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Fracture healing and wound healing Dr shermil sayd KMCT dental college

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Page 1: Fracture healing and wound healing

Fracture healing and wound healing

Dr shermil saydKMCT dental college

Page 2: Fracture healing and wound healing

Types of Bone

• Lamellar Bone• Woven Bone or immature bone (non-lamellar)

Page 3: Fracture healing and wound healing

Fracture

• Fracture is defined as a break in the continuity of bone

• Fracture results in loss of its mechanical stability and also partial destruction of blood supply

• Healing means to make whole or sound again, to cure, leaving a scar behind. But following fracture a scar is not formed, instead a bone has formed a new at the original fracture site. So rather than bone healing the appropriate nomenclature would be BONE REGENERATION

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TYPES OF FRACTURES(7,8,9)

• ON BASIS OF ETIOLOGY - Traumatic fracture - pathologic fractures due to some diseases - stress fracture• ON BASIS OF DISPLACEMenT - undisplaced - displaced translation ( shift ) angulation ( tilt ) rotation ( twist )

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• ON BASIS OF RELATIONSHIP WITH EXTERNAL ENVIRONMENT

- simple / closed fracture - open fracture• ON BASIS OF PATTERN - transverse - oblique - spiral - comminuted - segmental

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HEALING AFTER FRACTURE FIXATION

• DIRECT/PRIMARY:

• Mechanism of bone healing seen when there is no

motion at the fracture site (i.e. rigid internal fixation).

• Does not involve formation of fracture callus.

• Osteoblasts originate from endothelial and

perivascular cells.

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• INDIRECT/SECONDARY:

• Mechanism for healing in fractures that are not rigidly

fixed.

• Bridging periosteal (soft) callus and medullary (hard)

callus re-establish structural continuity.

• Callus subsequently undergoes endochondral

ossification.

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TYPES OF BONE HEALING

• PRIMARY

1. CONTACT HEALING: When there is direct contact between the

cortical bone ends, lamellar bone forms directly across the fracture

line , parallel to long axis of the bone, by direct extension of

osteons.

2. GAP HEALING: Osteoblasts differentiate and start depositing

osteoids on the exposed surfaces of fragment ends, mostly without

a preceding osteoclastic resorption which is later converted into the

lamellar bone

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• SECONDARY:

It is usual type consisting of formation of callus

either of cartilaginous or fibrous. This callus is

later replaced by lamellar bone. It is comparable

to healing of soft tissue by filling of gaps with

vascular granulation tissue

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MECHANISM OF BONE FORMATION

1. Cutting Cones 2. Intramembranous Bone Formation3. Endochondral Bone Formation

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CUTTING CONES

• Primarily a mechanism

to remodel bone.

• Osteoclasts at the front

of the cutting cone

remove bone.

• Trailing osteoblasts lay

down new bone

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INTRAMEMBRANOUS BONE FORMATION(PERIOSTEAL)

• Mechanism by which a long bone grows in width.

• Osteoblasts differentiate directly from pre osteoblasts and lay down seams of osteoid.

• Does NOT involve cartilage

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ENDOCHONDRAL BONE FORMATION

• Mechanism by which a long bone grows in length.

• Osteoblasts line a cartilage precursor.

• The chondrocytes hypertrophy, degenerate and calcify (area of low oxygen tension).

• Vascular invasion of the cartilage occurs followed by ossification (increasing oxygen tension).

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STAGES OF FRACTURE HEALING

• There are 3 major phases with sub divisions:

• A. Reactive Phase:– i. Fracture and inflammatory phase.– ii. Stage of hematoma formation.– iii. Granulation tissue formation.

• B. Reparative Phase:– iv. Cartilage Callus formation.– v. Lamellar bone deposition.

• C. Remodeling Phase:– vi. Remodeling to original bone contour.

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Components of Bone Formation

• Cortex

• Periosteum

• Bone marrow

• Soft tissue

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A.REACTIVE PHASE

• I .Fracture & inflammatory

phase :After fracture the first change

seen by light and electron microscopy is the presence of blood cells within the tissues

which are adjacent to the injury site. Soon after fracture,

the blood vessels constrict, stopping any further bleeding

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• ii. Stage of Hematoma formation:

Within a few hours after fracture, the extravascular blood cells form a blood clot, known as a hematoma. All of the cells within the blood clot degenerate and die.

The fracture hematoma immobilizes & splints the fracture.

