FRACTURES

Anandkumar Balakrishna
Wong Poh Sean
Mohd Hanafi Ramlee
CONTENT
 DEFINITION
 PRINCIPLE
MANAGEMENT
 COMPLICATIONS
DEFINITION

A fracture is a
break in the
structural
continuity of bone.
CAUSES
 Sudden trauma
 direct(fracture of the ulna caused by blow on
the arm)
 indirect(spiral fractures of the tibia and fibula
due to torsion of the leg, vertebral compression
fractures, avulsion fractures)
 Stress
or fatigue-repetitive stress(athletes,
dancers, army recruits)
 Pathological(osteoporosis, Paget’s disease,
bone tumour)
TYPES OF FRACTURES
CLOSED/ OPEN/
SIMPLE COMPOUND
•no opening •bone
in the skin. fragments
have broken
through the
skin.
 COMPLETE INCOMPLETE

• bone is completely • bone is incompletely

broken into 2 or divided and the
more fragments. periosteum remains
• -eg: in continuity.
• transverse fracture • -eg:
• oblique fracture • greenstick fracture
• spiral fracture • torus fracture
• impacted fracture • stress fracture
• comminuted • compression
fracture fracture.
• segmental fracture
COMPLETE FRACTURES
OBLIQUE FRACTURE

SEGMENTAL FRACTURE
 TRANSVERSE FRACTURE

SPIRAL FRACTURE
COMMINUTED FRACTURE

IMPACTED
FRACTURE
INCOMPLETE FRACTURE
GREENSTICK

TORUS
FRACTURES DISPLACEMENT
 Aftera complete fracture the fragments
usually displaced:
 partly by the force of injury
 partly by gravity
 partly by the pull of muscles attached to them.

4 types:
 Translation/Shift
 Alignment/Angulation
 Rotation/Twist
 Altered length
 SHIFT ANGULATION TWIST/
/TILT ROTATION

SIDEWAYS

OVERLAP
IMPACTION
HOW FRACTURES HEAL?
 Healing by callus
 Healing without callus
 Healing by callus
 Callus is the response to movement at the
fracture site to stabilize the fragments as
rapidly as possible.
 Steps:

Tissue destruction and haematoma formation.

Inflammation and cellular proliferation.

Callus formation: dead bone is mopped up & woven

bone(immature) appears in fracture callus.

Consolidation: woven bone(immature) is replaced by lamellar

bone(mature).

Remodelling:Newly formed bone is remodelled to resemble the

normal structure.
Healing without callus
 For fracture that is absolutely immobile:
 impacted fracture in cancellous bone.
 fracture rigidly immobilized by internal fixation
 New bone formation occurs directly between
fragments.
 Gaps between the fracture surfaces are invaded
by new capillaries & bone forming cells growing in
from edges.
 For very narrow crevices(<200um), osteogenesis
produces lamellar bone(mature).
 For wider gaps, osteogenesis begins with woven
bone (immature) first which is then remodelled to
lamellar bone (mature bone).
RATE OF REPAIR DEPENDS
UPON:
Patient’s
Type of Type of State of Patient’s
general
bone fracture blood flow age
constitution

cancell spiral
ous fracture poor healing
bone heals circulati healthy is faster
heals faster on will bone in
faster than slow the heals children
than transver healing faster. than
cortical se process. adults.
bone. fracture.
 CAUSES OF DELAYED UNION OR
NON-UNION OF THE FRACTURES
Interposition of
Distraction & Excessive
soft tissues
separation of the movement at the
between the
fragments fracture site
fragments.

Severe damage
to soft tissues
Poor local blood
which makes Infection
supply
them nearly/non-
viable.

Abnormal bone.
FRACTURES-
PRINCIPLE OF
TREATMENT
Management
of Closed
Fracture
First aid management
 Airway, Breathing and Circulation
 Splint the fracture
 Look for other associated injuries
 Check distal circulation – is distal circulation
satisfactory?
 Check neurology – are the nerve intact?
 AMPLE history- Allergies, Medications, Past
medical history, Last meal, Events
 Radiographs – 2 views, 2sides, 2 joints, 2 times.
 General Resuscitation

Manipulation
(improve position of fragments)

Splintage
(hold fragments together until
unite)

Exercise & weight-bearing

 Reduce Hold

Exercise

Principle Of Treatment
 Hold Safety

Speed Move

The Fracture Quartet

Outline Closed
Reduction
Mechanical
Reduce
Traction

Closed Fracture Open

Reduction
Sustained
Traction

Cast Splintage

Functional
Hold
Bracing

Exercise Internal Fixation

External
Fixation
Reduce
 Aim for adequate apposition and normal
alignment of the bone fragments
 The greater contact surface area between
fragments, the more likely is healing to occur
However, there are some
situations in which reduction is
unnecessary:
 When there is little or no displacement
 When displacement does not matter (e.g. in
some fractures of the clavicle)
 When reduction is unlikely to succeed (e.g.
with compression fracture of the vertebrae)
 Reduction

