General

Principles
of Fractures
Department of Orthopaedic Surgery

Liu Xueyong ( 刘学勇）

Introduction
Definition
A fracture indicates
disruption of the
continuity or
integrity of bone
 Etiology
direct trauma
indirect trauma
by transmission of stress: e.g.
fracture of clavicle
by muscular (quardriceps)
contraction: e.g. fracture of
patella
 continuous stress (fatigue fracture):
e.g. fracture of lower 1/3 fibular
shaft , fracture of the 2nd and 3rd
metatarsal bone
 pathological fracture: because of
cortical desruption which resulted
from bone diseases such as
osteomyelitis and benign, malignant,
or metastatic lesions of bone, the
fracture happened with slight
trauma
Classification
close fracture: the end of fracture
did not communicate with the
environment
open fracture: the end of fracture
communicated with the
environment, e.g. pubic fracture
with bladder or urethra injury,
coccyx fracture with rectal injury
incomplete fracture:
crack(fissure) fracture
and green stick
fracture(in children)
complete fracture
 Complete fracture
 transverse fracture
 oblique fracture
 spiral fracture
 comminuted fracture: T or Y type or
butterfly
 impacted fracture
 compression fracture: e.g. vertebral
body or calcaneus fracture
 sunken fracture: skull fracture
 epiphyseal injury
Stable fracture: crack, green
stick , transverse ,
compressive, impacted
fracture
Unstable fracture: easily
displace, e.g. oblique fracture,
spiral fracture,
comminuted fracture
 OTA classification of
long bone fractures
 Taylor and Martin proposed a
classification of metaphyseal
fractures (SUD) in which the main
fracture is characterized as stable
(S), unstable (U), or with diaphyseal
extension (D). These are further
divided into three subtypes: 0,
extraarticular; 1, less than 2 mm of
displacement; and 2, more than 2
mm of displacement
Classification
of
metaphyseal
fractures
(SUD)
Displacement of fracture
 angular displacement
 lateral displacement
 shortening displacement
  separated displacement
  rotational displacement
Clinical findings
and Radiological
findings
Systemic features
Shock: resulting from loss of
blood in patients with pelvic,
femoral or multiple fracture ,
severe open fracture or fracture
complicating with vital viscreal
injury
Fever: resulting from absorption
of hematoma, usually <38º
loss
of
blood
(ml)
Local features
Specific signs:
   Deformity
   Abnormal motion
Bony crepitus or grafting
Unspecific signs
 pain and tenderness
 swelling and visible
bruising (ecchymosis)
 dysfunction
Radiological findings
A-P and lateral view X-ray
including upper or low joint
X-ray findings: fracture line
If necessary, radiological
examination is performned
again after 2 weeks
Some special views
AP and oblique view for
fractures of metacarpus and
metatarsus
 lateral and axial view for
calcaneus fracture
AP and butterfly view for
fractures of scaphoid
Complications of
fracture
 Early period
  shock
 visceral injury such as liver, spleen,
lung, bladder and urethra, rectum
injury
 vital tissues injury such as arteries,
spinal cord, peripheral nerves
 fat embolism syndrome(FES)
 Compartment syndrome
Fat embolism syndrome(FES)

