Introductory course

Orthopaedics and
Traumatology
 The human skeleton contains
206 bones, 360 joints, 640
muscles
 Long bones, flat bones

 Long bones have two epiphysis,

one diaphysis and two
metaphysis with two growth
plates during childhood
 Orthopaedics and
Traumatology
 The term Orthopaedics is derived from the Greek words
orthos ("correct", "straight") and paidion ("child")
 Orthopaedics deals with chronic diseases of the ostheo-
articulary system : deformities, arthrosis, infections,
tumors, etc.
 Traumatology deals with acute diseases of the osteo-
articulary system: fractures, sprains, dislocations and
contusions.
Functions of the skeleton :
 Esthetic

 Mecanical and locomotion: protect soft structures

(heart, lungs, brain), mobility and the sense of hearing
 Hematopoetic: bone marrow

 Metabolic

 Systemic depository for Ca and PO4, growth factors

 Regulates systemic pH by absorbing or eliberating
alkaline salts
 Detoxifying by absorbing heavy metals
General notions about fractures:

 Definition: A traumatic disease of the bone

caracterised by interruption of bone continuity that has
a general impact over the entire body.
Classification:

I. Clasification by bone quality:

1. fractures of normal, healthy bone
2. fractures of pathological bone (tumors, infections,
severe ostheoporosis, genetic diseases, Lobstein diesease
= „glass bones disease”)
Classification:

II. Clasification by bone type: long or flat bones.

 Long bones
 Depending on localisation: metaphyseal,
epiphyseal and diaphyseal fractures.
 Epiphyseal fractures can be articular,
extraarticular or partially articular fractures
 Diaphyseal fractures can have transverse,
oblique, short, long lines of fractures, be
simple or cominutive
Classification:

III. Classification by fracture mechanism

1. Direct mechanism -> the line of fracture occurs at the
site of impact.
2. Indirect mechanism -> the line of fracture occurs at a
distance from the site of trauma, by bending, torsion or
compression-type effect on the bone.
Classification:

•IV. Classification by communication with the outside

environment
1. Closed fractures
2. Open fractures : the fracture communicates with the
outside environment.
General notions about fractures:

 Clinical impact of a fracture:

 Light fever
 Acrocyanosis
 Sweating
 Signs of shock
 Anxiety
 General notions about fractures:
 Certain local signs of fracture:

1. Abnormal bone mobility at the site of

fracture suspicion
2. Lack of motion from the
proximal to distal segments of bone, or
viceversa.
3. Clear, palpable bone interruption
4. Bone crepitations
General notions about fractures:
 Probability local signs of fracture:
1. Pain in a fixed point
2. Functional loss
3. Late echimosis
4. Blisters
5. Regional or segmental deformity (due to
hematoma, bone fragment displacement)
6. Shortening of the affected segment
General notions about fractures:

 Paraclinical investigations:
• RX = anterior-posterior and lateral views =
golden standard!!!
• CT
• MRI
• Ecography
• Artrography
General notions about fractures:

 Anatomy of a fractured bone site:

 Associated injuries:
 Always: Bone lesions, periostal lesions
 Possible/probable: muscles, tendons, fascia, nerve,
blood vessels, skin.
Complications:

• General :
• Venous ThromboEmbolism (VTE requires
prophylaxy!)
• Pulmonary Thromboembolism (fatal)
• Fatty embolism
• Shock
• Decompensation of any chronic dieseases
Complications:

• Local :
 Immediate:
- Open of fracture site
- Blood vessel injury
- Nervous injury (neuropraxis, axonotmesis,
neurotmesis)
• Associated lesions (dislocation, articular fractures)
Complications:

• Late: - Pseudarthrosis (non-union)

- Delay of bone fusion
- Algoneurodistrophy
- Vicious callus (hypertrophic, malalignment of
bone fragments, etc.)
- Vicious scarring
- Joint stiffness
- Arthrosis in articular fractures
Phases of bone consolidation = callus
formation

1. Inflamatory phase

2. Bone repair = fibrous callus, primitive bony

callus
3. Bone remodelation
1. Inflamatory phase (24-72h)

 The primary hematoma is produced by associated

tisuary lesionse
 Local blood vessels become thrombosed and thus
produce necrosis on the bony edge of the fracture
 Increase of capilary permeability produces a local
inflamatory web
 Osteoinductive growth factors stimulate the
proliferation and differentiation of mesenchimal stem
cells
2. Bone repair

 Periosteal callus is formed along the

fracture site periphery by
intramembraneous ossification
 Intramedulary callus is formed in the
center of fracture site, by endochondral
ossification in the primary hematoma
 Chemical and physical factors stimulate
callus formation and mineralization
3. Bone remodelation

 Non-lamelary tissue is gradually transformed into

lamelary tissue
 The medullar cavity is reconstructed.
 The bone is reconstructed as a resonse load bearing
and tension (according toWolff's Law)
3. Bone remodelation
 Callus formation
Necessary conditions

A.Adequated blood supply

B. The fracture site eliberates growth factors that
stimulate angiogenesis and determine local
vasodilatation
C. The bloodflow to the fracture is substantially
increased in a maximum of two weeks after the
fracture
Bone vascularisation

Long bones have 3 vasculary

supplies:

1. The nutritive artery

(intramedular) Perisotheal
vessels
2. Periostheal vessels

3. Metaphyseal vessels Nutritive artery

Metaphyseal
vessels
 Bone vascularisation

 The nutritive artery

– The majority of diaphyseal cortical vascularisation (80-85%)