Operative Non-operative

Closed reduction Open reduction

Mechanical Traction
Closed Reduction
 Suitable for
 Minimally displaced fractures
 Most fractures in children
 Fractures that are likely to be stable after
reduction
 Most effective when the periosteum and
muscles on one side of fracture remain intact
 Under anaesthesia and muscle relaxation, a
threefold manoeuvre applied:
 Distal part of the limb is pulled in line of the bone
 Disengaged, repositioned
 Alignment is adjusted
Mechanical Traction
 Some fractures (example fracture of femoral
shaft) are difficult to reduce by manipulation
because of powerful muscle pull
 However, they can be reduced by sustained
muscle mechanical traction; also serves to
hold the fracture until it starts to unite
Open Reduction
 Operative reduction under direct vision
 Indications:
 When closed reduction fails
 When there is a large articular fragment that
needs accurate positioning
 For avulsion fractures in which the fragments are
held apart by muscle pull
 When an operation is needed for associated
injuries
 When a fracture needs an internal fixation
Hold
• Sustained traction
Non • Cast Splintage
Operative • Functional Bracing

• Internal Fixation
Operative • External Fixation
 To alleviate
To prevent pain by some
displacement restriction of
movement

To allow free
To promote movement of
soft-tissue the
healing unaffected
parts

HOLD
 Sustained Traction
• Traction is applied to limb distal to the fracture
• To exert continuous pull along the long axis of
the bone

Hold Safety

Move
Speed
Advantage

•Can move joint

•Can exercise musle

Indication

•Useful for spiral fractures of long bone

shafts:
•Shaft of femur
•Tibia
•Lower humerus
 Disadvantage and complications
 Patient kept on bed for long time
 Pressure ulcer
 General weakness
 Pulmonary infection
 Contracture
 Pin tract infection
 Thromboembolic event

 Methods
 Traction by gravity
 Balanced traction
 Fixed traction
Traction By
Gravity
Example:
Fracture of
humerus
-Weight of arm to
supply traction
-Forearm is
supported in a
wrist sling
 Balanced Traction
Traction is applied to the limb
either by way of adhesive
strapping, kept in place by
bandages  skin traction
• Sustain a pull no more than 4-5 kg

Contraindications:

• Abrasion, dermatitis, wound

• Vascular insufficiencies
• When greater traction force in
needed
Thomas’s Splint
Traction applied via stiff Complications:
wire or pin inserted • Pin tract infection
through the bone distal • Damage to epiphyseal growth
to the fracture  skeletal plate
traction
• Vertical fracture of the bone
• Can apply several times • Injury to the vessels or nerves
as much force
Fixed Traction
 Principle = balanced traction
 Useful for when patient has to be transported
 Thomas’s splint
Cast Splintage
 Methods:
 Plaster of Paris
 Fibreglass
 Especially for distal limb # and for most
children #
 Disadvantage: joint encased in plaster cannot
move and liable to stiffen
 Can be minimized:
 Delayed splintage (traction initially)
 Replace cast by functional brace after few
weeks
 Complications

Tight cast  put on too

tightly/limb swells

Hold Safety
Pressure sores  even a
well-fitting cast may press
Speed upon the skin over a bony
Move prominence (the patella, the
heel)

Skin abrasion or laceration 

during removal of the plaster
 Functional Bracing

Principle 
functional long
Brace 
bone is supported
supportive device
externally by POP Indication 
that allows
or by a mouldable fractures of shaft
continued
plastic material of femur or tibia
function of the
but the function of
part
joints are
preserved
 Functional bracing is
not rigid  applied
when fracture is
beginning to unite, after Hold Safety
about 3-6 weeks of
traction or restrictive
splintage
Speed Move
Advantages:

• Fractures held reasonably well

• Joints can be moved
• Patient can leave hospital
• Method is safe
INTERNAL
FIXATION
Principle
Bony fragment may
be fixed with:
• screws,
• transfixing pins or nails,
• a metal plate held by
screws,
• a long intramedullary nails,
• circumferential band,
• or a combination with
these method
Indication
2. Fracture that are
1. Fracture that cannot
inherently unstable and
be reduced except by
prone to displacement
operation
after reduction

3.Fracture that unite 4.Pathological fracture

poorly and slowly • Bone disease may
• Principally fracture of prevent healing
the femoral neck

5.Multiple fracture
• Where early fixation
reduced the risk of
general complication
6.Fracture in patient
who present severe
nursing difficulty
Type of internal fixation
screw
• Interfragmentary screw (lag screw) are
used for fixing small fragment onto the
main bone

wires
• Kirschner wire (often inserted
percutaneously without exposing the
fracture
• Used in situation where fracture healing
is predictably quick
Plates and screw
• Useful for treating metaphyseal
fracture of long bones and diaphyseal
fracture of radius and ulna

