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FRACTURESAnandkumar BalakrishnaWong Poh SeanMohd 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 FRACTURESCLOSED/ SIMPLE
• no opening in the skin.
OPEN/ COMPOUND
• bone fragments have broken through the skin.
COMPLETE
• bone is completely broken into 2 or more fragments.
• -eg:• transverse
fracture • oblique fracture• spiral fracture• impacted
fracture• comminuted
fracture• segmental
fracture
INCOMPLETE
• bone is incompletely divided and the periosteum remains in continuity.
• -eg:• greenstick
fracture • torus fracture• stress fracture• compression
fracture.
COMPLETE FRACTURES
OBLIQUE FRACTURE
SEGMENTAL FRACTURE
SPIRAL FRACTURE
TRANSVERSE FRACTURE
COMMINUTED FRACTURE
IMPACTED FRACTURE
INCOMPLETE FRACTURE
GREENSTICK
TORUS
FRACTURES DISPLACEMENT After a 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 /TILT
TWIST/ROTATION
SIDEWAYS
OVERLAPIMPACTION
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:
Type of bone
cancellous
bone heals faster than
cortical bone.
Type of fracture
spiral fracture heals faster than
transverse
fracture.
State of blood flow
poor circulation will
slow the
healing proces
s.
Patient’s general
constitution
healthy bone heals faster.
Patient’s age
healing is
faster in
children than adults.
CAUSES OF DELAYED UNION OR NON-UNION OF THE
FRACTURES
Distraction & separation of the fragments
Interposition of soft tissues between the fragments.
Excessive movement at the fracture
site
Poor local blood supply
Severe damage to soft tissues which makes
them nearly/non-
viable.
Infection
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
Hold
Exercise
Reduce
Principle Of Treatment
Safety
MoveSpeed
Hold
The Fracture Quartet
Outline
Clo
sed
Fra
ctu
re
Reduce
Closed Reduction
Mechanical Traction
Open Reduction
Hold
Sustained Traction
Cast Splintage
Functional Bracing
Internal Fixation
External Fixation
Exercise
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)
Operative
Closed reduction
Mechanical Traction
Non-operative
Open reduction
Reduction
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
Non Operativ
e
• Sustained traction
• Cast Splintage• Functional
Bracing
Operative
• Internal Fixation
• External Fixation
Hold
HOLD
To prevent displaceme
nt
To alleviate pain by some
restriction of
movement
To promote soft-tissue
healing
To allow free
movement of the
unaffected parts
Safety
MoveSpeed
Hold
Sustained Traction• Traction is applied to limb distal to the
fracture• To exert continuous pull along the long axis
of the bone
• Can move joint• Can exercise musle
Advantage
• Useful for spiral fractures of long bone shafts:• Shaft of femur• Tibia• Lower humerus
Indication
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
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
Balanced Traction
Thomas’s Splint
Traction applied via stiff wire or pin inserted through the bone distal to the fracture skeletal traction• Can apply several
times as much force
Complications:• Pin tract infection• Damage to epiphyseal
growth plate• Vertical fracture of the
bone• Injury to the vessels or
nerves
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
Safety
MoveSpeed
Hold
Tight cast put on too tightly/limb swells
Pressure sores even a well-fitting cast may
press upon the skin over a bony
prominence (the patella, the heel)
Skin abrasion or laceration during
removal of the plaster
Complications
Brace supportive device that
allows continued
function of the part
Principle functional long
bone is supported
externally by POP or by a mouldable
plastic material but the function
of joints are preserved
Indication fractures of
shaft of femur or tibia
Functional Bracing
Functional bracing is not rigid applied when fracture is beginning to unite, after about 3-6 weeks of traction or restrictive splintage
Advantages:
• Fractures held reasonably well
• Joints can be moved• Patient can leave hospital• Method is safe
Safety
MoveSpeed
Hold
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
1. Fracture that cannot be reduced except by
operation
2. Fracture that are inherently unstable
and prone to displacement after
reduction
3.Fracture that unite poorly and slowly• Principally fracture of
the femoral neck
4.Pathological fracture• Bone disease may
prevent healing
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 reduction
