AIM : To manage the complications of fractures .

Early complications
Local:
Vascular injury causing haemorrhage, internal or external
Visceral injury causing damage to structures such as brain,
lung or bladder
Damage to surrounding tissue, nerves or skin
Haemarthrosis
Compartment syndrome (or Volkmann's ischaemia)
Wound infection, more common for open fractures
Systemic:
Fat embolism
Shock
Thromboembolism (pulmonary or venous)
Exacerbation of underlying diseases such as diabetes or CAD
Pneumonia
Late Complications
Local:
Delayed Union
Non-union
Malunion
Joint stiffness
Contractures
Systemic:
Gangrene, tetanus, septicaemia
Fear of mobilising
Osteoarthritis
Myositis ossificans
Avascular necrosis
Algodystrophy (or Sudeck's atrophy) Osteomyelitis
Growth disturbance or deformity
1. HYPOVOLAEMIC SHOCK
It is commonest cause of death following fractures if major
bones such as pelvis and femur. Its frequency is on the increase
due to arise in number of patients with multiple injuries the
cause of hypovolaemia could be extrenal or internal
haemorrhage. External may result from a compound fracture

with or without an associated injury to a major vessel to a limb.

Internal is difficultto diagnose, usually massive bleading such
as chest or abdomen.
Management:
Keep the person comfortable and warm (to avoid
hypothermia).
Have the person lie flat with the feet lifted about 12 inches to
increase circulation. However, if the person has a head, neck,
back, or leg injury, do not change the person's position
unless he or she is in immediate danger.
Do not give fluids by mouth.
If person is having an allergic reaction, treat the allergic
reaction, if you
know how.
If the person must be carried, try to keep him or her flat, with
the head down and feet lifted. Stabilize the head and neck
before moving a person with a suspected spinal injury.
The goal of hospital treatment is to replace blood and fluids. An
intravenous (IV) line will be put into the person's arm to allow
blood or blood products to be given.
Medicines such as dopamine, dobutamine, epinephrine, and
norepinephrine may be needed to increase blood pressure and
the amount of blood pumped out of the heart (cardiac output).
Chest physiotherapy to improve respiratory function
Limb supporting splint .
2. ARDS ACUTE RESPIRATORY DESTRESS SYNDROME
The exact mechanism is not known, but it is supposed to
be due release of inflammatory mediators which cause
disruption of microvasculature of pulmonary system.
ARDS typically occurs in people who are already critically
ill or who have significant injuries. Severe shortness of
breath the main symptom of ARDS usually develops
within a few hours to a few days after the original disease
or trauma.
Many people who develop ARDS don't survive. The risk of
death increases with age and severity of illness. Of the

people who do survive ARDS, some recover completely

while others experience lasting damage to their lungs.
Management :
Supplemental oxygen. For milder symptoms or as a
temporary measure, oxygen may be delivered through a
mask that fits tightly over your nose and mouth.
Mechanical ventilation. Most people with ARDS will
need the help of a machine to breathe. A mechanical
ventilator pushes air into your lungs and forces some of
the fluid out of the air sacs.
Fluids
Carefully managing the amount of intravenous fluids is
crucial. Too much fluid can increase fluid buildup in the
lungs. Too little fluid can put a strain on your heart and
other organs and lead to shock.
Medication
People with ARDS usually are given medication to:
Prevent and treat infections
Relieve pain and discomfort
Prevent clots in the legs and lungs
Minimize gastric reflux

3. FAT EMBOLISM
This is the most serious complications, the essential feature
being occlusion of small vessels by fat globules.
This is a relatively uncommon disorder that occurs in the first
few days following trauma with a mortality rate of 10-20%.
Various theories: Fat drops from bone marrow following
fracture, coalesce and form emboli in pulmonary capillary
beds and brain, with an inflammatory cascade and platelet
aggregation. Alternative theory suggests that FFAs are
released as chylomicrons following hormonal changes due to
trauma or sepsis. Also seen following severe burns, CPR,
bone marrow transplant and liposuction.
Risk factors
Closed fractures
Multiple fractures
Pulmonary contusion
Long bone/pelvis/rib fractures
Presentation
Sudden onset dyspnoea