Intramedullary nail
• Suitable for long bones
• Nail is inserted onto medullary canal
to splint the fracture
• Rotational of fracture are resisted by
introducing locking screw which
tranfix the bone cortices and the nail
proximal and distal to the fracture.
 advantages

Precise Immediate Early

reduction stability movement
•ORIF-open •Hold the •‘fracture
reduction fracture disease ‘
and securely like
internal oedema,s
fixation tifness,etc
may
abolish
 Infection

Refracture Complications Non-union

Implant
failure
 Iatrogenic infection  chronic

Infection osteomylitis
Risk of infection depends on:
1)The patient  devitalised tissue,
dirty wound, unfit patient
2)The surgeon  thorough
training, a high degree of surgical
dexterity and adequate assistant
are all essential
3)The facilities  aseptic routine
The infection should be rapidly
controlled by intravenous
antibiotic
If infection cannot be controlled,
the implant should be replaced
with some form of external fixation
 Cause:

Non union
1) excessive stripping
of soft tissue
2) unnecessary
damage to blood
supply in the course
of operative fixation
3)rigid fixation with a
gap between the
fragment
Implant failure
Metal is subjected
to fatigue
• Metal is subjected
to fatigue
• So, undue stress
should therefore
be avoided until
the fragment has
united.
• Pain at the site of
fracture site is a
danger signal.
Refracture
• It is important not to
remove the metal
implant too soon
• A year is minimum
and 18 to 24 month
is safer
• For several weeks
after the implant
removal the bone is
weak so full weight-
bearing should be
avoided
EXTERNAL
FIXATION
Principle

The bone is transfixed

above and below the
fracture with screw or
pins or tension wire and
these are then clamped
to a frame or connected
to each other by rigid
bars outside the skin
Indication
Fracture associated with soft
tissue injury
• Where the wound can be left
open for inspection, dressing
and definitive coverage
Fracture of the pelvis
• Which often cannot be
controlled quickly by any
other method
Infected fracture
• Where internal fixation
might not be suitable
Severely comminuted and
unstable fracture
• Which can be held out to
length until healing
commence
Fracture associated with
nerve and vessel damage
United fracture
• Where dead or sclerotic
fragment can be excised and
the remaining ends brought
together in the external fixator
(a)The patient was fixed with a plate and screw but did not
unite (b) external fixation was applied
Advantages

no soft tissue
technically quick
stripping;
and easy to perform

risk of infection at the

ease of removing
site of the fracture is
hardware;
minimal
 Complication

Damage
to soft Over Pin track
tissue distraction infection
structure
Damage to soft tissue structure

• Transfixing pins and wires may injure

the nerve and vessel or may tether
ligament and inhibit joint movement
• So, the surgeon must be thoroughly
familiar with the ‘safe corridor’ for
inserting the pins
Over distraction

•If there is no
contact between
the fragment, union
may be delayed or
prevented
Pin track infection

•There is a risk of infection

where the pins are inserted
from the skin into the bone.
•So, meticulous pin-site care
is essential
•Antibiotic should be
administered immediately if
infection occur
Exercise
 Prevention of edema
 active exercise and elevation
 Active exercise also stimulates the circulation.
Prevents soft-tissue adhesion and promotes
fracture healing.
 Preserve the joint movement
 Restore muscle power
 Functional activity
Management
of
Open
Fractures
A break in skin and
underlying soft tissues
leading directly to
communicating with
the fracture
Open Fracture
First Aid & Management of the Whole
Patient
Prompt wound debridement

Antibiotic prophylaxis

Stabilization of the fracture

Definitive wound cover

First Aid & Management of the
Whole Patient

Airway

Breathing

Circulation
 80

1. Emergency Management of
Open Fracture
 A,B,C
 Splint the limb
 Sterile cover - prevent contamination
 Look for other associate injury
 Check distal circulation – is distal circulation satisfactory?
 Check neurology – are the nerve intact?
 AMPLE history- Allergies, Medications, Past medical history,
Last meal, Events
 Radiographs – 2 view, 2sides, 2 joints, 2 times.
 Relieve pain
 Tetanus prophylaxis
 Antibiotics
 Washout / Irrigation
 Wound debridement
 fracture stabilisation
Open Fractures
Classification
 Preoperative
PHYSICAL
Assessment EXAMINATION
HISTORY ATLS

Age
Other injuries

General health & comorbidities Vascular status of limb

• Limb color, pulse, capillary refill
Neurological status of limb
Alcohol & drugs
• Power, sensation

Ambulatory status

Cause of injury

• High or low energy

• Potential for infection
• Previous injuries
 Preoperative Assessment
EXAMINATION OF OPEN
WOUND
Location & extent of the wound
Length of wound
Number of skin wounds
Degree of skin contamination

CT & MRI: open

RADIOLOGICAL X-ray: AP, lateral
pelvic, intra-
EXAMINATION articular, carpal,
tarsal fractures
Treatment- Outline

Irrigation

Debridement: Skin, Fat, Muscle, Bone

Wound closure

Analgesic + Antibiotic + Antitetanus

(AAA): IV, IM

Fracture stabilization
1) Analgesic + Antibiotic + Antitetanus
Prophylaxis
Analgesic
Pethidine/morphine

60-70% of open wound are associated with positive cultures, mostly

normal flora

Broad spectrum  3rd generation cephalosporin, aminoglycoside

Gentamicin or metronidazole for gram negative organism.