FES is the unexpected

occurrence of hypoxia,
confusion, and patechiae a few
days after long bone fractures
 The etiology of FES
 The broken bones liberate marrow fat that
embolizes to the lungs and brain in which fat
droplets enter the venous circulation via torn
veins adjacent to the fracture site
 The biochemical theory suggests that mediators
from the fracture site alter lipid solubility
causing coalescence, since normal chylomicrons
are less than 1 μm in diameter
 Elevated serum lipase levels hydrolyzes neutral
fat to free fatty acids and causes local
endothelial damages in the lungs and other
tissues
Compartment syndrome
Compartment syndrome is a
condition characterized by raised
pressure within a closed space
with a potential to cause
irreversible damage to the
contents of the closed space
 The prerequisites for the
development of a compartment
syndrome include a cause of
raised pressure within a confined
tissue space called osteofascial
compartment which is composed
of bone, deep fascia, interosseous
membrane and intermuscular
septum.
 Any condition that increases the
contents or reduces the volume
of a compartment could be
related to the development of an
acute compartment syndrome.
The most common cause associated with
decrease in the size of the compartment is
the application of a tight cast, constrictive
dressings, or pneumatic antishock
garments. Closure of fascial defects has
been shown to be associated with the
development of an acute compartment
syndrome. This condition most commonly
occurs in anterior compartment of the leg,
in patients who present with symptomatic
muscle hernias.
 A number of conditions have been
shown to increase the compartment
contents and lead to compartment
syndrome.
These involove hemorrage within the
compartment, or to accumulation of
fluid(edema) within the compartment .
The former is most commonly associated
with fractures of the tibia, elbow,
forearm, or femur, whereas the latter is
most commonly associated with
postischemic swelling after arterial
injuries or restoration of arterial flow
after thromosis of a major artery
 The symptom of pain out of proportion
to the known injury and the findings of a
tense, swollen compartment with some
degree of passively induced strench pain
represent the earliest manifestations of
an acute compartment syndrome
 By the time sensory deficits is obvious,
irreversible changes to nerves or muscles
may already have occurred. To wait the
development of frank motor weakness is
to invite diaster. Paresis is a late finding
and, if present, demands immediated
surgical intervention
 The only effective way to
decompress an acute
compartment syndrome is by
surgical fasciotomy.
Late period complication
of fracture
 hypostatic pneumonia
 bedsore
 deep venous thrombosis(DVT) of
lower limbs:
patients with injuries to the pelvis
and lower extremities are especially
prone to DVT
Infection: open fractures
myositis ossificans: the
ossification of soft tissues
adjacent to joints(elbow
commonly)
traumatic arthritis:
common in intraarticular
fractures
joint stiffness:
the most common
avascular necrosis of
bone:common in fractures of
hand scaphoid and femoral neck
ischaemic contracture of muscle:
the consequence of compartment
syndrome, claw hand
acute bone atrophy
(Sudeck atrophy)
the osteoporosis with pain
adjacent to the fracture site,
commonly in fractures of
hand and foot. The pain and
vascular systolic-diastolic
disorders are main features.
Biology of
fracture healing
Hunter and Brighton described
the classic stages of natural bone
repair
1. The impact stage: the interval from the
first application of force to the bone until
the energy of the force is completely
dissipated, resulting in energy absorption
by the bone until fracture occurs.
2. Inflammation stage: lasts 1 to 3 days,
and is evidenced by pain, swelling, and
heat. Inflammatory cells arrive at the
injured site accompanied by vascular
ingrowth and cellular proliferation.
 3.induction stage: begins during the
impact and inflammatory stages and
involves the formation of inducers and
humoral factors that direct the
regeneration of bone.
 4.soft callus stage: corresponds clinically
to the time when clinical union occurs by
fibrous or cartilaginous tissue.
Histologically it is characterized by
vascular ingrowth of capillaries into the
fracture callus and the appearance of
chondroblasts.
5.Hard callus stage: the
fibrocartilaginous union is replaced by
fibroosseous union. Clinically this
usually occurs at 3 to 4 months
6. Stage of remodeling begins with
clinical and roentgenographic union
and persists until the bone is returned
to normal, including restoration of the
medullary canal. Histologically the
fibrous bone is replaced with lamellar
one.
Two groups of growth-producing
substances at the site of fractures
 Peptide-signaling molecules (growth
factors): bone morphogenetic proteins,
fibroblast growth factors, platelet-derived
growth factor
 Immunomodulatory cytokines: interleukin-
1 and interleukin-6
 These substances are known to be produced
during fracture healing and to participate
in the regulation of the associated responses
In a word, the Process of
fracture Healing
 Organization of haemotoma and
interfragment stabilization by
fibrocartilage differentiation: 2 weeks
 Formation of original callus:restoration
of continuity by intramembranous and
endochondral ossification, 4-8 weeks
 Remodeling of the fracture site
8-12 weeks
The standard of healing
 No tenderness
  No abnormal mobility
  X-ray: continuous callus, fracture
line is opaque
  After removing the external
fixation, rehabilitation of function,
and no deformity within 2 weeks
Delayed union
Depending on the individual
bone,its vascularity, and its
biochemical environment,
fracture healing occurs in 2 to 6
months. failure of a fracture to
heal in the usual time is called
delayed union
Nonunion
Failure to heal 2 to 6 months, with
arrest of healing process demonstrated
by radiographically persistent fracture
lines, sclerosis at the fracture ends, a gap,
and hypertrophic or no callus, constitutes
nonunion. Clinically, there may be
motion, pain, tenderness, and thickening,
or deformity at fracture site
Factors influencing
fracture healing
The systmic and local factors
 1.   age
 2.   health status
 3.   the types and quantity of
fractures
 4.   blood supply
 5.   the degree of soft tissue injury
 6.   interposition of soft tissue
 7.   infetion
Iatrogenic factors

