
Gelberman, 1991)

NERVE INJURY

In open fracture any

nerve lesion is more
likely to be
complete; the nerve
is explored during
wound debridement
and repair, either
then or as a
secondary procedure
3 week later

COMPARTMENT SYNDROME

Bleeding, oedema or
inflamation may increase
the pressure within one of
the osteofascial
compartment.
There is reduced capillary
flow which result in muscle
ischaemia, further
oedema, still greater
pressure and yet more
profound ischaemia.

Ischaemia

Reduced
Blood flow

Painful
Pale
Pulseless
Paraesthetic

Oedema

Increase
Compartment
pressure

Paralysed
Fasciotomy

A Vicious circle that ends, after 12 hours or less, in necrosis of

nerve and muscle within compartment.
Nerve is capable of regeneration but muscle, once infarcted,
can never recover and is replaced by inelastic fibrous tissue
( VOLKMANNS ISCHAEMIC CONTRACTURE )

Clinical Features Compartment Syndrome

Ischaemic muscle is highly

sensitive to stretch, it should
be tested by stretching them
when the toes or fingers
are passively hyperextended
there is increase pain in the
calf or forearm.
The presence of a pulse does
not exclude the diagnosis.
In doubtful cases the
diagnosis can be confirmed
by measuring the
intracompartmental
pressure.

Treatment Compartment Syndrome

The threatened compartment

must be promptly
decompressed. Cast, bandage
and dressing must be
completely removed.
A differential pressure
between diastolic and
compartment should be
monitored, if it falls below 30
mmHg, immediate open
fasciotomy is performed

HAEMARTHROSIS

Fractures involving a joint may cause

acute haemarthrosis.
The joint is swollen and tense and
the patient resist any attempt at
moving it.
The blood should be aspirated before
dealing with the fracture.

INFECTION

Open fracture may become

infected.
Closed fractures hardly ever
do unless they are opened by
operation.
Post-traumatic wound
infection is now the most
common cause of chronic
osteitis.
This does not prevent the
fracture from uniting, but
union will be slow and chance
of refracturing is increase.

Clinical features - Infection

The history is of an
open fracture or an
operation on a closed
fracture.
The wound becomes
inflamed and starts
draining seropurulent
fluid, a sample of which
may yield a growth of
staphylococci or mixed
bacteria.

Treatment - Infection

All open fractures should

be regarded as
potentially infected
antibiotics and
meticulously excising all
devitalized tissue.
Signs of acute infection
and pus formation, the
tissue around the
fracture should be
opened and drained.
External fixation is useful
in such cases

GAS GANGRENE

Produced by Clostridial infection ,especially Clostridium

welchii anaerobic organism that can survive and multiply
only in tissues with low oxygen tension.
The prime site is a dirty wound with dead muscle that has
been closed without adequate debridement.

Toxins produced by the organisms destroy the cell wall and

rapidly lead to tissue necrosis, thus promoting the spread
of the disease.

Clinical feature Gas gangrene

Appear within 24 hours of injury.

Intense pain, swelling around the wound and a
brownish discharge may be seen. Gas formation
is usually not very marked.
Pulse rate is increase and a characteristic smell
becomes evident. Rapidly the patient becomes
toxaemic and may lapse into coma and death.

Clinical feature Gas gangrene

It is essential to distinguish gas gangrene, which

is characterized by myonecrosis, from anaerobic
cellulitis, in which superficial gas formation is
abundant but toxaemia usually slight.
Failure to recognize the difference may lead to
unnecessary amputation for the nonlethal
cellulitis.

Prevention Gas gangrene

Deep, penetrating wound in muscular tissue are

dangerous; they should be explored, all dead
tissue should be completely excised.
If there is the slightest doubt about tissue
viability, the wound should be left open.
Unhappily there is no effective antitoxin against
C.welchii.

Treatment Gas gangrene

The key to life-saving treatment is early

diagnosis.
Fluid replacement and intravenous antibiotic are
started immediately.
Hyperbaric oxygen has been used as a means of
limiting the spread of gangrene.
The mainstay of treatment is prompt
decompression of the wound and removal of all
dead tissue.
In advanced cases, amputation may be essential.

FRACTURE BLISTERS

These are due to elevation of the superficial

layers of skin by oedema, and can sometime be
prevented by firm bandaging.
They should be covered with a sterile dry
dressing.

PLASTER SORES AND PRESSURE SORES

Plaster sores occur where skin presses directly

onto bone. They should be prevented by padding
the bony points and by moulding the wet plaster
so that pressure is distributed to the soft tissue
around the bony points.
While a plaster sore is developing the patient
feels localized burning pain. A window must
immediately be cut in the plaster, or warning pain
quickly abates and skin necrosis proceeds
unnoticed.