Antitetanus
Toxoid for immunised Human antiserum for non-immunised
Antibiotic
• Gustilo Grade I- first generation of cephalosporin
for 72 hours
• Gustilo Grade II- first generation cephalosporin for
72 hours + Gram negative coverage (gentamicin)
for at least 72 hours
• Gustilo Grade III- first generation cephalosporin +G
–ve coverage for at least 72 hours
• For soil contamination- penicillin is added for
clostridial coverage
 2) Irrigation
Fluids such as Advantages:
normal isotonic
saline or antibiotic •Flushes away the
solutions + foreign matter and
hydrogen peroxide contaminated
blood clot
•Helps in
assessment of
A method of wound viability of tissues
cleansing by removing
debris mechanically •Reduces bacterial
with pressurised fluid. population
 3) Debridement

All dead and contaminated tissues

must be removed

Performed in a systematic manner

• Skin & fascia
• Muscles
• Tendon
• Bone
 89

Surgical Debridement
 Type II and type III require surgical
debridement.
 Important aspect of wound
management.
 Reduce bacteria, remove foreign
bodies, remove devitalized tissue.
 Removal of dead tissue reduces
bacterial burden and accelerate
healing.
4) Wound Closure
• For wounds less than 8 hours old
Primary closure
after debridement

• Wound left open after debridement

Delayed primary for 2-3 days
closure (<5days)
• If clean, close the wound

Another debridement • Type III

Secondary closure • For infected wound

• Partial thickness
Skin grafting
• Full thickness
Wound Closure
 Uncontaminated I & II can be sutured –
provided without tension
 All other wounds left open, packed with moist
sterile gauze, to be inspected 24-48 hours –
primary delayed closure
 If wound cannot be closed without tension –
skin grafting
 5) Fracture Stabilization
Immobilisation • A window is made in the plaster over the wound
for dressing
in a plaster

Skeletal • Eg. open fracture of tibia

traction
• Can be easily applied
• Readily reduced and adjusted
External fixator • Wound can be assessed for dressing
• Excellent stability

Internal fixator • Rarely used

Stabilization of the fracture
 To reduce infection and assist recovery of soft
tissue
 Depends on:
 degree of contamination
 length of time from injury to operation
 amount of soft tissue damage
 If <8 hours: up to IIIA treated as closed fractures:
 Splintage
 Intramedullary nailing
 Plating
 External fixation
 Others: External fixation
Aftercare

The limb is
elevated & it's
Antibiotic
circulation
cover
carefully
monitored

If the wound
has been left
open, it is Physiotherapy
inspected and
after 2-3 days rehabilitation
& covered
appropriately
COMPLICATION
OF FRACTURE
 Early Late
General Shock Crush Syndrome
Diffuse Coagulopathy Chest Infection
Tetanus
GENERAL
Respiratory Dysfunction
DVT & Pulmonary Emb.
Urinary Tract Infection
Gas Gangrene

Fat Emboli Syndrome

Bone Infection Non-union / Mal-union / Delayed

BONE
union
Avascular Necrosis
Length discrepancy
Disuse Osteoporosis
Joint Haemarthrosis Instability / Mal-alignment
Ligament injury
JOINT Osteoarthritis
Stiffness
Overuse injuries
Soft Tissue Plaster Sore Nerve compression
Tendon Rupture Volkmann’s contracture

SOFT TISSUE
Neurovascular Injury
Compartment Syndrome
Bedsores
Myositis Ossificans
Visceral injury Tendinitis & Tendon rupture
General
Complications

1. Shock
2. Diffuse coagulopathy
3. Respiratory
dysfunction
4. Crush syndrome
5. Venous thrombosis &
Pulmonary embolism
6. Fat embolism
7. Gas Gangrene
8. Tetanus
General 1: Shock
Altered physiologic status with generalized
inadequate tissue perfusion relative to metabolic
requirements.  irreversible damage to vital organs

Cardiogenic • direct injury to heart  effect the pump functions

• injury to brain stem (vasomotor center) spinal cord  loss of

Neurogenic sympathetic tone  increase venous capacitance  low
venous return àlow cardiac output (but bradycardia)

