2. Diaphysis
Shaft of a long bone
Epiphysis
Ends of the bone
Metaphysis
Area between the diaphysis and epiphyses
Hyaline cartilage
Found at the ends of the bone
Periostium
Membrane covering the bone
Marrow cavity
Space in the diaphysis
Endosteum
Lining of the medullary cavity
6. Primary fracture healing
Involves direct attempt by the cortex to reestablish
itself
Occurs only with anatomic reduction & rigid
fixation
Gaps in reduction heal by vessel ingrowth-
mesenchymal cells- osteoblasts-osteoclast cutting
cones
Direct contact areas heal by cutting cones allowing
passage of vessels
7. Secondary fracture healing
Response of periosteum/ external soft tissues
Recapitulation of embryonic intramembranous
ossification and endochondral bone formation
Intramembraneous= peripheral to fracture
Endochondral= adjacent to fracture
Motion enhances periosteal response
External soft tissue forms bridging calus
(endochondral)
8. Stages of Healing
Hematoma Formation 1-2 Days
Inflammation 2-7 Days
Soft Callus Formation 1-3 Weeks
Hard Callus Formation 3-6 Weeks
Remodelling Phase >8. Weeks
12. Soft Callus ( Fibrous Callus) Formation
Fibrous tissue forms at periphery where blood
supply is abundant
Fibrocartilage forms at center where blood supply
is limited
Increased instability results in increased callus
size
Tissues bridge fracture and decrease
interfragmentary strain
16. Remodelling Phase
Begins in middle of repair phase, continues until fx
clinically healed
Osteoclastic tunneling (cutting cones) in concert with
osteoblast deposition
Can continue up to 7 years
Remodeling based on stresses (Wolff’s law)
Bone formed in response to mechanical load
20. Distraction Osteogenesis
Gradual traction applied to cortical osteotomy
Bone forms under the law of tension stress
Wolff’s Law occurs even with tension
Typically intramembranous ossification
Used in limb lengthening
Treatment of limb deformities
Transportation of cortical bone
21. Conditions that interfere with fracture healing
High energy traumas brings soft tissue problems that
lead non unioun
Poor blood supply to the fractured area; could lead to
avascular or aseptic necrosis
Poor immobilization of fracture site may cause
misalignment, nonunion or deformity
Infection – more common with open fractures
Cortisone= negative effect, decreased callus
formation
25. Local complications
Early
1. Visceral injury (the lung, the bladder, the urethra,
and the rectum).
2. Vascular injury.
3. Nerve injury.
4. Compartment syndrome.
5. Haemoarthrosis.
6. Infection.
7. Gas gangrene.
8. Fracture blisters.
9. Plaster and pressure sores.
28. Shock
Three types of shock may complicate fractures
Hypovolemic or hemorrhagic shock
This type of shock is due to blood loss due to
vascular injury. The vessels may be injured by
the fracture pieces or in open fractures the
vessels are injured by the same cause like in
missile or bullet
29. injury.In hypovolemic shock there will be
reduction in the circulating volume causing
reduction in venous return and cardiac output.
The patient usually; severely pallor, shivering,
rigor, hypotensive and sometimes comatose.
Treatment by 1) control of hemorrhage (may
require surgery).
restoration of circulating volume (fluid and
blood products).
30. Occur in
Large bulk of muscle crushed
Tourniquet left for TOO long
What happened?
1st
theory =Compression releasedacid
myohaematin enter the
circulationkidneyblocks the tubules Renal
failure and death.
32. 1st
rule = Limb crushed severely(>6hrs)
How the amputation done?