The fracture haematoma provides a fibrin scaffold that facilitates migration of repair cells.

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iii. Granulation Tissue Formation:Within this same area, the fibroblasts survive and replicate. They form a loose aggregate of cells, interspersed with small blood vessels, known as granulation tissue which grows forward, outside and inside the bone to bridge the fracture.They are stimulated by vasoactive mediators like serotonin and histamine

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B. REPARATIVE PHASE• iv. Cartilage Callus formation :

Days after the # the periosteal cells proximal to the fracture gap and fibroblasts develop into chondroblasts which form hyaline cartilage.

The periosteal cells distal to the fracture gap develop into osteoblasts which form woven bone. These 2 tissues unite with their counterparts and culminate into new mass of heterogenous tissue called Fracture Callus restoring some of its original strength.

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• v. Lamellar bone deposition:

Or consolidation ..where hyaline cartilage and woven bone is replaced by lamellar bone. This process is called Endochondral ossification.

At this point, the mineralized matrix is penetrated by channels, each containing a microvessel and numerous osteoblasts.

This new lamellar bone is in the form of trabecular bone which restores bone’s original strength

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C. REMODELLING PHASE• vi. Remodelling to original bone

contour: The remodeling process substitutes the trabecular bone with compact bone. The trabecular bone is first resorbed by osteoclasts, creating a shallow resorption pit known as a "Howship's lacuna". Then osteoblasts deposit compact bone within the resorption pit. Eventually, the fracture callus is remodelled

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STAGES BASED ON REACTION TO TORSIONAL TESTING

• STAGE 1- A healing bone subjected to torsion fails through original # site with a low stiffness pattern.

• STAGE 2- The bone still fails through the # site , but the characteristic indicate high stiffness pattern(hard tissue pattern)

• STAGE 3 – The bone fails partly through the original # site and partly through the previously intact bone with a high stiffness pattern .

• STAGE 4 –Failure does not occur through the # site duplicates the mechanical properties of uninjured tissue

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# HEALING IN CANCELLOUS BONE

1.Cancellous bone heals by -

“CREEPING SUBSTITUTION” New blood vessels

can invade the trabeculae of cancellous bone

and bone opposition may take place directly on

to the surface of trabeculum.

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2.Heals at the point of direct contact:

• Cancellous bone certainly can unite very rapidly, but it

unites rapidly only at the points of direct contact.

3.No bridging callus :

Cancellous bone unites only by contact, not by throwing out

callus even when it is cut of due to dense attachment of the

periosteum.

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4.No death of osteocytes: Takes place in the cut edges of divided trabeculae in cancellous

bone. This must be because of the blood supply is good and large surface area of the trabecular spaces combined with relatively thin trabeculae, keep the osteocytes nourished.

5.Has tendency for late collapse :This lack of callus production by cancellous bone explains the

tendency to late collapse which have been distracted. Eg: after reduction of colle’s fracture a hallow cavity is left in the cancellous end of the radius

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FRACTURE HEALING IN CHILDREN

• Compared with the relatively static mature bone of adult, the changing structure and function, both physiological and biomechanical, of immature bones make them susceptible to different patterns of fracture.

• Fracture in children are more common and are more likely to occur after seemingly insignificant trauma. Damage involving specific growth regions such as the physis or epiphyseal ossification center may lead to acute and chronic growth disturbances.

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FRACTURE REPAIR IN CHILDREN

Fracture healing in children follow same pattern of adults but with some peculiarities :

PERIOSTEUM:• In the contrast to adults, the periosteum strips away

easily from the underlying bone in children. Allowing fracture haematoma to dissect along the diaphysis and metaphysis and this is evident in the subsequent amount of new bone formation along the shaft.

• Dense attachment of the periosteum into the zone of ranvier limit subperiosteal hematoma formation to the metaphysic and diaphysis

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REMODELLING IN CHILDREN

• The remodelling phase is the longest phase and in children may continue until skeletal maturation. Remodelling is better in children compared to adult, This is in response to constantly changing stress patterns in children during skeletal growth and development

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FACTORS INFLUENCING BONE HEALING

1. LOCAL FACTORS2. CHEMICAL FACTORS.3. VASCULAR FACTORS.4. SYSTEMIC FACTORS5. ELECTROMAGNETIC FACTORS6. TREATMENT FACTORS

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1.LOCAL FACTORS

A. Type of bone: Cancellous (spongy) bone or cortical bone.B. Degree of Trauma:

Extensive soft tissue injury and comminuted #‘s V/s Mild contusions C. Vascular Injury: Inadequate blood supply impairs healing. Especially vulnerable areas are the femoral head, talus, and scaphoid bones.