Hypovolemic • reduction of blood volume

 1500-3000ml 500-1000ml

1500-3000ml
100-300ml

1000-2000ml

1000-2000ml

VOLUME DISTRIBUTION
 General 1: Shock
Why we need to treat
shock?
• Blood redistribution
• Renal shutdown
• Intestinal ischemia
• Tissue hypoxia
• Metabolic acidosis
• Reduced hepatic blood
flow
• Acute Respiratory Distress
Sydrome
• Altered consciousness
How to manage shock?
• Identify: Thirst, rapid
shallow breathing, the lips
and skin are pale and the
extremities feel cold,
impaired renal function
test and decreased urinary
output.
• ABC
• IV lines: fluids and blood
• Oxygenation/Ventilation
• Urinary Catheter
• Central Venous Pressure
• Ionotropic drugs
General 2: DIFFUSE COAGULOPATHY
Consumptive
Management
Coagulopathy
•activation by •Stop the bleeding
tissue •Fresh Frozen
thromboplastin Plasma (FFP)
•endothelial injury •Cryoprecipitate
activating •Platelet transfusion
platelets
•Heparin
•massive blood
transfusion
General 3: RESPIRATORY DYSFUNCTION
Pathophysiology Management

•Alveolar edema •Oxygenation

•endothelial injury •Ventilation
•capillary •positive end
permeability expiratory pressure
•Poor lung (PEEP)
compliance
•inactivated
surfactant
•Arterial hypoxemia
 General 4: Crush Syndrome
[traumatic rhabdomyolitis]

Serious medical condition characterized by

major shock & renal failure following a
crushing injury to skeletal muscles or
tourniquet left too long

Bywaters’ Syndrome

Oliguria,
When Myohaemati
Nephrotoxic Block uremia,
compression n release
effects tubules metabolic
released from cells
acidosis
 General 4: Crush Syndrome
Clinically
• Shock
• Pulseless limb  redness 
swelling
• Loss of muscle sensation and
power
• Decrease renal secretion
• Uremia, acidosis
• Prognosis
• If renal secretion return
within 1 week the patient
survive
• But most of them die within
14 days
Management
• PREVENTION
• Strict tourniquet timing
• Amputation
• limb crushed severely
• tourniquet left on > 6 hrs
• above site of compression
& before compression
released
• Monitor intake & output
• Dialysis
• Correct electrolytes &
acidosis
• Antibiotics
General 5: Deep vein thrombosis
and pulmonary embolism.
 Virchow’s triad factor  Clot formation in
large vein  thrombus breaks off 
Emboli
 Site: leg, thigh and pelvic vein.
 Risk factors:

Knee and hip

Elderly Immobility Malignancy
replacement

Cardiovascul Hypercoagul
Trauma
ar disease able status
 General 5: Management Deep vein
thrombosis and pulmonary embolism.

 PREVENTION  Anticoagulation
 Correct hypovolemia  Ambulate patient
 Calf muscle exercise  Established
 Proper positioning thrombosis/embolism
Limb elevation
 Well fitting bandages &


cast  Heparinization
Thrombolysis
 Limb elevation

 Oxygenation or
 Graduated
ventilation
compression stockings
 Calf muscle stimulation
 General 6: Fat Embolism
Fat globules from marrow pushed into
circulation by the force of trauma that causing
embolic phenomena

Fractures Fat in bone Formation of

that most Closed/ope
marrow fat globules in
often cause n Fracture vessels
escape
FES
• Long
bones
• Ribs
• Tibia Triad of Stick in
Fat embolus
• Pelvis symptoms target organ
General 6: Fat Embolism
Triad of Symptoms Management

• Brain: mental • Prevent hypoxemia

confusion • oxygenation or
• Lung: breathlessness, ventilation
ARDS • Rule out head injury
• Skin: Petechia • CT Scan of brain
• Monitor fluid &
electrolyte balance
• CVP, urinary
catheter
General 6: Fat Embolism
SKIN: Fat droplets 
obstruct alveolar
capillaries 
thromboplastin release 
consumption of
coagulation fx & platelets
 DIVC/Skin necrosis 
Petechia

LUNG: Fat droplets 

obstruct alveolar
capillaries 
thromboplastin release 
alter membrane
permeability / lung
surfactant  oedema  BRAIN: Fat droplets  obstruct
respiratiory failure [V/Q capillaries  confusion 
Mismatch] coma/fits  death
 General 7: Gas Gangrene
Rapid and extensive necrosis of the muscle
accompanied by gas formation and systemic toxicity
due to clostridium perfringens infection

Clinical Features Management

• sudden onset of pain localized • early diagnosis .

to the infected area.
• swelling , edema
• +/- pyrexia
• profuse serous discharge with
sweetish and mousy odor .
• Gas production
• surgical intervention and
debridement are the mainstay
of treatment.
• IV antibiotics
• fluid replacement.
• hyperbaric Oxygen
General 7: Gas Gangrene

Prevention: ALL DEAD TISSUE [4C]

SHOULD BE COMPLETELY EXCISED,
 General 8: Tetanus
A condition after clostridium tetani infection that
passes to anterior horn cells where it fixed and cant
be neutralized later produces hyper-excitability and
reflex muscle spasm

