Transcript Complications of fractures

Complications of fractures
1-The general complications of fractures (blood loss,
shock, fat embolism, cardiorespiratory failure etc.)
2-Local complications can be divided into :
a-early (thosethat arise during the first few weeks
following injury).
b- late.
Local complications of fractures
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Urgent
Local visceral injury
Less urgent
Fracture blisters
Late
Delayed union
Vascular injury
Plaster sores
Malunion
Nerve injury
Pressure sores
Non-union
Compartment
Nerve entrapment
Avascular necrosis
syndrome
Haemarthrosis
Myositis ossificans
Ligament injury
Muscle contracture
Infection
Gas gangrene
Tendon lesions
Joint stiffness
Algodystrophy
joint instability
Osteoarthritis
EARLY COMPLICATIONS
• Early complications may present as part of the
primary
• injury or may appear only after a few days or weeks.
1-VISCERAL INJURY
• Fractures around the trunk are often complicated
by injuries to underlying viscera, the most
important being penetration of the lung with lifethreatening pneumothorax following rib fractures
and rupture of the bladder or urethra in pelvic
fractures. These injuries require emergency
treatment.
2-VASCULAR INJURY
The fractures most often associated with damage to
a major artery are those around the knee and
elbow, and those of the humeral and femoral
shafts.
The artery may be cut, torn, compressed or
contused,either by the initial injury or
subsequently by jagged bone fragments. The
effects vary from transient diminution of blood
flow to profound ischaemia, tissue death and
peripheral gangrene.
• Clinical features
The patient may complain of paraesthesia or numbnessin the toes or the
fingers. The injured limb is cold and pale, or slightly cyanosed, and the pulse
is weak or absent.
X-rays will probably show one of the ‘highrisk’fractures listed above. If a
vascular injury is suspected an angiogram should be performed
immediately; if it is positive, emergency treatment must be started without
further delay.
• Treatment
All bandages and splints should be removed. The fracture is re-x-rayed and, if
the position of the bones suggests that the artery is being compressed or
kinked, prompt reduction is necessary.
The circulation is then reassessed repeatedly over the next half hour. If there
is no improvement, the vessels must be explored by operation preferably
with the benefit of preoperative or peroperative angiography.
A cut vessel can be sutured, or a segment may be replaced by a vein graft;
if it is thrombosed, endarterectomy may restore the blood flow. If vessel
repair is undertaken, stable fixation is a must and where it is practicable, the
fracture should be fixed internally.
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3- NERVE INJURY
Nerve injury is particularly common with fractures of the humerus or injuries
around the elbow or the knee
A- Closed nerve injuries
In closed injuries the nerve is seldom severed, and spontaneous recovery
should be awaited – it occurs in90 per cent within 4 months. If recovery
has not occurred by the expected time, and if nerve conduction studies
and EMG fail to show evidence of recovery, the nerve should be explored.
B- Open nerve injuries
With open fractures the nerve injury is more likely to be complete. In these
cases the nerve should be explored at the time of debridement and
repaired at the time or at wound closure.
C- Acute nerve compression
Nerve compression, as distinct from a direct injury, sometimes occurs with
fractures or dislocations around the wrist. Complaints of numbness or
paraesthesiain the distribution of the median or ulnar nerves should be
taken seriously and the patient monitored closely; if there is no
improvement within 48 hours of fracture reduction or splitting of
bandages around the splint, the nerve should be explored and
decompressed.
Common nerve injuries
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Injury
Shoulder dislocation
Humeral shaft fracture
Humeral supracondylar fracture
median
Elbow medial condyle
Monteggia fracture–dislocation
interosseous
Hip dislocation
Knee dislocation
Nerve
Axillary
Radial
Radial or
Ulnar
PosteriorSciatic
Peroneal
INDICATIONS FOR EARLY EXPLORATION
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Nerve injury associated with open fracture
Nerve injury with fractures that need internal
fixation
Presence of a concomitant vascular injury
Nerve damage diagnosed
4- COMPARTMENT SYNDROME
Fractures of the arm or leg can give rise to severe
ischaemia, even if there is no damage to a major
vessel. Bleeding, oedema or inflammation (infection)
may increase the pressure within one of the
osseofascial compartments; there is reduced capillary
flow, which results in muscle ischaemia, further
oedema,
still greater pressure and yet more profound ischaemia
a vicious circle that ends, after 12 hours or less, in
necrosis of nerve and muscle within the compartment.
Nerve is capable of regeneration but muscle, once
infarcted, can never recover and is replaced by
inelastic fibrous tissue (Volkmann’s ischaemic
contracture).