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D. Degree of Immobilization: Immobilized for vascular ingrowth and bone healing to occur. Repeated disruptions of repair tissue, especially to areas with marginal blood supply or heavy soft tissue damage, will impair healing.E. Type of Fractures: Intraarticular fractures communicate with synovial fluid, which contains collagenases that retard bone healing Open fractures result in infections Segmental fractures have disrupted blood supply.F.Soft Tissue Interposition: G.others: Bone death caused by radiation, thermal or chemical burns or infection.

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1.MESSENGER 2.GROWTH 3.PERMEABILITYSUBSTANCES FACTORS FACTORS-Serotonin -Transforming GF -Proteases-Prostaglandins -Fibroblast GF - Amines Polypeptides - Platelet derived GF -Histamines -BMP-Thromboxane -Insulin like GF

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2.CHEMICAL FACTORS

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C.LEUKOTRINES-Stimulate osteoblastic bone formation and enhance the capacity of isolated osteoclasts to form resorption pits

• 1.MESSENGER SUBSTANCE:A.CYTOKINES--IL-1,4,6,11, macrophage and granulocyte/macrophage (GM) (CSFs) & (TNF) stimulate bone resorption.-IL-1 ,6 synthesis is decreased by estrogen

B. PROSTAGLANDINS of the E series--Stimulate osteoblastic bone formation and inhibit activity of isolated osteoclasts.

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2.GROWTH FACTORS:

A. Transforming growth factor(TGF):Superfamily of growth factors (~34 members) Act on serine/threonine kinase cell wall receptors Promotes proliferation and differentiation of osteoblasts, osteoclasts and chondrocytes Stimulates both endochondral and intramembranous bone formation and collagen type 2 synthesis.B.Fibroblast growth factors(FGF):Both acidic (FGF-1) and basic (FGF-2) forms Increase proliferation of chondrocytes and osteoblastsEnhance callus formation & stimulates angiogenesis.

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C.Platelet derived growth factor(PDGF):

A dimer, genes PDGF-A and PDGF-BStimulates bone cell growthIncreases type I collagen synthesis by increasing the number of osteoblasts.PDGF-B stimulates bone resorption.

D.Insulin like growth factor(ILGF): Two types, IGF1 &IGF2, out of which IGF1 is produced in liver and stimulated by growth hormone.Stimulates bone collagen & matrix synthesis and replicates osteoblasts . It also inhibits collagen degradation.

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• E.Bone Morphogenic Proteins (BMP):BMP was discovered by Marshall Urist in 1965. They are

Osteoinductive proteins initially isolated from demineralized bone matrix

FUNCTIONS: 1. Induce cell differentiation : BMP 3(osteogenin). 2. Promote endochondral ossification: BMP 2 & 7. 3. Regulate extracellular matrix production :BMP1. 4.Increase fusion rates in Spinal fusions): BMP 2 5.Non unions: BMP 7 as good as bone grafting

These are included in the TGF-β family except BMP 1. Must be applied locally because of rapid systemic clearance .

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3.PERMEABILITY FACTORS:-Protease – Plasmin , Kalikrein, Globulin permeability factor.-Polypeptides –leucotaxime, Bradykinin, Kallidin-Amines – Adrenalin, nor-adrenalin, Histamine

These factors work in ways that :– Increase capillary permeability– Alteration in diffusion mechanism in intracellular matrix– Cellular migration– Proliferation & differentiation– New blood vessel formation– Matrix synthesis– Growth & development

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3.VASCULAR FACTORS

A. Metalloproteinases Degrade cartilage and bones to allow invasion of vessels

B. Angiogenic factors:Vascular-endothelial growth factors mediate neo-

angiogenesis & endothelial-cell specific mitogensC. Angiopoietin (І & ІІ)

Regulate formation of larger vessels and branches.

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4.SYSTEMIC FACTORS

A.Age: Young patients heal rapidly and have a remarkable ability to remodel V/S old .

B.Nutrition: An adequate metabolic stage with sufficient carbohydrates and protein is necessary.

