Introduction

These are the associated pathologies other than the loss

of bone continuity which either co exist or originate
due to the fracture.
early diagnosis and aggressive treatment is necessary
to minimize disabilities.
Classification
I.IMMEDIATE
A.Systemic
hypovolaemic Shock
B.Local
injury to
1. major vessels
2. Muscles and tendons
3. Joints
4. viscera
II.EARLY
A.Systemic
1. Hypovolaemic shock
2. ARDS
3. Fat embolism
4. DVT & pulmonary embolism
5. Aseptic traumatic fever
6. Septicaemia
7. Crush syndrome
B. Local
1. Infection
2. Compartment syndrome
III. LATE COMPLICATIONS
A. Related to imperfect union
1. Delayed union
2. Non union
3. Mal union
4. Cross union
B.Others
1. Avascular necrosis
2. Shortening
3. Joint stiffness
4. Sudeck’s dystrophy
5. Osteomyelitis
6. Ischemic contracture
7. Myositis ossificans
8. OA
Hypovolaemic shock
Commonest cause of death in fractures of major bones
Like pelvis or femur
cause
External or internal haemorrhage.
External: compound fractures injuring major vessels of
the LIMB
Internal: injury to body cavities- chest or pelvis
Internal is more difficult to diagnose.
# pelvis (1.5-2 litres) # femur (1-1.5 litres) produces
major haemorrhage.
Prevention
Early stopping of bleeding
Avoiding shifting of the patients
For # pelvis- temporary stabilization with external
fixator
Emergency angiography and embolisation of bleeding
vessels for deeper vessels.
Management
Starts even before the cause is established
Two large bore iv cannulas put
Infuse 2000 ml of crystalloids (ringer lactate) followed
by colloid (haemaccel) and blood if needed
Cut down if peripheral vasoconstriction is present
Localise the site of lesion- if in body cavities, perform
chest aspiration or diagnostic peritonial lewage.
Sometimes a simple x ray is enough.
Chest bleeding-ICDT
Abdominal bleeding- laperotomy
ARDS
Respiratory distress following a trauma
Cause- not definite. Hypothesized to be by release of
Inflammatory cells and proteinaceous fluid that
accumulate in the alveolar spaces leading to a decrease
in diffusing capacityand hypoxemia. The
microvasculature in dysrupted.
Onset- 24 hours after injury
 Features:
Tachypnea
Laboured breathing
X- ray- diffused
pulmonary infiltrates
Arterial Po2 below 50
management
100% O2 and assisted ventilation
It takes upto 7 days to get the chest clear
If not detected early death occurs by multiorgan
failure or cardiorespiratory failure.
Fat Embolism
It is a life threatening complication of fracture where fat
globules occlude the small blood vessels.
Embolism is the process of occlusion of blood vessel by
any material which is brought to the site from
elsewhere by bloodstream.
Pathogenesis
Injury to large bones (e.g. femur) release fat globule
from bone marrow to blood stream. Alternatively fat
can also be released from the adipose tissue.
The fat globules obstruct capillary vasculature of the
lungs.
Also, fat is converted to free fatty acid, which induces
toxic vasculitis followed by thrombosis which obstruct
the microvasculature.
Clinical features

COMMON PULMONARYTYPE
Patechial rash ofanterior Tachypnoea
neck, anterior axillary Tachycardia
fold or conjunctiva Respiratory failure
CEREBRALTYPE
Drowsiness
Restlessness
Disorientation
Coma
Diagnosis
Retinal artery emboli
Urine: fat globules
CXR: pulmonary infiltration/
Snow storm appearance
Clinical features
management
Respitarory support
Heparinisation
i.v. low mol wt dextran
Corticosteroid
Dextrose and alcohol infusion to emulsify fat.
 Deep Vein Thrombosis
It is a common complication
originating from altered Pathology:
hemodynamics in lower
limb and spinal injuries.
pathology
Virchow's triad trauma
1. decreased flow rate of
the blood
2. damage to the blood immobilisation
vessel wall
3. hypercoagulability
Venous stasis

thrombosis
Clinical features
Elderly and obese patients are at risk.
Leg swelling
Local redness, warmth
Calf tenderness
Pain in passive dorsiflexion (Homan sign)
Venography shows DVT
 Sequale
1. The venous thrombosis can get dislodged and
produce embolism elsewhere. If it is pulmonary
embolism the condition is life threatening.
Embolism usually occurs within 4-5 days after injury.
2. A late complication of DVT is the post-phlebitic
syndrome, which can manifest itself as edema, pain
or discomfort and skin problems.
Other causes Risk factor:
Surgery
compression of the veins hospitalization
physical trauma immobilization
cancer orthopedic casts
infections economy class syndrome
inflammatory diseases smoking
stroke Obesity
heart failure age
nephrotic syndrome certain drugs (such as estrogen
or erythropoietin)
thrombophilia
pregnancy
postnatal period.
diagnosis
D-dimers
doppler ultrasound
venography
Clinical features
treatment
Prophylaxis Management
Active/ passive calf pump Complete rest with elevation
and toe movement thrombolysis
Elevation Anticoagulant therapy
Deep breathing exercise graduated compression
Elastic TED stockings stockings (
Early internal fixation to thromboembolic deterrent
provide early mobility. stockings) or
intermittent pneumatic
compression devices.
Respiratory support in case
of pulmonary embolism
 Crush syndrome
It is renal failure following Clinical features
extensive crushing injury (appear within 2-3 days of injury)
of muscles. Signs of deficient renal function:
Pathogenesis: Oliguria (Scanty urine)
Crushing of muscles causes Apathy
entry of myoglobin into Restlessness
circulation. Myoglobin
precipitates in renal Delirium
tubules causing acute Cardiac arrhythmia &failure
tubular necrosis, Hypothermia
metabolic acidosis & Shock
hperkalemia
Treatment