Clinical Features Management

• Tonic and clonic • Prophylaxis

contractions of esp. jaw,
face, around the wound
itself ,neck ,trunk, finally
spasm of the diaphragm
and intercostal muscles
leads to asphyxia and
death.
• Treatment
• Antitoxin & antibiotic
• Muscle relaxant
• Tracheal intubation
• Respiration control
Early
Complications

1. Visceral Injury
2. Vascular Injury
3. Compartment
Syndromes
4. Nerve injury
5. Haemarthrosis
6. Infection
Early 1: Visceral injury
 Fractures
around the trunk are
often complicated by visceral
injury.
 E.g. Rib fractures 
pneumothorax / spleen trauma
/ liver injuries.
 E.g. Pelvic injuries  bladder or
urethral rupture / severe
hematoma in the retro-
peritoneum .
 Rx: Surgery of visceral injuries
 Early 2: Vascular injury
 Commonly associated with high-
energy open fractures. They are rare
but well-recognized.
 Mechanism of injuries:
 The artery may be cut or torn.
 Compressed by the fragment of bone.
 normal appearance, with intimal
detachment that lead to thrombus
formation.
 segment of artery may be in spasm.
 It may cause
 Transient diminution of blood flow
 Profound ischaemia
 Tissue death and gangrene
 Early 2: Vascular injury
Pain
5P’s of ischemia

Pallor

Pulseless

Paralysis

Paraesthesia

X-ray: suggest high-risk fracture.

Angiogram should be performed to confirm diagnosis.
 Early 2: Vascular injury
Injury Vessel
 muscle ischaemic is 1st rib fracture subclavia
irrevesible after 6 hours. n

 Remove all bandages Shoulder dislocation Axillary

and splint & assess Humeral supracondylar Brachial

fracture
circulation
Elbow dislocation Brachial
 Skeletal stabilization – Pelvic fracture Presacral
temporary external and
fixation. internal
iliac
 Definitive vascular Femoral supracondylar Femoral
repair. fracture
 Vesselsutured Knee dislocation Popliteal
 endarterectomy Proximal tibial fracture Popliteal
or its
branches
Early 3: Compartment Syndrome
A condition in which increase in pressure within a
closed fascial compartment leads to decreased
tissue perfusion.
Untreated, progresses to tissue ischaemia and
eventual necrosis

Leg Forearm

•4 compartments: •3 compartments: dorsal,

anterior, lateral, superficial and deep
superficial and deep volar
posterior •interconnected, hence
•NOT interconnected fasciotomy of 1
compartment may
decompress the other 2
Early 3: Compartment Syndrome
 Mostcommon sites (in ↓ freq): leg (after tibial
fracture) → forearm → thigh → upper arm.
Other sites: hand, foot, abdomen, gluteal and
cervical regions.

 High risk injuries:

 # of elbow, forearm bones, and proximal 3rd of
tibia (30-70% after tibial #)
 multiple fracture of the foot or hand
 crush injuries
 circumferential burns
Early 3: Compartment Syndrome
[aetiology]
↑ Compartmental volume (↑
fluid content)
• Trauma – fractures
/osteotomies, crush injury
• Vascular – haemorrhage,
post-ischaemic swelling
• Soft tissue injury – burns,
prolonged limb compression
• Iatrogenic – intraosseous
fluid resuscitation in children,
intraarterial drug injection
• Extreme muscular exertion
↓ Compartment volume
(constriction of the
compartment)
• Constrictive dressings/plaster
casts
• Thermal injuries with eschar
formation
• Pneumatic antishock
garments (MAST)
• Surgical closure of fascial
defects
 Early 3: Compartment
Syndrome

Vicious cycle
↑ fluid content Constriction of compartment

↑ INTRACOMPARTMENTAL PRESSURE

Obstruct venous return Capillary basement

membranes become
leaky → oedema
Vascular congestion
Muscle and nerve ischaemia

Further ↑ intracompartmental ↓ capillary perfusion

pressure
Compromise arterial circulation
→ PROGRESSIVE NECROSIS OF MUSCLES AND NERVES !!
Sequence started with:

severe pain/bursting
sensation (early)

paraesthesia/hypoaesthesia

motor weakness

loss of peripheral pulses and

capillary refill (late signs,
poor prognosis)
A vicious circle that ends after 12 hours or less

Necrosis of the nerve and muscle within the compartment

Nerve Muscle
-capable to regenerate -infarcted

Never recover

Replaced by inelastic fibrous tissue

( Volkmann’s ischaemic contracture)
Investigations of compartment
sydromes
 Intra-compartment Pressure Measurement (ICP)
 Use of slit catheter; quick and easy
 Indications:
 Unconscious patient
 Those who are difficult to assess
 Concomitant neurovascular injury
 Equivocal symptoms