C.Systemic Diseases: And those causing an immunocompromised state will likely delay healing. Illnesses like Marfan’s syndrome and Ehlers-Danlos syndrome cause abnormal musculoskeletal healing

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D.HORMONES:• Estrogen

Stimulates fracture healing through receptor mediated mechanism.

• Thyroid hormonesThyroxine and triiodothyronine stimulate osteoclastic bone resorption.

• Glucocorticoids Inhibit calcium absorption from the gut causing increased PTH and

therefore increased osteoclastic bone resorption. • Parathyroid Hormone• Growth Hormone: Mediated through IGF-1 (Somatomedin-C) Increases callus formation and fracture strength

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5.ELECTROMAGNETIC FACTORS

In vitro bone deformation produces piezoelectric currents and streaming potentials.Electromagnetic (EM) devices are based on Wolff’s Law that bone responds to mechanical stress: Exogenous EM fields may simulate mechanical loading and stimulate bone growth and repair

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6.TREATMENT FACTORS

APPOSITION OF FRACTURE FRAGMENTS.

LOADING AND MICROMOTION . FRACTURE STABILIZATION.

RIGID FIXATION.

BONE GRAFTING.

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RECENT ADVANCES• GROWTH FACTOR THERAPY(3) Due to their ability to stimulate proliferation and differentiation

of mesenchymal and osteoprogenitor cells they have shown great promise for their ability to promote fracture repair .

• APPLICATION OF PLATELET RICH PLASMA(4) Injecting platelet rich plasma at fracture site helps in fracture

healing .

• TISSUE ENGINEERING, STEM CELLS AND GENE THERAPIES(5) In past decade tissue culture and stem cells have been

implicated in enhancing fracture healing and articular cartilage regeneration.

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• Nanotechnology(1)based on understanding cell-implant interactions. Cells

do not interact directly with an implant but instead interact through a layer of proteins that absorb almost instantaneously to the implant after insertion. Scientists have improved numerous implant materials, including titanium and titanium alloys, porous polymers, bone cements and hydroxyapatite, by placing nanoscale features on their surfaces. The bulk materials' properties remain unchanged, maintaining their desirable mechanical properties, but the surface changes enhance the interactions with proteins. This causes bone-forming cells to adhere to the implant and activates them to grow more bone.

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COMPLICATIONS OF FRACTURE HEALING

• MALUNION

• DELAYED UNION

• NONUNION

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MAL UNION

• A MALUNITED Fracture is one that has healed with the fragments in a non anatomical position

• CAUSES 1 INACCURATE REDUCTION2 INEFFECTIVE IMMOBILIZATION

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MALUNION can IMPAIR FUCNTION byABNORMAL JOINT SURFACEROTATION or ANGULATIONOVERRIDINGMOVEMENT OF NEIGHBOURING JOINT MAY

BE BLOCKED

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CHARACTERISTICS FOR ACCEPTABILITY OF FRACTURE REDUCTION

ALIGNMENT (MOST IMPORTANT) ROTATION RESTORATION OF NORMAL LENGTHACTUAL POSITION OF FRAGMENTS (LEAST IMPORTANT)

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Correction

• Operative treatment for most malunited fracture should not be considered until 6 to 12 months but in INTRA ARTICULAR fracture early operative treatment is needed.

• Surgeon should look for before surgery--OSTEOPOROSISSOFT TISSUE HOW MUCH FUNCTION CAN BE GAINED

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ILIZAROV TECHNIQUE is BEST Simultaneous restoration of

ALIGNMENT

ROTATION

LENGTH

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Delayed Union

• The exact time when a given fracture should be united cannot be defined

• Union is delayed when healing has not advanced at the average rate for the location and type of fracture (Btn 3-6 mths)

• Treatment usually is by an efficient cast that allows as much function as possible can be continued for 4 to 12 additional weeks

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• If still nonunited a decision should be made to treat the fracture as nonunion

• External ultrasound or electrical stimulation may be considered

• Surgical treatment should be carried out to remove interposed soft tissues and to oppose widely separated fragments

• Iliac grafts should be used if plates and screws are placed but grafts are not usually needed when using intramedullary nailing, unless reduction is done open

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Nonunion

• FDA defined nonunion as “established when a minimum of 9 months has elapsed since fracture with no visible progressive signs of healing for 3 months”

• Every fracture has its own timetable (ie long bone shaft fracture 6 months, femoral neck fracture 3 months)

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Delayed/Nonunion

Factors contributing to development:• Systemic• Local

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Systemic factors:• Metabolic• Nutritional status• General health• Activity level• Tobacco and alcohol use