Prophylaxis Treatment
Application of tourniquet Treated as acute renal
and gradual release to failure.
slowly allow the
myoglobin to reach the
kidneys
Compartment syndrome
An increased pressure within enclosed
osteofascial space that reduces capillary per-
fusion below level necessary for tissue
viability; the underlying mechanism is:
- increased volume within space
- decreased space forcontents
- combination of both
Etiology
Trauma with
bleeding/swelling
Bleeding disorders
Burns
Tight wraps
Traction
Surgical positioning
Pneumatic antishock
garment
Reprefusion swelling
Casting &Wraps
Pathophysiology:
Increased compartment pressure
leads to increased venous pressure
which decreases A-V gradient resulting
in muscle and nerve ischemia.
Compartments
Most common
Forearm
Leg
Other compartments
Hand
Finger
Gluteal
Thigh
Foot
Diagnosis
History
Clinical exam: the Ps
Compartment pressures
Laboratory tests
CPK
Urine myoglobin
Clinical features
The six ‘Ps’:
Pressure: palpation of compartment and its tension or
firmness
Pain: Exaggerated with passive stretch of the involved
muscles in compartment
Earliest symptom but inconsistent

Paresthesia:Peripheral nerve tissue is more sensitive than

muscle to ischemia
Will progress to anesthesia if pressure not relieved

Paralysis: late finding

Pallor
Pulselessness
Treatment
Lower leg to level of the heart
Remove cast
Split all dressings down to skin
Fasciotomy if continued clinical findings and/or
elevated compartment pressure
Forearm
Leg Anatomy
Leg Single Incision Technique
Leg Two Incision Technique
Hand Compartments
Foot Compartments
Delayed/ Non union
When a fracture takes more than the usual time to unite
it is said to have gone in delayed union.
When the process of healing stops before completion
the fracture is said to have gone for non union. To
diagnose non union the fracture has to be minimum
six months old.
causes
I. Related to patient
Old age
Associated systemic illness: ex.Malignancy
II. Related to fracture
Distraction at fracture site
Muscle pulling the fragments: ex. # patella
Gravity: ex. # shaft of humerus
Soft tissue interposition: ex. # shaft of humerus
Bone loss during fracture: ex. # tibia open type
Infection from open fracture: ex. # tibia
Damage to blood supply of # fragment: ex. # scaphoid
Pathological fracture: ex. # osteomyelitic tibia
III causes related to treatment:
Inadequate reduction: # shaft of long bones
Inadequate immobilisation:# shaft of long bones
Distraction (excessive) during treatment::# shaft of
femur.
types
1. Atrophic: no or minimal callus formation
2. Hypertrophic: callus is present but it does not bridge
the fracture site.
Common sites
Neck of femur
Scaphoid
Lower third oftibia
Lower third ofulna
Lateral condyle of humerus
Clinical features
Pain
Deformity
Abnormal mobility
Refracture
Radiological findings
Delayed union: inadequate callus, visible fracture line
Non union: ends are rounded, smooth sclerotic.
Medullary cavity may be obliterated. visible fracture
line.
Treatment: Delayed union
1. Most commonly prolonged conservative
management
2. Surgical intervention: bone grafting with or without
internal fixation.
Treatment: non union
Depends upon site and resulting disability. Following are
the options.
1. Bone grafting: commonest.
2. Excision of fragments: when it can be done with
minimal loss of function. A prosthesis may be used
to replace the lost part, eg. In # neck of femur the
head can be replaced with an austin moore
prosthesis.
3. Illizarov menthod
4. No treatment: when there is no disability, eg. #
scaphoid.
Mal union
When a fracture does not unite in proper position it is
said to havemalunited.
Causes:
1. Improper reduction
2. Unchecked muscle pull
3. Excessive communication
Consequences
Deformity
Shortening of limb
Limitation of movements
treatment
1. osteoclasis: refracture, done in children to correct
mild to moderate angular deformities under GA.
2. Redoing the fracture surgically: most common. ORIF
is generally done along with bone grafting.
3. Corrective osteotomy: performed at a site away from
the fracture. Eg. Supracondyle # of humerus.
4. Excision of protruding bone.
No treatment may be necessary if remodelling occurs.