1.  imperfect reduction
2.  inadequate immoilisation
3.  excessive traction
4.  surgical interference
5. inappropriate rehabilitation
Uhthoff proposed a more
detailed classification
It emphasizes factors under the
physician’s control .His system
divides by the injury, depend
on treatment, or are associated
with complications
Systemic factors
 A. Age
 B. Activity level including
1.General immobilization
2.Space flight
 C. Nutritional status
 D. Hormonal factors
1.Growth hormone
2.Corticosteroids (microvascular avascular
necrosis [AVN])
3.Others (thyroid, estrogen, androgen,
calcitonin, parathyroid hormone [PTH],
prostaglandins)
 E.Diseases: diabetes, anemia,
neuropathies,
 F.Vitamin deficiencies: A, C, D, K
 G.Drugs: nonsteroidal antiinflammatory
drugs (NSAIDs), anticoagulants, factor
XIII, calcium channel blockers
 H.Other substances (nicotine, alcohol)
 I.Hyperoxia
 J.Systemic growth factors
 K.Environmental temperature
 L.Central nervous system trauma
Local factors
A. Factors independent of injury,
treatment, or complications
 1.Type of bone
 2.Abnormal bone
a.Radiation necrosis
b.Infection
c.Tumors and other pathological
conditions
 3.Denervation
B.Factors depending on injury
 1.Degree of local damage
a.Compound fracture
b.Comminution of fracture
c.Velocity of injury
d.Low circulatory levels of
vitamin K1
 2.Extent of disruption of vascular
supply to bone, its fragments
(macrovascular AVN), or soft
tissues; severity of injury
 3.Type and location of fracture (one
or two bones, e.g., tibia and fibula or
tibia alone)
 4.Loss of bone
 5.Soft tissue interposition
 6.Local growth factors
C.Factors depending on
treatment
 1.Extent of surgical trauma (blood supply,
heat)
 2.Implant-induced altered blood flow
 3.Degree and kind of rigidity of internal or
external fixation and the influence of timing
 4.Degree, duration, and direction of load-
induced deformation of bone and soft
tissues
 5.Extent of contact between
fragments (gap, displacement,
overdistraction)
 6.Factors stimulating posttraumatic
osteogenesis (bone grafts, bone
morphogenetic protein [BMP],
electrical stimulation,
surgical technique, intermittent
venous stasis)
D.Factors associated
with complications
1.Infection
2.Venous stasis
3.Metal allergy
Treatment of
fracture
Our goal is to
conserve as much
functional
potential of the
injured extremity
as possible
 Priciples of fracture
treatment
Reduction
Immobilization
Rehabilitation
 Reduction
Manipulation
Traction
Open reduction