 Hypoxia
Fever
Confusion, coma, convulsions
Transient red-brown petechial rash affecting upper body,
especially axilla
Management
Supportive treatment
Corticosteroid drugs
Surgical stabilisation of fracture
4. DEEP VEIN THROMBOSIS (DVT) AND PULMONARY
EMBOLISM
DVT is a common complication associated with lower limb
injuries and with spinal injuries.
Clinical features of a DVT
Swelling of the extremity
Tenderness or a feeling of cramping of the calf muscles that
is increased with dorsiflexion (Homan's sign)
Inflammation and discoloration/redness of the extremity
Clinical features of a Venous Thromboembolism
Calf pain and/or tenderness
Swelling with pitting edema
Swelling below the knee (distal deep vein thrombosis) or
up to the groin (proximal deep vein thrombosis)
Increased skin temperature
Superficial venous dilation
Management :

Anticoagulation is the usual treatment for DVT. Patients are

generally initiated on a brief course (i.e., less than a week) of
heparin treatment while they start on a 3-6 month course of
warfarin (or related vitamin K inhibitors). Once the thrombosis is
treated with RBC-thinning agents, the affected area has a fair
chance of returning to its normal proportions. However, thinning
agents do not lessen the chance of embolism to the pulmonary or
coronary arteries.

Thrombolysis
Thrombolysis is generally used for an extensive clot. Although a
meta-analysis of randomized controlled trials by the Cochrane
Collaboration shows improved outcomes with thrombolysis, there
may be an increase in serious bleeding complications.

 Compression stockings

Elastic compression stockings should be routinely applied "beginning

within 1 month of diagnosis of proximal DVT and continuing for a
minimum of 1 year after diagnosis".

5. CRUSH SYNDROME
This syndrome results from massive crushing of the muscles,
commonly associated with crush injuries sustained during
earthquakes, mining and other such accidents. A similar effect may
follow the application of tourniquet for an excessive period.
Causes: crushing of muscles results in entry of myohaemoglobin
into circulation , which precipitates in renal tubules , leading to
acute renal tubular necrosis.
Symptoms :
Scanty urine
Apathy
Restlessness
Delirium

6. INJURY TO MAJOR BLOOD VESSELS

Blood vessels lie in close proximity to the bones, and hence are liable
to injury with different fractures and dislocations. The popliteal artery
is the most frequently damaged vessel.
Causes: the artery maybe damaged by the object causing the fracture
or by a sharp edge of a bone fragment. The damage to the vessel may
vary from just a pressure from outside to a complete rupture
Consequences: obstruction to the blood flow will not always lead to
gangrene. where the collateral circulation is good
the following may result:
1. No effect
2. Exercise ischeaemia
3. Ischaemic contracture
4. Gangrene
Management:
Localised pressure at bleeding points
Compression bandage
Limb support and keep in elevation

Early possible active , or assisted movements to distal joints.

7. PROBLEMS WITH BONE HEALING ( DELAYED UNION,

MAL UNION , NON UNION )
Delayed union is failure of a fracture to consolidate within
the expected time - which varies with site and nature of the
fracture and with patient factors such as age. Healing
processes are still continuing, but the outcome is uncertain.
Non-union occurs when there are no signs of healing after
>3-6 months (depending upon the site of fracture). Nonunion is one endpoint of delayed union..
Malunion occurs when the bone fragments join in an
unsatisfactory position, usually due to insufficient reduction.
Management :
Non-surgical approaches:
Early weight bearing and casting may be helpful for delayed
union and non-union.
Bone stimulation can sometimes be used. This delivers
pulsed ultrasonic or electromagnetic waves to stimulate new
bone formation. It needs to be used for up to an hour every
day, and may take several weeks to be effective.
Medical treatments such as teriparatide have also been used
to promote fracture healing, particularly in patients with
osteoporosis.
Surgical approaches:
Debridement to establish a healthy infection-free
vascularity at the fracture site.
Bone grafting to stimulate new callus formation. Bone may
be taken from the patient or may be cadaveric.
Bone graft substitutes/osteobiologics.
Internal fixation to reduce and stabilise the fracture. (Bone
grafting provides no stability).
Depending on the type of non-union, any combination of the
above.