Above the compression or crushed injury
Before compression is released
33. CommonestCommonest Complications of Trauma &
Surgery
Most frequently
Calf
Less frequent in proximal of thigh & pelvis
Pulmonary Embolism
From Proximal of thigh & pelvis
Incidence=5% & Fatal = 0.5%
34. The primary cause in surgical
HYPERCOAGULABILITYHYPERCOAGULABILITY of the Blood
due to activation of Factor XFactor X by ThromboplastinThromboplastin from
damaged tissues
Thrombosis occurssecondary factors are
Stasis
Pressure
Prolonged immobility
Endothelial damage
Increase in no & stickiness of platelet
35. Old people
Cardiovascular Disease
Bedridden patient
Patients undergoing hip arthroplasty
36. Pain the calf or thigh
Soft tissue tenderness
Sudden slight increase in temperature
Sudden increase in pulse rate
Homann’s Sign positiveHomann’s Sign positive
38. Difficult to diagnose =only minority have
symptoms (chest pain, dyspnoe, heamoptysis)
So high risk patients should be examine for
pulmonary consolidation
X-ray
Pulmonary angiography
39. Prophylactic treatment
Foot elevation
Graduated compression stockings
Exercise
Anticoagulant treatment
Subcut low dose heparin 5000 units preops & 3/7
postops (but CI in older patientbleeding)
Change to low molecular weight heparin (less likely to
cause bleeding)
40. Localized DVT
Elastic stockings
Low dose subcut heparin (5000 unit)
More extensive DVT
Bed rest
Elastic stockings
Full anticoagulation
Heparin IV (10000 units 6 hourly)
Continue for 5-7/7 with last 2/7 warfarin introduce
42. What is Tetanus?
Tetanus organism live only in dead tissueexotoxin
blood & lymph to CNS anterior horn cell
Will develop
Tonic clonic contraction
Jaw and face (trismus and risus sardonicus)
Neck and trunk
Diaphragm and Intercostal muscle spasmASPHYXIA
43. Active immunization (tetanus toxoid)
Booster doses (immunized patients)
Non Immunized patients
Wound toilet & antibiotics
If wound contaminated antitoxin
44. IV antitoxin
Heavy Sedation
Muscle Relaxant drug
Tracheal Intubation
Controlled respiration
45. By clostridial infection (esp C.welchii)
Anaerobic with low oxygen tension
Produce toxinsdestroy cell walltissue
necrosis Spreading
46. Within 24 hours
Intense pain
Swelling
Brownish discharge
Pulse rate increased
Charasteristis smell
Little or no pyrexia
Gas formation not marked
ToxaemiccomaDEATH
47. Deep penetrating wound should be
EXPLORED
ALL dead tissue completely EXCISED
Doubt about tissue viabilityleft it OPEN
No antitoxin
48. The key = EARLY DIAGNOSIS
General measures (fluid, IV antibiotics)
Hyperbaric oxygen (limiting spread)
Decompression of wound
Removal of all dead tissue
Amputation (advanced case)
49. Only minority patients with circulating fat
globules will develop POST TRAUMATIC
RESPIRATORY DYSFUNCTION
Source of fat emboli=bone marrow
Usually in MULTIPLE CLOSED FRACTURE
But other condition also reported (burns, renal
infarction, cardiopulmonary operation)
50. Usually young adults with LL fracture
Early warning signs (72 hrs. of injury)
Rise in temperature and pulse rate
More pronounced case
Breathlessness
Mild mental confusion
Petechia (chest & conjuntival fold)
Most severe case
Marked respiratory distress coma ARDS
51. Mild case
Monitoring of blood PO2
Signs of hypoxia
Oxygen
If severe
Intensive care with sedation and assisted ventilation
Swan ganz Catheterization (monitor cardiac Fx)
Fluid balance
Supportive
Heparin-thromboembolism
Steroids-pulmonary oedema
Aprotinin-prevent aggregation of chylomicrons
52. General Local
Early Late
* Early complication : those that arise during the first few weeks
following injury.
54. Fracture around the trunk are often Cx by injury
to the adjacent viscera :
Pelvic fracture
Rib fracture penetration to the lungs
Pneumothorax
Bladder and urethral
rupture
55. Most commonly – knee, femoral shaft, elbow,
and humerus.
Artery may be cut, torn, compressed or
contused.