DELAYED UNION

If the time is unduly

prolonged, the term
delayed union is used.
Factors causing delayed
union can be summarized
as :
Biological
Biomechanical
Patient related

BIOLOGICAL FACTORS
INADEQUATE BLOOD SUPPLY
A badly displaced fracture of a long bone will
cause tearing of both the periosteum and
interruption of the intramedullary blood supply.
. SEVERE SOFT TISSUE DAMAGE
- Reducing the effect of muscle splintage.
- Damaging blood supply.
- Diminishing the osteogenic stimulus.
. PERIOSTEAL STRIPPING

BIOMECHANICAL FACTORS
.

IMPERFECT SPLINTAGE
Excessive traction, excessive movement or
isolated fracture of forearm or leg will delay
ossification in the callus.
. OVER-RIGID FIXATION
Contrary to popular belief, rigid fixation delays
rather than promotes fracture union. Union by
primary bone healing is slow.
. INFECTION
There is bone lysis, necrosis and pus formation
but also implants which are used to hold the
fracture tend to loosen.

Clinical features Delayed Union

Fracture tenderness persists and if the bone is

subjected to stress, pain may be acute.
X-Ray
- The fracture line remains visible and there is
very little callus formation or periosteal reaction.
- The bone ends are not sclerosed or athropic.

Conservative Treatment Delayed Union

The two important principles are:
1.
To eliminate any possible cause of delayed
union.
2.
To promote healing by providing the most
appropriate biological environment.
Fracture loading is an stimulus to union by:
a. By encouraging muscular exercise
b. By weightbearing in the cast or brace

Operative Treatment Delayed Union

If union is delayed for more than 6 months and
there is no sign of callus formation, fixation and
bone grafting are indicated.
The operation should be planned in such a way as
to cause the least possible damage to the soft
tissue.

NON-UNION
The fracture gap become a type
of pseudoarthrosis.
In hyperthropic non-union the
bone ends are enlarged,
suggesting that osteogenesis
is still active but not quite
capable of bridging the gap.
In athropic non-union
osteogenesis semms to have
ceased. The bone ends are
often tapered or rounded with
no suggestion of new bone
formation.

Causes of non-union
The Injury

The bone

Soft tissue loss

Bone loss
Intact fellow bone
Soft tissue interposition

Poor blood supply

Poor haematoma
Infection
Pathologic lesion

The surgeon

The patient

Distraction
Poor splintage
Poor fixation
Impatience

Immense
Immoderate
Immovable
Immpossible

CONSERVATIVE TREATMENT
With hyperthropic non-union,
- Functional bracing may be sufficient to induce
union.
- Pulse electromagnetic fields.
- Low frequency pulsed ultrasound can

OPERATIVE TREATMENT

Hypertrophic non-union,
rigid fixation alone may
lead to union.
Atrophic non-union,
fixation alone is not
enough. Fibrous tissue in
the fracture gap, as well as
the hard, sclerotic bone
ends, are excised and bone
grafts are packed arround
the fracture.

MALUNIION

When the fragments join in

an unsatisfactory position
(unacceptable angulation,
rotation or shortening) the
fracture is said to be
malunited.
Causes are failure to
reduce a fracture
adequately, failure to hold
reduction while healing
proceeds or gradual collaps
of comminuted or
osteoporotic bone.

Clinical features - Malunion

The deformity is usually

obvious, but sometimes
apperent only on X-ray.
Rotational deformity of the
femur, tibia, humerus or
forearm may be missed
unless the limb is
compared with its opposite
fellow.

Clinical features - Malunion

Rotational deformity of a
metacarpal fracture is
detected by asking the
patient to flatten the
fingers onto the palm and
seeing whether the normal
regular fan-shaped
appearance is reproduced.

Treatment Malunion
A few guidelines are offered
1.

2.

3.

4.

In adults, angulation of more than 10 150 in a long

bone, or a noticeable rotational deformity, may need
correction by remanipulation, or by osteotomy and
internal fixation.
In children, angular deformities near the bone ends will
usually remodel with time; rotational deformity will not.
In the lower limb, shortening of more then 2.0cm is
seldom acceptable to the patient and a limb lengthening
procedure may be indicated.
The patients expectation (often prompted by cosmesis)
may be quite different from the surgeons; they are not
to be ignored.

Treatment Malunion
A few guidelines are offered
5. Early discussion with the patient, and a guided view of the
X-rays, will help in deciding on the need for treatment and
may prevent later misunderstanding.
6. Malalignment of more than 150 in any plane may cause
asymmetrical loading of the joint above or below and the
late development of secondary osteoarthritis; this applies
particularly to the large weightbearing joints.

AVASCULAR NECROSIS
Certain regions are notorious for
their propensity to develop
ischaemia and bone necrosis
after injury:
1. The head of the femur
(after fracture of femoral neck
or dislocation of the hip).
2. The proximal part of the
scaphoid (after fracture
through its waist).
3. The lunate (following
dislocation).
4. The body of the talus (after
fracture of its neck).