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Local factors• Open• Infected• Segmental (impaired blood supply)• Comminuted• Insecurely fixed• Immobilized for an insufficient time• Treated by ill-advised open reduction• Distracted by (traction/plate and screws)• Irradiated bone• Delayed weight-bearing > 6 weeks• Soft tissue injury > method of initial treatment

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Nonunited fractures form two types of pseudoarthrosis:

• Hypervascular or hypertrophic• Avascular or atrophic

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Hypervascular or Hypertrophic:

1. Elephant foot (hypertophic, rich in callus)

2. Horse foot (mildly hypertophic, poor in callus)

3. Oligotrophic (not hypertrophic, no callus)

Hypervascular nonunions. A, "Elephant foot" nonunion. B, "Horse hoof" nonunion. C, Oligotrophic nonunion (see text). (Redrawn from Weber BG, Cech O, eds: Pseudarthrosis, Bern, Switzerland, 1976, Hans Huber.)

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Vascular or Atrophic• Torsion wedge

(intermediate fragment)• Comminuted (necrotic

intermediate fragment)• Defect (loss of fragment of

the diathesis)• Atrophic (scar tissue with

no estrogenic potential is replacing the missing fragment)

Avascular nonunions. A, Torsion wedge nonunion. B, Comminuted nonunion. C, Defect nonunion. D, Atrophic nonunion (see text). (Redrawn from Weber BG, Cech O, eds: Pseudarthrosis, Bern, Switzerland, 1976, Hans Huber.)

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Classification (Paley et al)• Type A<2cm of bone loss A1 (Mobile deformity) A2 (fixed deformity) A2-1 stiff w/o

deformity A2-2 stiff w/ fixed

deformity• Type B>2cm of bone loss B1 with bony defect B2 loss of bone length B3 both

A, Type A nonunions (less than 1 cm of bone loss): A1, lax (mobile); A2, stiff (nonmobile) (not shown); A2-1, no deformity; A2-2, fixed deformity. B, Type B nonunions (more than 1 cm of bone loss): B1, bony defect, no shortening; B2, shortening, no bony defect; B3, bony defect and shortening.

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Treatment:1. Electrical2. Electromagnetic3. Ultrasound4. External fixation (ie deformity, infection, bone loss)5. Surgical

• Hypertrophic: stable fixation of fragments• Atrophic: decortications and bone grafting• According to classification: type A : restoration of alignment, compression type B : cortical osteotomy, bone transport or

lengthening

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Surgical guidelines:• Good reduction• Bone grafting• Firm stabilization

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Reduction of the fragments:• Extensive dissection is undesirable, leaving

periosteum, callus, and fibrous tissue, to preserve vascularity and stability, resecting only the scar tissue and the rounded ends of the bones

• External fixator, Intramedullary nailing, Ilizarov frame

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Bone Grafting origins:• Autogenous “the golden standard”• Allograft• Synthetic substitute

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Bone grafting techniques:• Onlay• Dual onlay• Cancellous insert• Massive sliding graft• Whole fibular transplant• Vascularized free fibular graft• Intramedullary fibular graft

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CRITERTIA FOR SUCCESSFUL BONE GRAFT

• OSTEOCONDUCTION

• OSTEOGENICITY

• OSTEOINDUCTION

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Stabilization of bone fragments:• Internal fixation (hypertrophic #):

intramedullary, or plates and screws• External fixation(defects associated#): ie Ilizarov

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Factors complicating nonunion• Infection• Poor tissue quality• Short periarticular fragments• Significant deformity

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Mandible Fractures

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Healing Primary Healing • In rigid fixation techniques • Lag screws, compression plates, Recon plate,

external fixation, Wire fixation, Miniplate fixation

• No callus formation • Question of bone resorption

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Secondary bone healing • Callus formation • Remodeling and strengthening • MMF, Wire fixation, Miniplate fixation

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Closed Reduction

• Favorable, non-displaced fractures• Grossly comminuted fractures when

adequate stabilization unlikely• Severely atrophic edentulous mandible• Children with developing dentition

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• Length of MMF– De Amaratuga – 75% of children under 15 healed by 2 weeks, 75% young adults 4 wks– Juniper and Awty – 82% had healed at 4 wks– Longer period for edentulous fractures 6- 10wks