Intima may be detached, thrombus block,
artery spasm
Effect ?? ↓↓ bld flow coz Ischemia leads to
tissue death & peripheral gangrene
56. Common vascular injuries may associate with the
following fractures.
1. First rib or clavicle fracture (subclavian artery).
2. Shoulder dislocation (Axillary artery).
3. Humeral supracondylar fracture (brachial artery).
4. Elbow dislocation (Brachial artery).
57. 5. Pelvic fracture (presacral and internal iliac).
6. Femoral supracondylar fracture (Femoral artery).
7. Knee dislocation (Popliteal artery).
8. Proximal tibia (popliteal or its branches).
59. Pt with ischemia may have 5 P’s:
- paraesthesia/numbness
- pain
- pallor
- pulselessness
- paralysis
Investigate if suspect vascular injury :
Angiogram
60. Emergency treatment
All bandages/splints removed
The fracture X-Ray again
Circulation reassessed for next half hour
If no improvement, do vessels exploration
Suture torn vessels, vein grafting, if
thrombosed do endarterectomy
Aim: to restore bld flow
61. Variable degree of motor and sensory loss
along the distribution of the nerve
May be neurapraxia, axonotmesis or
neurotmesis
Radial nerve is most frequently damaged
nerves.
62. NerveNerve TraumaTrauma EffectEffect
AxillaryAxillary Dislocation ofDislocation of
shouldershoulder
Deltoid paralysisDeltoid paralysis
RadialRadial # of humerus# of humerus Wrist dropWrist drop
MedianMedian Supracondylar # ofSupracondylar # of
humerushumerus
Pointing indexPointing index
UlnarUlnar # medial epicondyl# medial epicondyl
humerushumerus
Claw handClaw hand
SciaticSciatic Post dislocation of hipPost dislocation of hip Foot dropFoot drop
CommonCommon
peronealperoneal
Knee dislocation #Knee dislocation #
neck of fibulaneck of fibula
Foot dropFoot drop
63. In closed injuries – nerve is seldom severed and
spontaneous recovery should be awaited.
In open fractures – complete
lesion(neurotmesis) : the nerve is explored
during wound debridement and repaired.
64. Definition
Compartment syndrome involves the compression of
nerves and blood vessels within an enclosed space,
leading to impaired blood flow and nerve damage.
Fascia separate groups of muscles in the arms and legs
from each other. Inside each layer of fascia is a confined
space, called a compartment, that includes the muscle
tissue, nerves, bones and blood vessels.
A rise in pressure within these compartments may
jeopardize the blood supply to the muscles & nerves
within the compartment.
65. Causes:
-any injury/infection leading to edema of muscle
-fracture haematoma within the compartment
-ischemia to the compartment leading to muscle
oedema
-Due to tight bandages or casts
Hallmark Symptoms:
- severe pain that does not respond to elevation
or pain medication.
- In more advanced cases, there may be
decreased sensation, weakness, and paleness
of the skin.
66. Injuries with a high risk of developing
Compartments synd:
# of the elbow
# of the forearm bone
# of the proximal third of the tibia
68. A vicious cycle cont. until the total vascularity
of the muscles and nerves is jeopardized.
This result in ischaemic muscle necrosis and
nerve damage. (within 12 hours)
The necrotic muscle undergo healing with
fibrosis, leading to Volkmann’s contracture.
Nerve damage may result in motor and
sensory loss. In extreme case gangrene
69. clinically:
- should be tested by stretching the
muscles when the toes or fingers are
passively hyperextended there is ↑ pain
in the calf or forearm.
Early preventing : limb elevation
Dx : confirmed by direct intracompartmental
pressure measuring > 40mmHg is an indication
of compartment decompression and
fasciotomy.
71. Treatment
First removed all the bandages & dressing.
Fasciotomy is performed.
The wound should be left open and
inspected 2 days later.
If there is muscle necrosis debridement
If muscle is healthy suture (w/o tension)/
skin grafted / simply heal by 2˚ intention.
74. Fractures involve joints, leads to acc. of blood
within the joints.