– Enters the bone through a single site (nutritive foramen)

– It forms intramedulary arteries proximal and distal of the

nutritive foramen
 Bone vascularisation
 Periostheal arteries

– Emerge from a rich network of periostheal capilaries

– Supply 15-20% of cortical vascularization

– They are capable to assume a greater percent of cortical

vascularisation in case of normal intramedulary
vascularisation damage

 Metaphyseal vessels

– Emerge from the periarticular vascularisation

– They enter the bone through the thin cortical present in the
metaphyseal region and form an anasthomosis with the
intramedular vascular network
 Mechanisms of bone healing

A. Direct bone healing (primary)

B. Indirect bone healing (secundary)

 A. Direct bone healing (primary)

 Is produced when there is no motion at the fracture site

 Does not imply the formation of callus

 A cutting cone is formed that tranverses the fracture site

 The osteoblasts excrete lamelar bone behind the

osteoclasts, thus forming secondary bone
 The fracture gradually heals by the forming of several
secondary osteons
 A process that takes time: months or years
 The components of direct healing

 Contact healing

 Direct contact of the fractured bone segments forms

lamelar bone tissue.

 Healing by diastasis

 A diastasis smaller than 200-500 microns is filled by

non lamelar bone tissue that is subsequently molded
into lamelar bone tissue
 A bigger diastasis in indirectly healed - > it is partially
filled with fibrous tissue that is subsequently ossified
Direct bone healing
 B. Indirect bone healing
 Healing mechanish for
fractures that are not
rigidly fixed
 Soft periostheal callus that
acts as a bridge and hard
medular callus reestablish
bone continuity
 The callus thus formed in
followed by an endostheal
ossification
 Relatively fast process –
takes weeks
Umoral factors that regulate the bone
healing process

1. Growth factors
2. Cytokines
3. Prostaglandines/Leucotrienes
4. Hormones
Anatomical factors that influence bone
healing

 The interposition of soft tissue between bone

fracture fragment.
 Bone necrosis caused by irradiation, thermic or
chemic pain or infection
Anatomical factors that influence bone
healing

 Soft tissue damage

 The degree of local

vascularisation
damage
 Sistemic factors that affect bone
healing

 Malnutrition
 Diminishes osteocondral cells activity and proliferation

 Inhibits callus formation

 Smoking
 Inhibits the osteoblasts

 Nicotine determines vasoconstriction that restricts local

bloodflow to the fracture site
 Sistemic factors that affect bone
healing

 Diabetes

– Associated with collagen defects, organic matrix decrease,

inefficient fibrilar connections and collagen subtypes
proportions alterations
 Fracture treatment

 Regardless of fracture particularities, the treatment of a

fracture implies three main steps:
1. Reduction of the fracture
2. Maintaining of the reduction
3. Functional rehabilitation
 Fracture treatment

I. Orthopaedic treatment: treatment without scalpel.

1. Closed reduction
2. Plaster or continuous extenstion for immobilisation
3. Rehabilitation
 Fracture treatment

II. Surgical treatment:

1. Closed or open reduction

2. Biomecanical ostheosynhesis: the ostheosynthesis
device takes all the load for which the fragmented bone
segment was responsible and maintains the bone
fragments in their place.
3. Immediate start of rehabilitation is possible.
Open fractures

Classification -> Gustilo-Anderson Classification.

This takes into consideration:

- the amount of energy
- the extent of soft-tissue injury
- the extent of contamination for determination
of fracture severity.
 Open fractures:

Progression from grade I to IIIC:

 implies a higher degree of energy involved in the
injury,
 higher soft tissue and bone damage
 higher potential for complications.
 Important to recognize that grade 3C fracture implies
vascular injury as well!
Gustilo-Anderson Classification
I. Low energy, wound less than 1 cm

II. Open fracture, wound > 1 cm but < 10 cm in length without

extensive soft-tissue damage, flaps, avulsions
III. Open fracture with extensive soft-tissue laceration (>10 cm),
damage, or loss or an open segmental fracture.
IIIA Type III fracture with adequate periosteal coverage of the
fracture bone despite the extensive soft-tissue laceration or
damage

IIIB Type III fracture with extensive soft-tissue loss and

periosteal stripping and bone damage. Usually associated
with massive contamination.

IIIC Type III fracture associated with an arterial injury requiring

repair, irrespective of degree of soft-tissue injury.
Open fractures:

Classification -> Cauchoix and Duparc :

Type 1: punctiform opening, usually produced from

the inside to the outside

Type 2: a several centimeters opening, through

witch you can see the bone. Produced from the
outside -> inside and is always contaminated

Type 3: big opening, lack of skin, foreign bodies

present in the wound, bare bone fragment.
Maximum risk of infection
Conclusion
 Treatment of open fracture:

 Transform it in a closed fracture!!!

 In first 6 to 12 hours:

 Type 1 and 2: cleaning, debridement, regular

osteosinthesis.
 Type 3: cleaning, debridement, regular and
external fixation.
Conclusion
 Treatment of open fracture:

 Transform it in a closed fracture!!!

 After 6 to 12 hours:

 Type 1, 2 and 3: cleaning, debridement and

external fixation.

 Antibioprophilaxy: shouldn’t be longer than 3-5 days.

 See local protocols.

Conclusion

 Bone healing is influenced by several variables

including mechanical stability, the local environment,
biochemical factors and local vascularisation
Thank you!