Dr Shoaib Shaikh

Orthopaedic consultant
- Modern Hospital
- Sarwat Memorial Hospital
- ZVM Unani Hospital
- BJMC Sassoon General Hospital
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
8. Infection
9. 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
 # pelvis (1.5-2 litres) # femur (1-1.5 litres) produces
major haemorrhage.
Prevention
 Early stopping of bleeding
 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
 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- Chest tube
 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 capacity and 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.
The fat globules obstruct capillary vasculature of
the lungs or brain
Also, fat is converted to free fatty acid, which
induces toxic vasculitis followed by thrombosis
which obstruct the microvasculature.
Clinical features

COMMON PULMONARY
Patechial rash of TYPE
anterior neck, Tachypnoea
anterior axillary fold Tachycardia
or conjunctiva
Respiratory failure
CEREBRAL TYPE
Drowsiness
Restlessness
Disorientation
Coma
Diagnosis
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
It is a common
Thrombosis
complication originating Pathology:
from altered
hemodynamics in lower
limb and spinal injuries.
pathology
Virchow's triad trauma
1. decreased flow rate
of the blood
2. damage to the immobilisation
blood 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.
Diagnosis
D-dimers
doppler
ultrasound
venography
Treatment
Prophylaxis
 Active/ passive calf pump
and toe movement
 Elevation
 Deep breathing exercise
 Elastic TED stockings
 Early internal fixation to
provide early mobility.
Management
Complete rest with
elevation thrombolysis
Anticoagulant therapy
graduated compression
stockings
( thromboembolic
deterrent stockings) or
intermittent pneumatic
compression devices.
Respiratory support in
case of pulmonary
embolism
 Crush syndrome
It is renal failure following Clinical features
extensive crushing (appear within 2-3 days of
injury of muscles. injury) Signs of deficient renal
Pathogenesis: function: Oliguria (Scanty
Crushing of muscles urine)
causes entry of
Restlessness
myoglobin into
circulation. Myoglobin Delirium
precipitates in renal Cardiac arrhythmia &
tubules causing acute failure Hypothermia
tubular necrosis, Shock
metabolic acidosis &
hperkalemia
Treatment

Prophylaxis Treatment
Application of Treated as acute
tourniquet and renal failure.
gradual release to
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 for contents
- combination of both
Etiology
Trauma with
bleeding/swelling
 Bleeding
disorders
 Burns
 Tight wraps
 Surgical
positioning
 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
 Elevation
 Remove cast
 Split all dressings down to skin
 Fasciotomy if continued clinical findings and/or
elevated compartment pressure
Leg Anatomy
Leg Single Incision Technique
Leg Two Incision Technique
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

III causes related to treatment:
 Inadequate reduction: # shaft of long bones
 Inadequate immobilisation:# shaft of long bones
 Distraction (excessive) during treatment::# shaft of
femur.
Common sites
Neck of
femur
Scaphoid
Lower third tibia
Lower third of
ulna
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.
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 method – Producing compression
forces across the non union site with the help
of regular manipulation of external ring
fixators
Mal union
 When a fracture does not unite in proper position it
is said to have malunited.
Causes:
1. Improper reduction
2. Unchecked muscle pull
3. Excessive communition
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.
 VOLKMANN’S CONTRACTURE

• Results from unrelieved compartment syndrome.

• Due to ischemia muscle is gradually replaced
by fibrous tissue.
• Leads to a permanently stiff , claw- like deformity of
the hand and arm.
• Prevention by prompt recognition followed by
limb splinting and compartment decompression.
 No treatment may be necessary if remodelling
occurs.