• ORIF-open reduction and internal fixation
Immediate stability
• Hold the fracture securely
Early movement
• ‘fracture disease ‘ like oedema,s tifness,etc may abolish
Complications
Infection
Non-union
Implant failure
Refracture
Infe
ctio
nIatrogenic infection chronic osteomylitisRisk of infection depends on:1)The patient devitalised tissue, dirty wound, unfit patient2)The surgeon thorough training, a high degree of surgical dexterity and adequate assistant are all essential3)The facilities aseptic routineThe infection should be rapidly controlled by intravenous antibioticIf infection cannot be controlled, the implant should be replaced with some form of external fixation
Non
un
ion
Cause:1) excessive stripping of soft tissue2) unnecessary damage to blood supply in the course of operative fixation 3)rigid fixation with a gap between the fragment
Implant failureMetal 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
IndicationFracture associated with soft tissue injury• Where the wound can be left
open for inspection, dressing and definitive coverage
Severely comminuted and unstable fracture• Which can be held out to
length until healing commence
Fracture of the pelvis• Which often cannot be
controlled quickly by any other method
Fracture associated with nerve and vessel
damage
Infected fracture• Where internal fixation
might not be suitable
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
technically quick and easy to
perform
no soft tissue stripping;
ease of removing hardware;
risk of infection at the site of the
fracture is minimal
Complication
Damage to soft tissue
structure
Over distracti
on
Pin track infection
• 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
Damage to soft tissue structure
• If there is no contact between the fragment, union may be delayed or prevented
Over distraction
• 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
Pin track infection
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 FracturesA 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 Assessment
HISTORY
Age
General health & comorbidities
Alcohol & drugs
Ambulatory status
Cause of injury
• High or low energy• Potential for infection• Previous injuries
PHYSICAL EXAMINATION
ATLS
Other injuries
Vascular status of limb
• Limb color, pulse, capillary refillNeurological status of limb
• Power, sensation
Preoperative Assessment
EXAMINATION OF OPEN WOUNDLocation & extent of the wound
Length of wound
Number of skin wounds
Degree of skin contamination
RADIOLOGICAL EXAMINATION
X-ray: AP, lateral
CT & MRI: open pelvic, intra-
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
Antitetanus
Toxoid for immunised Human antiserum for non-immunised
Broad spectrum 3rd generation cephalosporin, aminoglycosideGentamicin or metronidazole for gram negative organism.
60-70% of open wound are associated with positive cultures, mostly normal flora
AnalgesicPethidine/morphine
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) IrrigationFluids such as
normal isotonic saline or antibiotic
solutions + hydrogen peroxide
A method of wound cleansing by removing
debris mechanically with pressurised fluid.
Advantages:
• Flushes away the foreign matter and contaminated blood clot
• Helps in assessment of viability of tissues
• Reduces bacterial 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 after debridementPrimary closure
• Wound left open after debridement for 2-3 days
• If clean, close the wound
Delayed primary closure (<5days)
• Type IIIAnother debridement
• For infected woundSecondary closure
• Partial thickness • Full thicknessSkin grafting
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
• A window is made in the plaster over the wound for dressing
Immobilisation in a plaster
• Eg. open fracture of tibiaSkeletal traction
• Can be easily applied• Readily reduced and adjusted• Wound can be assessed for dressing• Excellent stability
External fixator
• Rarely usedInternal fixator
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 circulation carefully
monitored
Antibiotic cover
If the wound has been left open, it is inspected after 2-3 days & covered
appropriately
Physiotherapy and
rehabilitation
COMPLICATION OF FRACTURE
Early Late
General ShockDiffuse CoagulopathyTetanusRespiratory DysfunctionDVT & Pulmonary Emb.Fat Emboli Syndrome
Crush SyndromeChest InfectionUrinary Tract InfectionGas Gangrene