 Especially long bone # in lower limb

 Perform as soon as dx considered
 > 40mmHg – urgent Rx! (normal 0 – 10 mmHg)
Investigations of compartment
syndromes
 OtherIx – limited value; +ve only when CS is
advanced
 Plasma creatinine and CPK
 Urinanalysis – myoglobinuria
 Nerve conduction studies
 Ix to establish underlying cause or exclude
differentials
 X-ray of affected extremity
 Doppler US/arteriograms – determine presence
of pulses; exclude vascular injuries and DVT
 PT/APTT – exclude bleeding disorder
 Management
 Prompt DECOMPRESSION of affected
compartment
 Remove all bandages, casts and dressings
 Examination of whole limb
 Limb should be maintained at heart level
 Elevation may ↓ arterio-venous pressure gradient
on which perfusion depends
 Ensure patient is normotensive.
 Hypotension ↓ tissue perfusion, aggravate the
tissue injury.
Management
 Measure intra-compartment pressure
 If > 40mmHg
 Immediate open fasciotomy
 If < 40mmHg
 Close observation and re-examine over next hour
 If condition improve, repeated clinical evaluation
until danger has passed

Don’t wait for the obvious sings of ischemia to appear. If you suspect
An impending compartment syndrome, start treatment straightaway
Fasciotomy
 Opening all 4 compartments
 Divide skin and deep fascia for the whole
length of compartment
 Wound left open
 Inspect 5 days later
 If muscle necrosis, do debridement
 If healthy tissue, for delayed closure or skin
grafting
Complications
 Volkmann’s ischaemic contracture
 Motor/sensory deficits
 Kidney failure from rhabdomyolysis (if very severe)
 Infection – fasciotomy converts closed # to open
#
 Loss of limb
 Delay in bone union

Prognosis
excellent to poor, depending on how quickly CS is
treated and whether complications develop
 Early 4: Nerve Injury
 It’s more common than Injury nerve

arterial injuries. 1. Shoulder

dislocation
Axillary

 The most commonly 2. Humeral shaft Radial

injured nerve is the radial fracture

3. Lower end of Median
nerve [in its groove or in the radius
lower third of the upper arm 4. Humeral Radial or
especially in oblique fracture supracondylar (esp. median(ant.inteross
children) eous)
of the humerus]
5. Medial condyle Ulnar
 Common with humerus, 6. Elbow dislocation Ulnar
elbow and knee fractures 7. Hip dislocation Sciatic

 Most nerve injuries are due 8. Knee dislocation Peroneal

to tension neuropraxia. 9. Fracture of fibular

neck
Peroneal
 Early 4: Nerve Injury
 Damaged by laceration, traction, pressure or
prolonged ischaemia

Neurapraxia Axonotmesis Neurotmesis

• axon remains • axonal • nerve completely

intact but separation with divided.
conduction degeneration of Spontaneous
ceases due to distal portions. recovery unlikely.
segmental Sheath remains
demyelination. intact, thus
Spontaneous recovery likely
recovery in a few but delayed
days or weeks
 Early 4: Nerve Injury
Investigations
Clinical features  Electromyography
 Numbness and  Nerve conduction
study
weakness
 May help to establish
 Skin smooth and level and severity of
shiny but feels dry lesion
 Muscle wasting and
weakness
 Sensation blunted
 Tinel’s sign +ve
 Early 4: Nerve Injury
Open injuries
• Exploration
• Cleanly divided – repair
immediately
• Torn/crushed – left alone
or ends lightly tacked
together, re-explore 2 – 3
weeks later for scar tissue
removal and suturing
Closed injuries
• Usually nerve sheath
intact
• Rate of axonal
regeneration = 1mm/day
• If no sign of recovery –
re-exploration with
excision of scar tissue
and suturing of clean-cut
ends, nerve grafting if
gap too large
• Splinting 3-6 weeks then
physiotherapy
 Early 5: Haemarthrosis
 Bleeding into a joint spaces.
 Occurs if a joint is involved in
the fracture.
 Presentation:
 swollen tense joint; the patient
resists any attempt to moving it
 treatment:
 blood aspiration before dealing
with the fracture; to prevent the
development of synovial
adhesions.
Early 6: INFECTION
 Closed fractures – hardly ever
 Open fractures – may become infected
 Post traumatic wound – may lead to
chronic osteomyelitis

Clinical features Treatment

• wound is inflammed • antibiotic

• draining seropurulent • excise the devitalised
fluid tissue
• tissues opened &
drained the pus
Late
Complications

1. Delayed Union
2. Non-union
3. Mal-union
4. Avascular Necrosis
5. Osteoarthritis
6. Joint Stiffness
Late 1: DELAYED UNION
Union of the upper limbs - 4-6
weeks
Union of the lower limbs - 8-12
weeks(rough guide)
Any prolong time taken is
considered delayed
Late 1: DELAYED UNION
 Factors are either biological or biomechanical
 Biological :
 Poor blood supply
 Tear of periosteum, interruption of intramedullary
circulation
 Necrosis of surface# and healing process will take
longer
 Severe soft tissue damage
 Most important factor
 Longer time for bone healing due less inflammatory
cell supply
 Infection: bone lysis, tissue necrosis and pus
 Periosteal stripping
 Less blood circulation to bone
Late 1: DELAYED UNION
 Mechanical
 Over-rigid fixation-fixation devise