C/Feature :The joint is swollen and tense and
patient will resists any movement.
Tx : the blood should be aspirated before
dealing with the fracture.
75. Causes:
Open fracture (common)
Use of operative method in the Tx of #
Wound becomes inflamed and starts draining
seropurulent fluid.
Infection may be superficial, moderate
(osteomyelitis), severe (gas gangrene).
Post-traumatic wound infx is most common
cause of chronic osteomyelitis union will be
slow and ↑ chance of refracturing.
76. Treatment:
Antibiotic
Excising all devitalised tissue
If Sx of acute infx and pus formation : tissue
around the fracture should be opened &
drained
77. Produced by anaerobic orgs : Clostridium sp infections.
These orgs can survive in ↓ O2 tension
Toxins produced will destroy the cell wall and leads to
tissue necrosis
C/feature: within 24hr. Pt complains:
- intense pain
- swelling around the wound
- brownish discharge
- gas formation
- pyrexia
- characteristic smelling
- PR ↑
- toxaemic coma death
Inability to recognize may lead to unnecessary amputation
for the non-lethal cellulitis.
78.
swelling around the wound,swelling around the wound,
brownish dischargebrownish discharge
gas formationgas formation
79. Prevention:
deep penetrating wound in muscular tissue are
dangerous;should be explored, all dead tissue
should be completely excised, and if there doubt
about the tissue viability should left open the
wound
Treatment:
Early Dx is life saving
General measures:
Fluid replacement & IV Antibiotic (immediate)
Hyperbaric O2(limiting the spread of gangrene)
Mainstay : prompt decompression & remove
dead tissue
83. Clinical featuresClinical features
Fracture tenderness
(Esp when subjected to stress)
X-RayX-Ray
Visible fracture line
Very little callus formation or
periosteal reaction
85. TreatmentTreatment
ConservativeConservative
- To eliminate any possible cause
- Immobilization
- Exercise
OperativeOperative
- Indication :
Union is delayed > 6 mths
No signs of callus formation
- Internal fixation & bone grafting
86. Condition when the fracture will never unite w/o
intervention
Healing has stopped.
Fracture gap is filled by fibrous tissue
(pseudoarthrosis)
CausesCauses
Improper Tx of delayed union
Too large a gap
Interposition of periosteum, muscle or cartilage between
the fragments
87. Clinical featuresClinical features
Painless movement at the fracture site
X-RayX-Ray
Fracture is clearly visible
Fracture ends are rounded, smooth and sclerotic
Atrophic non-unionAtrophic non-union : - Bone looks inactive
(Bone ends are often tapered / rounded)
- Relatively avascular
Hypertrophic non-unionHypertrophic non-union : - Excessive bone formation
` - on the side of the gap
- Unable to bridge the gap
89. TreatmentTreatment
Ununited scaphoid fracture → asymptomatic
Hypertrophic non-union (Esp long bone)
→ Rigid fixation (internal / external)
sometimes need bone grafting
Atrophic non-union
→ Fixation & bone grafting
90. Condition when the fragments join in an
unsatisfactory position (unaccepted angulation,
rotation or shortening)
CausesCauses
Failure to reduce a fracture adequately
Failure to hold reduction while healing proceeds
Gradual collapse of comminuted or osteoporotic bone.
91. Clinical featuresClinical features
Deformity & shortening of the limb
Limitation of movements
TreatmentTreatment
Angulation in a long bone (> 15 degrees)
→ Osteotomy & internal fixation
Marked rotational deformity
→ Osteotomy & internal fixation
Shortening (> 3cm) in 1 of the lower limbs
→ A raised boot OR
Bone operation
92.