AVASCULAR NECROSIS
Ischaemia occurs during the first few
hours following fracture or
dislocation.
However, the clinical and radiological
effects are not seen until weeks or
even months later.

Clinical feature Avascular Necrosis

There are no symptoms

associated with avascular
necrosis, but if the fracture fails
to unite or if the bone collaps the
patient may complain of pain.
The X-ray shows:
- Increase in bone density.
- New bone ingrowth in the
necrotic segment.
- Disuse osteoporosis in the
surrounding parts

Treatment Avascular Necrosis

In old people with necrosis

of the femoral head an
arthroplasty is the obvious
choice, in younger people,
realignment osteotomy (or
even arthrodesis) may be
wiser.
Avascular necrosis in the
scaphoid or talus may need
no more than symptomatic
treatment, but vascular bone
grafting, or arthrodesis of
the wrist or ankle, is
sometime needed.

GROWTH DISTURBANCE

In children, damage to the physis may lead to

abnormal or arrested growth.
Fractures that split the epiphysis inevitably
traverse the growing portion of the physis, and so
further growth may be asymmetrical and the
bone end characteristically angulated.

TENDON LESIONS

Rupture of the extensor

pollicis tendon may occur 6
12 weeks after a fracture
of the lower radius.
Direct suture is seldom
possible and the resulting
disability is treated by
transferring the extensor
indicis proprius tendon to
the distal stump of the
ruptured thumb tendon.

TENDON LESIONS

NERVE COMPRESSION

Peroneal nerve may

damage if an elderly
patient lies with the leg
in full external rotation.
Radial palsy may follow
the faulty use of
crutches.

NERVE COMPRESSION

Bone or joint deformity may result

in local nerve entrapment with
typical feature such as numbness
or paraesthesia, loss of power and
muscle wasting in the distribution
of the affected nerve.
Common site are :
1. the ulnar nerve, due to a
valgus elbow following an ununited lateral condyle fracture.
2. the median nerve, following
injuries around the wrist.
3. the posterior tibial nerve,
following fractures around the
ankle.

TREATMENT NERVE COMPRESSION

Treatment is by early
decompression of the
nerve.
In the case of the ulnar
nerve this may require
anterior transposition.

MUSCLE CONTRACTURE

Following arterial injury or

a compartment syndrome,
the patient may develop
ischaemic contractures of
the affected muscles
(Volkmanns ischaemic
contracture).
The sites most commonly
affected are the forearm
and hand, the leg and the
foot.

JOINT INSTABILITY

Following injury a joint

may give way. Causes
include :
1. Ligamentous laxity
2. Muscle weakness
3. Bone loss

Injury may also lead to

recurrent dislocation. The
commonest sites are the
shoulder and the patella.

JOINT STIFFNESS

A haemarthrosis forms and

leads to synovial adhesions.
Oedema and fibrosis of the
capsule, the ligaments and
the muscles around the
joint.
Adhesion of the soft tissues
to each other or to the
underlying bone.

All these condition are made

worse by prolonged
immobilization.

Treatment Joint Stiffness

The best treatment is prevention:
- by exercises that keep the joints mobile from
the outset.
- if the joint has to be splinted, make sure that it
is held in the position of safety.

Treatment Joint Stiffness

Joints that are already stiff take time to mobilize,

but prolonged and patient physiotherapy can
work wonders.
If the situation is due to intra-articular adhesions,
gentle manipulation under GA may free the joint
sufficiently to permit a more pliant response to
further exercise.
Occasionally, adherent or contracted tissues need
to be released by operation.

ALGODYSTHROPHY (COMPLEX
REGIONAL PAIN SYNDROME)

Sudeck, in 1900, describe a condition

characterized by painful osteoporosis of the hand
after fracture, it was called Sudecks atrophy.
Now recognized as the late stage of a post
traumatic reflex sympathetic dystrophy (also
known as algodystrophy)

ALGODYSTHROPHY (COMPLEX
REGIONAL PAIN SYNDROME)

The patient complains of

continuous pain.
Local swelling, redness and
warmth as well as
tenderness and moderate
stiffness of the nearby
joints.
X-ray characteristically
show patchy rarefaction of
the bone.

Treatment

In the early stage; anti-inflamatory drugs are

helpful.
If this does not produce improvement,
amitriptyline may help to control the pain.
Sympathetic block or sympatholytic drugs such as
intravenous guanethidine have been advocated
for this condition.
Prolonged and dedicated physiotherapy will
usually be needed.

OSTEOARTHRITIS

A fracture involving a joint

may severely 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

OSTEOARTHRITIS

Malunion of a metaphyseal
fracture may radically alter
the mechanics of a nearby
joint and this, too, can
give rise to secondary
osteoarthritis.