 Imperfect splintage
 Excessive traction creates a gap#(delay ossification
in the callus)
Late1: DELAYED UNION
 Clinical features:
 Tenderness persist
 Acute pain if bone is subjected to stress*
( * ask pt to walk, move affected limb)

X RAYS -visible line# and very little callus

formation/periosteal reaction
- bone ends are not sclerosed/ atrophic
(it will eventually unite)
Late 1: DELAYED UNION
 Tx: conservative and operative
 Eliminate possible causes of delay
 Promote healing
 Immobilization should be sufficient to prevent movement at
# site(cast / internal fixation)
 Not to neglect # loading so, encourage muscle exercise
and weight bearing in the cast/brace
 Operation
 > 6 mths & no signs of callus formation
 Internal fixation and bone graffting
(operation-least possible damage to the soft tissue)
 Late 2 : NON-UNION
 In a minority of cases, delayed union--non-union
 Factors contributing to non-union:-
 inadequate treatment of delayed union
 too large gap
 interposition of soft tissues between the fragments
 The growth has stopped and pain diminished-
replaced by fibrous tissue - pseudoarthrosis
 Treatment :-
 conservative / operative
 atrophic non-union – fixation and grafting
 hypertrophic non-union – rigid fixation
Late 2: NON UNION
 bone ends are rounded off or exuberant
 Hypertrophic non union
 Bone ends are enlarged, osteogenesis is still active
but not capable of bridging the gap
 ‘elephant feet’ on X ray

 Atrophic non union

 Cessationof osteogenesis
 No suggestion of new bone formation
A B

Non-union
X- ray
A – Atrophic non- union
B – Hypertrophic non-
union
Late 2: Non union
 Tx:
 Mostly symptomless
 Conservative
 Removable splint
 For hypertrophic non-union, functional bracing-induce union
 Pulsed electromagnetic fields and low frequency pulsed u/s
can also be used to stimulate union.
 Operative
 Hypertrophic--Rigid fixation (internal or external)
 Atrophic--Excision of fibrous tissue ,sclerotic tissue at bone
end, bone grafts packed around the fracture
Late 3: MALUNION

fragments that are joined in

an unsatisfactory position

 Factors:-
 failure to reduce the fracture
 failure to hold the reduction while healing
proceed
 gradual collapse of comminuted / osteoporotic
bone
MALUNION
Late 3: Mal-union
 X-ray are essential to check the position of the
fracture while uniting. important- the first 3
weeks so it can be easily corrected
 Clinical features:
 Deformity usually obvious , but sometimes the true
extent of malunion is apparent only on x-ray
 Rotational deformity can be missed in the femur,
tibia, humerus or forearm unless is compared with
it’s opposite fellow
 Treatment
 Decision about the need for re-manipulation
and correction-difficult
In adults Fracture-reduced as near to the anatomical position as possible
apposition for healing
alignment and rotation is important for function
Angulation(>10-15) in long bone or apparent rotational deformity may
need correction by re-manipulation or by osteotomy and internal
fixation
In children angular deformity near the bone ends often remodel with time
Rotational deformity will not

In lower limb Shortening less than 2 cm: compensated by shoe raise

shortening
Shortening more than 2 cm: limb lengthening should be consider.

Long term effect of mal-alignment (>15) results in asymmetrical loading

of joint and results in late development of 2 osteoarthritis.
Late 4: AVASCULAR NECROSIS
Certain region-known for their propensity to
develop ischaemia and bone necrosis
 Head of femur
 Proximal part of scaphoid
 Lunate
 Body of talus
 (Actually this is an early complication however
the clinical and radiological effects are not seen
until weeks or even months)
 Noclinical feature of avascular necrosis but if
there is a failure to unite or bone collapse-pain
 A B

The cardinal X-ray feature – increased bone density in the weight-

bearing part of the joint(new bone ingrowth in necrotic segment)
Treatment:-
 Avascular necrosis can be prevented by early
reduction of susceptible fractures and
dislocations.
 Arthroplasty - Old people with necrosis of the
femoral head.
 Realignment osteotomy or arthrodesis - for
younger people with necrosis of the femoral
head
 Symptomatic treatment for scaphoid or talus
Late 5: OSTEOARTHRITIS
A fracture-joint may 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
Late 6: JOINT STIFFNESS
 Commonly occur at the joints close to
malunion or bone loss eg: knee, elbow,
shoulder
 Causes of joint stiffness
 haemarthrosis → lead to synovial adhesion
 oedema and fibrosis
 adhesion of the soft tissues
 Worsen by prolong immobilization
 Treatment
 prevented with exercise
 physiotherapy
THANK YOU!!!!