93. Common complication of fracture Tx following
immobilization
Common siteCommon site : knee, elbow, shoulder,
small joints of the hand
CausesCauses
Oedema & fibrosis of the capsule, ligaments, muscle
around the joint
Adhesion of the soft tissue to each other or to the
underlying bone (intra & peri-articular adhesions)
Synovial adhesions d/t haemarthrosis
94. TreatmentTreatment
Prevention :Prevention :
- Exercise
- If joint has to be splinted → Make sure in correct position
Joint stiffness has occurred:Joint stiffness has occurred:
- Prolonged physiotherapy
- Intra-articular adhesions
→ Gentle manipulation under anaesthesia
followed by continuous passive motion
- Adherent or contracted tissues
→ Released by operation
95. Heterotopic ossification in the muscles after an
injury
Usually occurs in
Dislocation of the elbow
A blow to the brachialis / deltoid / quadriceps
CausesCauses
(thought to be due to) muscle damage
w/o a local injury (unconscious / paraplegic patient)
96. Clinical featuresClinical features
Pain, soft tissue tenderness
Local swelling
Joint stiffness
Limitation of movements
Extreme cases: - Bone bridges the joint
- Complete loss of movement
(extra-articular ankylosis)
X-RayX-Ray
Normal
Fluffy calcification in the soft tissue
97. TreatmentTreatment
Early stage : Joint should be rested
Then : Gentle active movements
When the condition has stabilized :
Excision of the bony mass
Anti-inflammatory drugs may ↓ joint stiffness
98. Circumscribed bone
necrosis
CausesCauses
Interruption of the arterial
blood flow
Slowing of the venous
outflow leading to
inadequate perfusion
Common siteCommon site ::
Femoral headFemoral head
Femoral condyls
Humeral head
Capitulum of humerus
ScaphoidScaphoid (proximal part)
TalusTalus (body)
Lunate
100. Clinical featuresClinical features
Joint pain, stiffness, swelling
Restricted movement
X-RayX-Ray
↑ bone density
Subarticular fracturing
Bone deformity
101.
102. TreatmentTreatment
Avoid weight bearing on the necrotic bone
Revascularisation (using vascularised bone grafts)
Excision of the avascular segment
Replacement by prostheses
103. Previosly known as Sudeck’s atrophy
Post-traumatic reflex sympathetic dystrophy
Usually seen in the foot / hand
(after relatively trivial injury)
Clinical featuresClinical features
Continuous, burning pain
Early stage : Local swelling, redness, warmth
Later : Atrophy of the skin, muscles
Movement are grossly restricted
104. X-RayX-Ray
Patchy rarefaction of the bones (patchy osteoporosis)
OsteoporosisOsteoporosis AlgodystrophyAlgodystrophy
106. Post-traumatic OAPost-traumatic OA
Joint fracture wt severely damaged articular cartilage
Within period of months
22OO
OAOA
Cartilage heals
Irregular joint surface may caused localized stress → 2O
OA
Years after joint injury
These require Emergency Treatment…………chest tube insertion
Most common artery injury is popliteal art
Knee – poppliteal artery, femoral art, brachial art…….cut, torn – by initial inj or jagged by bone fragments
In this operation, the fracture can be fixed internally at the same time
Radial N – Humerus fracture
Neurapraxia-minimal damage, axonotmesis- axon damage but sheath intact, neurotmesis- complete damage
About 90% cases recover within 4 months
If blood supply is impaired more than 12 hours, coz necrosis of the muscles and nerves within the compartments. Nerve is still capable of regeneration but muscles once infarcted, can never recover n will be replaced by inelastic fibrous tissue.(volkmann’s contracture)
This results in further swelling, a further increase in pressure, and a further reduction in capillary blood flow. Necrosis develops within about 12 hours - nerve function may be recoverable in time but infarcted muscle is damaged permanently. Eventually, the dead muscle fibroses and shortens, and an ischaemic contracture results.
As ischemic muscles is sensitive to stretch,
Different pressure btwn diastolic pressure and compartment pressure
Within 6 hour in total ischema…muscles necrosis
Fasciotomy :do a long incision to the fascia to release the pressure
un
All open fracture shud be regarded as potentially infecte
C.perfringens, welchii
Cth dead muscle, dirty wound, inadequate debridement
Once experienced this will never be forgotten