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Open Reduction

• Displaced unfavorable fractures • Mandible fractures with associated midface

fractures • When MMF contraindicated or not possible • Patient comfort • Facilitate return to work

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Intraosseous wiring • Semirigid fixation • Cheap • Technically difficult • Primary and Secondary bone healing

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Lag Screws • Rigid fixation (Compression) • Good for anterior mandible fractures, Oblique

body fractures, mandible angle fractures • Cheap • Technically difficult • Injury to inferior alveolar neurovascular

bundle

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Lag Screw Technique

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Compression plates • Rigid fixation • Allow primary bone healing • Difficult to bend • Operator dependent • No need for MMF

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• Miniplates– Semi Semi-rigid fixation– Allows primary and secondary bone healing– Easily bendable– More forgiving– Short period MMF Recommended

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Reconstruction Plates • Good for comminuted fractures • Bulky, palpable • Difficult to bend

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External Fixation

• Alternative form of rigid fixation

• Grossly comminuted fractures,contaminated fractures, non-union

• Often used when all else fails

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MAXILLARY FRACTURES

• Fractures of the maxilla occur less frequently than those of the mandible or nose due to the strong structural support of this bone

• Reestablishing continuity of these buttresses is the foundation on which maxillary fracture treatment is based.

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LeFort classification of midfacial fractures.

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• The Lefort I fracture, or transverse fracture,extends through the base of the maxillary sinuses above the teeth apices essentially separating the alveolar processes, palate, and pterygoid processes from the facial structures above. This transverse fracture across the entire lower maxilla separates the alveolus as a mobile unit from the rest of the midface. Fracture dislocations of segments of the alveolus may be associated with this fracture.

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• A pyramidal fracture of the maxilla is synonymous with a LeFort II fracture. This fracture pattern begins laterally, similar to a LeFort I, but medially diverges in a superior direction to include part of the medial orbit as well as the nose.

• The fracture extends diagonally from the pterygoid plates through the maxilla to the inferior orbital rim and up the medial wall of the orbit to the nose. This separates the maxillary alveolus, medial wall of the orbit and nose as a separate piece

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• A LeFort III fracture or craniofacial dysjunction denotes a complete separation of the midface or facial bones from the cranium. This fracture transverses the zygomaticofrontal suture, continues through the floor of the orbit, and finally through the nasofrontal suture. The bones of the orbit are separated through the lateral wall, floor, and medial wall.

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Treatment

• by reduction and immobilization• Establishment of preinjury occlusion and midface buttress

alignment• reestablish normal height and projection of the face • To accomplish this, the structural buttress of the maxilla

must be aligned and stabilized to provide the necessary support and contour to the midface.

• The proper occlusal relationship between the dental arches is established with intermaxillary fixation (IMF), or more appropriately termed maxillomandibular fixation

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Wound healing

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Wound Healing

• Wound- Discontinuity of the skin, mucous membrane or tissue caused by physical, chemical or biological insult

• Wound healing is a complex and dynamic process of restoring cellular structures and tissue layers

• There are 3 distinct phases• There are various categories of wound healing the ultimate outcome of any healing process is repair of

a tissue defect

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• The types of wound healing:o 1° healingo Delayed 1° healingo 2° healingo (Epithelialisation)Even though different categories exist, the

interactions of cellular and extracellular constituents are similar.

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Primary wound healing

• Also known as “healing by primary intention”• Think of a typical surgical wound: the wound

edges are approximated• Minimal number of cellular constituents die• Results in a small line of scar tissue• Minimizes the need for granulation tissue so

scarring is minimized

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The importance factors for good wound healing

• Technique• Choice of suture• Choice of needle• Training• Instruments• Antibiotics• Aftercare

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Delayed Primary healing

• Occurs if wound egdes are not approximated immediately

• May be desired in contaminated wounds• By day 4: phagocytosis of contaminated tissues

has occurredUsually wound is closed surgically at this stageIf contamination is present still : chronic

inflammation ensues leading to prominent scar eventually

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Secondary Healing

• Also called healing by secondary intention• A full thickness wound is allowed to heal by

itself: there is no approximation of wound edges

• Large amounts of granulation tissue formed• Wound eventually very contracted• Takes much longer to heal

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Fungal sinusitis

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Post op

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2 weeks post op – healing by 2° intention

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Epithelialization

• Epithelization is the process by which epithelial cells migrate and replicate via mitosis and traverse the wound