A similar cascade of events may be caused by swelling of
a limb inside a tight plaster cast.
Clinical features
• High-risk injuries are fractures of the elbow,
forearm bones, proximal third of the tibia, and also
multiple fractures of the hand or foot, crush injuries
and circumferential burns. Other precipitating
factors are operation (usually for internal fixation)
or infection.
• The classic features of ischaemia are the five Ps:
PAIN
Paraesthesia
Pallor
Paralysis
Pulselessness
• However in compartment syndrome the ischaemia occurs at the
capillary level, so pulses may still be felt
• and the skin may not be pale! The earliest of the ‘classic’features are pain
(or a ‘bursting’ sensation), altered sensibility and paresis (or, more usually,
weakness in active muscle contraction).
• Ischaemic muscle is highly sensitive to stretch. If the limb is unduly
painful, swollen or tense, the muscles (which may be tender) should be
tested by stretching them. When the toes or fingers are passively
hyperextended,there is increased pain in the calf or forearm.
• Confirmation of the diagnosis can be made by measuring the
intracompartmental pressures. So important is the need for early
diagnosis that some surgeons advocate the use of continuous
compartment pressure monitoring for high-risk injuries (e.g. fractures of
the tibia and fibula) and especially for forearm or leg fracture in patients
who are unconscious. A split catheter is introduced into the compartment
and the pressure is measured close to the level of the fracture. A
differential pressure (ΔP) – the difference between diastolic pressure
and compartment pressure – of less than30 mmHg (4.00 kilopascals) is
an indication for immediate compartment decompression.
Treatment
The threatened compartment (or compartments) must be
promptly decompressed. Casts, bandages and dressings
must be completely removed – merely splitting the plaster
is utterly useless – and the limb should be nursed flat
(elevating the limb causes a further decrease in end
capillary pressure and aggravates the muscle ischaemia).
The ΔP should be carefully monitored; if it falls below 30
mmHg, immediate open fasciotomy is performed. In the
case of the leg, ‘fasciotomy’ means opening all four
compartments through medial and lateral incisions. The
wounds should be left open and inspected 2 days later:
if thereis muscle necrosis, debridement can be carried out; if
the tissues are healthy, the wounds can be sutured (without
tension) or skin-graft
5-HAEMARTHROSIS
Fractures involving a joint may cause acute
haemarthrosis. The joint is swollen and tense and
the patient resists any attempt at moving it. The
blood should be aspirated before dealing with the
fracture.
6-INFECTION
Open fractures 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.
LATE COMPLICTIONS
1-DELAYED UNION
• Causes
A-BIOLOGICAL
• 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. The fracture edges will become necrotic and dependent on the formation of
an ensheathing callus mass to bridge the break. If the zone of necrosis is extensive,
as might occur in highly comminuted fractures, union may be hampered.
• Severe damage to the soft tissues affects fracture healing by: (1) reducing the
effectiveness of muscle splintage; (2) damaging the local blood supply and (3)
diminishing or eliminating the osteogenic input from mesenchymal stem cells
within muscle.
• Periosteal stripping Over-enthusiastic stripping of periosteum during internal
fixation is an avoidable cause of delayed union.
• Infection Both biology and stability are hampered by active infection: not only is
there bone lysis, necrosis and pus formation, but implants which are used to hold
the fracture tend to loosen
B- BIOMECHANICAL
• Imperfect splintage Excessive traction (creating a fracture gap) or excessive
movement at the fracture site will delay ossification in the callus. In the forearm
and
• leg a single-bone fracture may be held apart by
anntact fellow bone.
• Over-rigid fixation Contrary to popular belief,
rigid fixation delays rather than promotes
fracture union.
C-PATIENT RELATED
• In a less than ideal world, there are patients who
are:
• • Immense
• • Immoderate
• • Immovable
• • Impossible.
• Clinical features
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Fracture tenderness persists and, if the bone is subjectedto stress, pain may be acute.
On x-ray, the fracture line remains visible and there is very little or incomplete callus
formation or periosteal reaction. However, the bone ends are not sclerosed or atrophic.
The appearances suggest that, although the fracture has not united, it eventually will.
• Treatment
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CONSERVATIVE
The two important principles are: (1) to eliminate any possible cause of delayed union
and (2) to promote healing by providing the most appropriate environment.
Immobilization (whether by cast or by internal fixation) should be sufficient to prevent
shear at the fracture site, but fracture loading is an important stimulus to union and can
be enhanced by: (1) encouraging muscular exercise and (2) by weightbearing in the
cast or brace. The watchword is patience; however, there comes a point with every
fracture where the illeffects of prolonged immobilization outweigh the advantages of
non-operative treatment, or where the risk of implant breakage begins to loom.