anatomical reduction &

functional reduction
The criteria of
functional reduction
 1) Alignment of the axis of the bone
should be corrected in
anteroposterior and mediolateral
planes
 2) Length correction is difficult
when bone is lost, and up to 1 cm of
shortening or lengthening is well
tolerated if it does not compromise
fracture regeneration biology
 3) Rotation of the axis of the bone should
be corrected to be as close as possible to
that of the normal opposite extremity.
Malrotation is better tolerated in the
upper extremity than in the lower
extremity .External malrotation seems
better tolerated than internal malrotation
in the lower extremity. 5 to 10 degrees of
angulatory deformation and 10 to 15
degrees of rotary deformity may be
functionally tolerated.
 Immobilization
 splint
 casting
 Traction (skin, skeletal)
 external fixation
 internal fixation (pin and wire
fixation, screw fixation, plate and
screw fixation, intramedullary nail
fixation)
The indications of open
reduction and internal fixation
 1) Major avulsion fractures associated
with disruption of important
musculotendinous units or ligamentous
groups that have been shown to have a
poor result with nonoperative treatment
 2) Multiple fracture
 3) Displaced intraarticular fractures
suitable for surgical reduction and
stabilization
 4) Unstable fractures in which an
appropriate trial of nonoperative
management has failed
 5) Fractures associated with vascular or
neurological deficits that require surgical
repair, including long bone fractures in
patients with spinal cord, conus, or
proximal nerve root lesions
 6) Fractures for which nonoperative
treatment is known to yield poor
functional results, such as femoral neck
fractures, Galeazzi racture-dislocations,
and Monteggia fracture-dislocations
Disadvantages of surgical
reduction and stabilization
 1)Operative treatment adds further trauma
to any injury
 2) It increases the dangers of infection and
further vascular destruction to the injured
tissues
 3) Any surgical dissection will produce scar
tissue to heal the incision, the dissection in
itself may create complications of
contracture and debilitation of the muscle-
tendon units
 4) The possibility of nerve and vascular
damage is constant
 5)  Surgical treatment also involves the use
of anesthesia and its attendant risks
 6) Blood transfusions carry the risks of
hepatitis, acquired immune deficiency
syndrome (AIDS), and immunological
reactions etc
 7) Implants or external fixation systems
frequently require removal, with the
attendant risks of a second operative
procedure. Refractures have been
reported after implant and external
fixation removal.
 External fixation
External fixation with hybrid fixators and frames
Screw fixation of articular fragment
combined with external fixation.
Internal fixation
Examples of screws for fracture fixation:
cancellous and cortical, lag, pretapped
and self-tapping
Lag screw technique

A, To determine best location and inclination, forceps temporarily compress

fracture. B, Lag screw replaces forceps in location and position (inclination).
C, Lag screw is best positioned at right angle to fracture plane. Use of
bisecting angle is correct only for osteotomies with less than 40 degrees of
inclination. If inclination is, for example, 60 degrees, osteotomy will be
displaced because of insufficient inclination of lag screw.
Dynamic
and static
locking of
intramedullary
nail
 Intraarticular epiphyseal and metaphyseal
fractures reconstructed with lag screws

A, Cancellous screw (6.4 mm) for posterior lip ankle fracture. B, Two 4-mm
partially threaded small fragment cancellous bone screws used for medial
malleolar fracture. C, Two 4-mm partially threaded small fragment cancellous
bone screws used for type A fracture of medial malleolus. D, Two 4-mm
partially threaded small fragment cancellous bone screws used for lag screw
fixation of epiphysis and fixation of condyle to metaphysis of distal humerus.
Plate is
acting as
protection
plate and
compression
plate
Open fractures
Open
fractures are
surgical
emergencies
 Open fractures are surgical
emergencies
 Surgery should be begun as soon as
the patient’s general condition will
permit it
 With the passage of time the
probability of infection rapidly
increases. A contaminated wound
usually is considered to be infected
after 12 hours
 The care of the
open fracture
 1.Treat all open fractures as an
emergency
 2.Perform a thorough initial evaluation
to diagnose other life-threatening injuries
 3.Begin appropriate antibiotic therapy in
the emergency room or (at the latest) in
the operating room and continue the
therapy for 2 or 3 days only
 4.Immediately debride the wound
using copious irrigation and, for
types II and III fractures, repeat the
debridement in 24 to 72 hours

Debridement is a term that cover

the following procedure: exploration
of the wound, excision of devitalized
tissue, and removal of foreign
material
Assessment of viability of
damaged muscle
Color, consistency, and the capacity of the
muscle to bleed can be used as guidelines and
will assist in determining viability
Muscle that is a normal, beefy-red color
usually is viable. Viable muscle usually is firm
in consistency, usually will contract when
incised with a scalpel or touched with
eletrocautery, and will demonstrate its
vascularity by punctate bleeding from the cut
edges
5.Stabilize the fracture
6.Leave the wound open for 5 to
7 days
7.Perform early autogenous
cancellous bone grafting
8.Rehabilitate the involved
extremity