Bone Infection Non-union / Mal-union / Delayed unionAvascular NecrosisLength discrepancyDisuse Osteoporosis
Joint HaemarthrosisLigament injury
Instability / Mal-alignmentOsteoarthritisStiffnessOveruse injuries
Soft Tissue
Plaster SoreTendon RuptureNeurovascular InjuryCompartment SyndromeVisceral injury
Nerve compressionVolkmann’s contractureBedsoresMyositis OssificansTendinitis & Tendon rupture
GENERAL
BONE
JOINT
SOFT TISSUE
General Complications
1. Shock2. Diffuse coagulopathy3. Respiratory
dysfunction4. Crush syndrome5. Venous thrombosis &
Pulmonary embolism6. Fat embolism7. Gas Gangrene8. Tetanus
General 1: ShockAltered physiologic status with generalized
inadequate tissue perfusion relative to metabolic requirements. irreversible
damage to vital organs
• direct injury to heart effect the pump functionsCardiogenic
• injury to brain stem (vasomotor center) spinal cord loss of sympathetic tone increase venous capacitance low venous return àlow cardiac output (but bradycardia)
Neurogenic
• reduction of blood volumeHypovolemi
c
500-1000ml
100-300ml
1000-2000ml
1000-2000ml
1500-3000ml
1500-3000ml
VOLUME DISTRIBUTION
General 1: ShockWhy 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 Coagulopathy
• activation by tissue thromboplastin
• endothelial injury activating platelets
• massive blood transfusion
Management
• Stop the bleeding• Fresh Frozen
Plasma (FFP)• Cryoprecipitate• Platelet
transfusion• Heparin
General 3: RESPIRATORY DYSFUNCTION
Pathophysiology
• Alveolar edema• endothelial
injury• capillary
permeability• Poor lung
compliance• inactivated
surfactant• Arterial
hypoxemia
Management
• Oxygenation• Ventilation• positive end
expiratory pressure (PEEP)
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
When compressi
on released
Myohaematin release from cells
Nephrotoxic effects
Block tubules
Oliguria, uremia,
metabolic acidosis
Bywaters’ Syndrome
General 4: Crush SyndromeClinically
• 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 replacement Elderly Immobility Malignancy
Cardiovascular disease Trauma Hypercoagul
able status
General 5: Management Deep vein thrombosis and pulmonary embolism.
PREVENTION Correct hypovolemia Calf muscle exercise Proper positioning Well fitting bandages &
cast Limb elevation Graduated compression
stockings Calf muscle stimulation
Anticoagulation Ambulate patient Established
thrombosis/embolism Limb elevation Heparinization Thrombolysis Oxygenation or
ventilation
General 6: Fat EmbolismFat globules from marrow pushed into circulation by the force of trauma that
causing embolic phenomena
Fractures that most often cause FES• Long
bones• Ribs• Tibia• Pelvis
Closed/open
Fracture
Fat in bone
marrow escape
Formation of fat
globules in vessels
Fat embolus
Stick in target organ
Triad of symptoms
General 6: Fat Embolism
Triad of Symptoms
• Brain: mental confusion
• Lung: breathlessness, ARDS
• Skin: Petechia
Management
• Prevent hypoxemia• oxygenation or
ventilation• Rule out head
injury• CT Scan of brain
• Monitor fluid & electrolyte balance• CVP, urinary
catheter
General 6: Fat EmbolismSKIN: 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 respiratiory failure
[V/Q Mismatch]
BRAIN: Fat droplets obstruct capillaries
confusion coma/fits death
General 7: Gas GangreneRapid and extensive necrosis of the muscle accompanied by gas formation and systemic
toxicity due to clostridium perfringens infection
Clinical Features
• sudden onset of pain localized to the infected area.
• swelling , edema• +/- pyrexia• profuse serous discharge
with sweetish and mousy odor .
• Gas production
Management
• early diagnosis .• 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: TetanusA 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
• Tonic and clonic contractions of esp. jaw, face, around the wound itself ,neck ,trunk, finally spasm of the diaphragm and intercostal muscles leads to asphyxia and death.
Management
• Prophylaxis• Treatment• Antitoxin & antibiotic• Muscle relaxant• Tracheal intubation• Respiration control
Early Complications
1. Visceral Injury2. Vascular Injury3. Compartment
Syndromes4. Nerve injury5. Haemarthrosis6. 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 injury5P
’s o
f is
ch
em
ia
Pain
Pallor
Pulseless
Paralysis
Paraesthesia
X-ray: suggest high-risk fracture.Angiogram should be performed to confirm diagnosis.