OPERATIVE
Each case should be treated on its merits; however, if union is delayed for more than 6
months and there is no sign of callus formation, internal fixation and bone grafting are
indicated.
2-NON-UNION
• In a minority of cases delayed union gradually turns into
non-union – that is it becomes apparent that the fracture
will never unite without intervention.
• Movement can be elicited at the fracture site and pain
diminishes; the fracture gap becomes a type of
pseudoarthrosis.
• X-ray The fracture is clearly visible but the bone on either
side of it may show either exuberant callus or atrophy. This
contrasting appearance has led to nonunion being divided
into hypertrophic and atrophic types. In hypertrophic nonunion the bone ends are enlarged, suggesting that
osteogenesis is still active but not quite capable of bridging
the gap. In atrophic non-union, osteogenesis seems to have
ceased. The bone ends are tapered or rounded with no
suggestionof new bone formation.
Treatment
• CONSERVATIVE
Non-union is occasionally symptomless, needing no treatment
or, at most, a removable splint. Even if symptoms are present,
operation is not the onlyanswer; with hypertrophic nonunion, functional bracing may be sufficient to induce union,
but splintage often needs to be prolonged. Pulsed
electromagnetic fields and low-frequency, pulsed ultrasound
can also be used to stimulate union.
• OPERATIVE 1- With hypertrophic non-union and in the
absence of deformity, very rigid fixation alone (internal or
external) may lead to union.
2-With atrophic non-union, fixation alone is not enough. Fibrous
tissue in the fracture gap, as well as the hard, sclerotic bone
ends is excised and bone grafts are packed around the
fracture with internal or illizarov fixation
3-MALUNION
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 collapse of comminuted or
osteoporotic bone.
• Clinical features
• The deformity is usually obvious, but sometimes the true extent of
malunion is apparent 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. 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 I
reproduced
• X-rays are essential to check the position of the fracture while it is
uniting. This is particularly important during the first 3 weeks, when the
situation may change without warning. At this stage it is sometimes
difficult to decide what constitutes ‘malunion’; acceptable norms differ
from one site to another and these are discussed under the individual
fractures
• Treatment
• Incipient malunion may call for treatment even before the fracture has
fully united; the decision on the need
• for re-manipulation or correction may be extremely
• difficult. A few guidelines are offered:
• 1. In adults, fractures should be reduced as near to the anatomical
position as possible. Angulation of more than 10–15 degrees in a long
bone or a noticeable rotational deformity may need correction by
remanipulation,
• or by osteotomy and fixation.
• 2. In children, angular deformities near the bone ends (and especially if
the deformity is in the same plane as that of movement of the nearby
joint) will usually remodel with time; rotational deformities will not.
• 3. In the lower limb, shortening of more than 2.0 cm is seldom acceptable
to the patient and a limb length equalizing procedure may be indicated.
• 4. The patient’s expectations (often prompted bycosmesis) may be quite
different from the surgeon’s; they are not to be ignored
• 5. Very little is known of the long-term effects of small angular deformities
on joint function. However, it seems likely that malalignment of more than
15 degrees in any plane may cause asymmetrical loading of the joint
above or beloand the late development of secondary osteoarthritis; this
applies particularly to the large weightbearing joints.
4- AVASCULAR NECROSIS
• Certain regions are notorious for their propensity tovdevelop ischaemia and
bone necrosis after injury , They are: (1) the head of the femur (after fracture of
the femoral neck or dislocation of the hip);
(2) the proximal part of the scaphoid (after fracture through its waist);
(3) the lunate (following dislocation) and
(4) the body of the talus (after fracture of its neck).
• Accurately speaking, this is an early complication of bone injury, because
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 features
There are no symptoms associated with avascular necrosis, but if the fracture fails
to unite or if the bone collapses the patient may complain of pain. X-ray shows
the characteristic increase in x-ray density, which occurs as a consequence of two
factors:
Disuse osteoporosis in the surrounding parts gives the impression of ‘increased
density’ in the necrotic segment, and
collapse of trabeculae compacts the bone and increases its density. Where
normal bone meets the necrotic segment a zone of increased radiographic
density may be produced by new bone formation.
Treatment
• Treatment usually becomes necessary when joint
function is threatened.
• In old people with necrosis of the femoral head
an arthroplasty is the obvious choice;
• in younger people, realignment osteotomy (or, in
some cases, arthrodesis) may be wiser.
• Avascular necrosis in the scaphoid or talus may
need no more than symptomatic treatment, but
arthrodesis of the wrist or ankle is sometimes
needed.