• Common in the healing of ulcers and erosions• Occurs by one of 2 mechanisms

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Epithelialization: Mechanisms

• Mechanism 1If basement membrane is intact ie some

dermis or dermal appendages remainEpithelialization occurs by epithelial cells

migrating upwards

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• Mechanism 2Occurs in a deeper woundA single layer of epithelial cells advance from

the wound edges to cover the woundThey then stratify so wound cover is complete

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Normal Wound Healing

• There are 3 phasesI. Inflammatory phase: Days 0-4II. Proliferative phase : Days 5-21III. Remodelling phase: Days 22-60

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• It can also be classified in 4 stages:I. HaemostasisII. InflammationIII. GranulationIV. Remodelling

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Haemostasis

• Injury causes local bleeding• Vasoconstriction is mediated by :o Adrenalineo Thrombaxane A2o Prostaglandin 2α

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• Platelets then adhere to damaged endothelium and discharge ADP

o Which promotes thrombocyte clumping and “dams” the wound

• Inflammation is initiated by cytokine release from platelets

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• α-granules from platelets release:Platelet Derived Growth Factor (PDGF)Platelet factor IVTransforming Growth Factor β• Thrombocyte dense bodies release:HistamineSerotonin

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• PDGF attracts fibroblasts chemotacticallyLeading to collagen deposition in later stages

of wound healing

• Fibrinogen → FibrinThus providing the structural support for the

cellular components of inflammation

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Inflammatory Phase

• Capillary dilatation occurs due to:HistamineBradykininProstaglandins• This dilatation allows inflammatory cells to

reach the wound site

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• These PMNs or leukocytes have several functions:

• Scavenge for debris• Debride the wound• Help to kill bacteria by: -oxidative burst mechanisms -opsonisation

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• Opsonin“factor which enhances the efficiency of

phagocytosis because it is recognized by receptors on leucocytes

2 major opsonins are:fragment of IgGA product of complement, C3b

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• Monocytes now enter the wound and become macrophages

• They have numerous functions-Secretion of numerous enzymes and cytokines

Collagenases and elastases-To break down injured tissues

PDGF, TGFβ, IL, TNF-To stimulate proliferation of fibroblasts, endothelial and smooth muscle cells

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• AngiogenesisThe formation of new blood vesselsFormed by endothelial cells becoming new

capillaries within the wound bedAngiogenesis stimulated by TNFα

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Proliferative Phase

• Collagen depositionType III collagen is laid down by fibroblastsFibroblasts are attracted by TGFβ and PDGFTotal collagen content increases until day 21• Granulation TissueIs the combination of collagen deposition and

angiogenesis

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Granulation Tissue

• Definition:Newly formed connective tissue, often found

at the edge or base of ulcers and wounds made up of : capillaries, fibroblasts, myofibroblasts, and inflammatory cells embedded in a mucin rich ground substance during healing

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Occasionally overgranulation can occur (as above following a flexor tendon repair) Treatment is steroid topical cream (1% hydrocortisone cream)

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• Re-epithelialization occurs next:By upward migration of epithelial cells if BM is

intactOr from wound edges

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Remodelling Phase

• Fibroblasts become myofibroblastsAnd wound begins to contractCan contract 0.75mm per dayCan over contract howeverContraction allows wound to become smallerA large wound can contract by up to 40-80%

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• Type III collagen is degradedAnd replaced with Type I• Water is removed from the scar, allowing collagen

to cross-link• Wound vascularity decreases• Collagen cross linkage allows: Increased scar strengthScar contractureDecreased scar thickness

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Wound Strength

• During phase 1 and 2 (inflammatory and proliferative phases)

Wounds have very little strength• During remodelling:Wounds rapidly gain strengtho @ 6 weeks: wound is 50% of final strengtho @12 months: wound is maximal strength: but

this is only 75% of pre-injury tissue strength

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Healing complications

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Abnormal Scars

• Hypertrophic Scars• Keloid Scars

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Hypertrophic Scars

• Raised, red and thickened• Limited to boundaries of scar• Occurs shortly after injury• Common on anterior chest and deltoids• Regresses over time• Related to wound tension and prolonged

inflammatory phase of healing

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Hypertrophic Scars

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• Treatment:Surgical excisionIntralesional Triamcenelone acetate injection

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Keloid Scars

• Raised, red and thickened scar• Extends beyond original scar boundary• Occurs months after injury• Does not regress• Commoner in darker skinned people• Familial tendency• Autoimmune phenomenon• Worsened by surgery and in pregnancy• Regresses post menopause