8. COMPARTMENT SYNDROME
Fractures of the limbs can cause severe ischaemia by damage
to a major artery or by increasing the osteofascial compartment
pressure by swelling due to bleeding or oedema.
capillary flow muscle ischaemia. more oedema more
pressure capillary flow.
Thus rapid pressure build-up, leading to muscle and nerve
necrosis.
Compartment syndromes can also result from crush injuries
(falling debris or simple
compression if patient unconscious for length of time) or an
over-tight cast.
Any compartment, but tibia shaft # & forearm # greatest risk.
Esp if age<35y.
Presentation
Signs of ischaemia (5 P's: Pain, Paraesthesia, Pallor, Paralysis,
Pulselessness) - but
diagnosis should be made before all these features are present.
The presence of a pulse
does not exclude the diagnosis.
Signs of raised intracompartmental pressure:
o Swollen arm or leg
o Tender muscle - calf or forearm pain on passive extension of
digits o Pain out of proportion to injury
o Redness, mottling and blisters
Watch for signs of renal failure (low-output uraemia with
acidosis)
When uncertain, measure intracompartmental pressure directly.
Management
Remove/relieve external pressures
Prompt decompression of threatened compartments by open
fasciotomy
Debride any muscle necrosis
Treat hypovolaemic shock and oliguria urgently
Renal dialysis may be necessary
Complications
Acute renal failure secondary to rhabdomyolysis
DIC
Volkmann's contracture (where infarcted muscle is replaced
by inelastic fibrous tissue).
Management :

 regular monitoring of the immobilisation

Vigorous active and resisted fingers toe movements
Early protected functional use of related limb .
9. MYOSITIS OSSIFICANS
Myositis Ossificans is extra-skeletal ossification that occurs in
muscles & other soft tissues. If you have a bad muscle strain or
contusion (dead leg!) and it is neglected then you could be
unlucky enough to get Myositis. It is usually as a result of
impact which causes damage to the sheath that surrounds a
bone (periostium) as well as to the muscle. Bone will grow
within the muscle (called calcification) which is painful. The
bone will grow 2 to 4 weeks after the injury and be mature
bone within 3 to 6 months.
Muscles most often involved are brachialis, quadriceps
femoris and adductor muscles of thigh. It is significant that
these muscles gain attachment to bone over a wide surface
area, suggesting that periosteum participates to some extent in
the process.
Symptoms :

Restricted range of movement

Pain in the muscle when you use it

A hard lump in the muscle

An X-ray can show bone growth

Management :

Rest

Immobilization

Anti-inflammatory drugs

physiotherapy management

surgical debridement
Physiotherapy management of myositis ossificans includes :

Rest
Immobilization
pulsed Ultra sound and phonophoresis

 Maintain available range of motion but avoid stretching

and massage, until maturation.
iontophoresis with 2 % acetic acid solution.
extra corporeal shock wave therapy.

10.
REFLEX SYMPATHETIC DYSTROPHY (SUDECKS
DYSTROPHY )
Complex Regional Pain Syndrome (CRPS) is also known as
reflex sympathetic dystrophy, causalgia, Sudeck's atrophy,
algoneurodystrophy, among other names. It is a disease
causing severe pain, disproportional to the expected
amount of pain from a stimulus. It is typically confined in
one limb, but may spread to other limbs or even to the
entire body. A person with CRPS will experience sensory,
motor, autonomic, and skin/bone changes.
There are two types of CRPS. CRPS type I occurs after any
type of trauma. CRPS type II may also occur after trauma,
but has neuronal involvement. CRPS most commonly
occurs after surgery (including arthroscopies), upper and
lower motor neuron injuries, traumatic brain injury,
cerebrovascular accident, central nervous system lesion,
neuropathies, or nerve entrapments.
Signs and Symptoms :