Early 2: Vascular injury muscle ischaemic is
irrevesible after 6 hours. Remove all bandages
and splint & assess circulation
Skeletal stabilization – temporary external fixation.
Definitive vascular repair. Vessel sutured endarterectomy
Vessel Injury
subclavian
1st rib fracture
Axillary Shoulder dislocation
Brachial Humeral supracondylar fracture
Brachial Elbow dislocation
Presacral and internal iliac
Pelvic fracture
Femoral Femoral supracondylar fracture
Popliteal Knee dislocation
Popliteal or its branches
Proximal tibial fracture
Early 3: Compartment Syndrome
Leg
• 4 compartments: anterior, lateral, superficial and deep posterior
• NOT interconnected
Forearm
• 3 compartments: dorsal, superficial and deep volar
• interconnected, hence fasciotomy of 1 compartment may decompress the other 2
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
Early 3: Compartment Syndrome
Most common 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
↑ fluid content Constriction of compartment
↑ INTRACOMPARTMENTAL PRESSURE
Obstruct venous return
Vascular congestion
Further ↑ intracompartmental pressure
↓ capillary perfusion
Muscle and nerve ischaemia
Capillary basement membranes become leaky → oedema
Compromise arterial circulation
→ PROGRESSIVE NECROSIS OF MUSCLES AND NERVES !!
Vicious cycle
Early 3: Compartment Syndrome
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-capable to regenerate
Muscle-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
Other Ix – 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
Prognosisexcellent to poor, depending on how quickly CS is treated and whether complications develop
Early 4: Nerve Injury It’s more common than
arterial injuries. The most commonly
injured nerve is the radial nerve [in its groove or in the lower third of the upper arm especially in oblique fracture of the humerus]
Common with humerus, elbow and knee fractures
Most nerve injuries are due to tension neuropraxia.
nerve Injury
Axillary 1. Shoulder dislocation
Radial 2. Humeral shaft fracture
Median 3. Lower end of radius
Radial or median(ant.interosseous)
4. Humeral supracondylar (esp. children)
Ulnar 5. Medial condyle
Ulnar 6. Elbow dislocation
Sciatic 7. Hip dislocation
Peroneal 8. Knee dislocation
Peroneal 9. Fracture of fibular neck
Early 4: Nerve Injury
Damaged by laceration, traction, pressure or prolonged ischaemia
Neurapraxia
• axon remains intact but conduction ceases due to segmental demyelination. Spontaneous recovery in a few days or weeks
Axonotmesis
• axonal separation with degeneration of distal portions. Sheath remains intact, thus recovery likely but delayed
Neurotmesis
• nerve completely divided. Spontaneous recovery unlikely.
Early 4: Nerve InjuryClinical features Numbness and
weakness Skin smooth and
shiny but feels dry Muscle wasting
and weakness Sensation blunted Tinel’s sign +ve
Investigations Electromyography Nerve conduction study May help to establish
level and severity of lesion
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
• wound is inflammed• draining seropurulent
fluid
Treatment
• antibiotic• excise the devitalised
tissue• tissues opened &
drained the pus
Late Complications
1. Delayed Union2. Non-union3. Mal-union4. Avascular Necrosis5. Osteoarthritis6. Joint Stiffness
Late 1: DELAYED UNION Union of the upper limbs - 4-6
weeksUnion 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
Mechanical Over-rigid fixation-fixation devise
Imperfect splintage Excessive traction creates a gap#(delay
ossification in the callus)
Late 1: 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)
Late1: 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 1: DELAYED UNION
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 Cessation of osteogenesis No suggestion of new bone formation
Non-unionX- rayA – Atrophic non- unionB – Hypertrophic non- union
A B
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
Factors:- failure to reduce the fracture failure to hold the reduction while healing
proceed gradual collapse of comminuted / osteoporotic
bone
fragments that are joined in an unsatisfactory position
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 possibleapposition 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 timeRotational deformity will not
In lower limb shortening
Shortening less than 2 cm: compensated by shoe raise
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)
No clinical 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
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