pain (pain may not be present in 7%of CRPS sufferers)

swelling
tremor
trouble initiating movements
muscle spasms (may be present in the cervical and lumbar
spine regions in advanced cases)
muscle atrophy
temperature changes
color changes (red, blue)
thick, brittle, or rigid nails
weakness

 thin, shiny, clammy skin

stiffness or decreased joint motion
painful or decreased sensation on skin (some patients report
intolerance to air moving over skin)
strange, disfigured, or dislocated feelings in limbs.

Physical Therapy Management :

TENS: Somers, et al found that high frequency TENS
contralateral to the nerve injury reduces mechanical
allodynia, while low frequency reduces thermal allodynia in
rats.
aquatics: Aquatic therapy allows activities to be performed
with decreased weight bearing on the lower extremities.
mirror therapy
desensitization
gradual weight bearing
stretching
fine motor control
It is important for physical therapists to recognize that CRPS
typically follows blood vessel pathways, and therefore
symptoms may not always follow neural patterns. Also, due to
the spread pattern, CRPS treatment should be provided
bilaterally, due to the contralateral connections present
between the extremities.
11.

STIFFNESS OF JOINTS

It is common complication of fracture treatment.

Shoulder,elbow and knee joints are particularly prone to
stiffness following immobilisation.
Stiffness of joints hamper the normal physical activity of the
patient , and results in late osteoarthritis.
Management :
Cold therapy

Heat pack application

Transcutaneous electrical nerve stimulation (TENS)
Ultrasound therapy
Soft tissue mobilization
Manual stretching
Joint mobilization
Physical therapy exercises
1 Range of motion exercises
2 General conditioning exercises
3 Stretching exercises
4 Progressive strengthening exercises
Use of assistive or walking device (e.g. cane, walker)
Postural training
Patient education
About joint stiffness and your specific condition
Precautions to observe
Home self-care of symptoms
Home exercise program
Injury prevention

12.

AVASCULAR NECROSIS

Avascular necrosis (also known as osteonecrosis, bone

infarction, aseptic necrosis, ischemic bone necrosis and AVN) is
a condition where bone tissue dies due to a lack of blood
supply. This decrease in blood supply causes a decrease in
oxygen and nutrient delivery to the bone, which leads to
multiple breaks in the bone and eventual collapse of the
affected bone.
Symptoms include :
pain and decreased range of motion in the affected joint.
The most common location for this condition to manifest, is the
head or neck of the femur or humerus, and the knee joint.
Management :

 Adequate support to relieve ambulatory body support

Maintenance of functional ROM
exercises to maintain joint mobility and strengthen the
muscles around the affected joint.
Electrical stimulation
ultrasound can be used to stimulate bone growth
During physical therapy, excessive compressive and shear
forces on the joint should be avoided.
13.

LIMB LENGTH DISPARITY

Causes :
Malunion overlapping or angulation at fracture site
Loss of bone piece at the time of injury
Bone compression
Damage or bone disease
Reduced blood supply
Lengthening
Clinical features :
Limp during ambulation
Cosmtic deformity
Management:
Growth stimulating procedures
Compensatory shoe raise
Vigorous strenghtening exercise
14.

VOLKMANNS ISCHAEMIC CONTRACTURE

Causes:
Impaired vascular integrity
.
Tight bandage or POP cast is the main cause
Ischaemia may damage peripheral nerves
Clinical features :
Severe pain from forearm to hand
Gradual progress to sensory and motor paresis to paralysis
Progresses to flexion deformity at wrist and fingers
Management:

 Early ROM exercises with full finger extension and wrist

joint extended fully .
Dynamic VIC splint
Active mobilization
Re education of muscle function and full ROM