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Keloid Scars

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• Treatment:Surgical excision : caveat- recurrence = 65%Compression treatmentCO2 lasersCryotherapy

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Factors influencing scarring

• These can be broken down into:i. Patient factorsii. Surgical factors

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Patient Factors

• AgeElderly scar well• Skin typeCeltics : hypertrophic scar tendencyDark skinned: keloid scars

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• Anatomic regionMidlineDeltoid regionSternotomy • Patient morbidityNutritional stateDiabetesWound infections

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• Local tissueOedemaPrevious radiotherapyVascular insufficiency

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Surgical factors

• Atraumatic skin handling• Eversion of wound edgesInversion places keratinised epidermis

between the healing surfaces = delayed healing

• Tension free closure• Clean and healthy wound edges

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Everted Edges

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Inverted Edges

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• Scar orientationParallel to lines of relaxed skin tensionLangers lines• Suture tensionOver-tight: pressure necrosisUnder-tight: wound gaping and widened scar

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Langers Lines

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Acute Inflammation

• Definitiono The cellular and vascular response to injuryo Short in durationo Has cellular and chemical components

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Acute Inflammation: Causes

• Injury by:o Pathogens Bacteria, viruses, parasitesoChemical agents Acids, alkalisoPhysical agents Heat, trauma (surgery), radiationoTissue death Infarction

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Stages of Acute Inflammation

• Dilatation of local capillaries• endothelial permeability• Leakage of protein-rich fluid into interstitial

space – including fibrinogen• Fibrinogen → fibrin• Margination of leukocytes to peripheries of

capillariesMostly neutrophils

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Stages of Acute Inflammation

• Acute Inflammation is mediated by:Chemicals: interleukins and histamineProteins: complement cascade

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Complement Cascade

• Component of innate immune system• Cascade of proteins Resulting in formation of Membrane-

Attack-Complex (MAC) which canI. Destroy invading bacteriaII. Recruit other cells ie neutrophils Can also act as opsonins: enhancing

phagocytosis

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Complement Cascade

• 2 main activating arms of CC:I. Classic pathway: consists of antigen-

antibody complexesII. Alternative pathway: activated directly by

contact with micro-organisms

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Chronic Inflammation

• Definitiono Tissue response to persistent injuryo Long in durationo Cellular components differ from acute

inflammation

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Chronic Inflammation

• CausesForeign bodies: ie suturesBacteria: ie TBChronic abscess: ie osteomyelitisTransplant: ie chronic rejectionIBDProgression from AI

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Chronic Inflammation

• Key pointsHistological pattern not as predictable as

acute inflammationThere may be areas of acute inflammation

occurring simultaneouslyGranulation tissue and fibrosis may both be

present: indicating the tissues attempts at repair

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Chronic Inflammation

Lymphocytes predominateMacrophages present too• In granulomatous inflammation they fuse

forming multinucleate Langhans giant cellsPlasma cells are also present

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Chronic Inflammation

• MacrophagesDerived from monocytesPhagocytosis and killing of pathogens by

lysosomesLanghans giant cell formation

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Chronic Inflammation: Effects

• Secondary infection ie chronic epithelial injury• Scarring• Resolution: restoration of normality• Local lymphadenopathy

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The Surgical Wound

• It is often said that it is “controlled trauma”Carried out in a sterile environmentUnder aseptic conditions

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• Many protocols are put in place to prevent infections in surgical wounds

o Hand washingo Gowns and gloveso Painting and drapingo Drainso Antibioticso Laminar flow theatreso Sterile instrumentso Sterile dressings

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Surgery

• But wound infections can occur despite these measures causing:

• Death• Morbidity• Longer hospital stays• Cosmetically displeasing wounds

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Healthy Wound

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Wound Infection

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Wound Dehiscence

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Operation Types

• The risk of a wound infection depends on the operation

• For that reason, operations are classified into distinct types

o Cleano Clean-Contaminatedo Contaminatedo Dirty

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Class I :Clean wounds

• Elective operations (non emergency)• Non traumatic injury• Good surgical technique• Respiratory, gastrointestinal, biliary and

genitourinary tracts not breached• Risk of infection < 2%• Eg: mastectomy, hernia repair

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Class II: Clean - Contaminated

• Urgent or emergency case that is otherwise clean

• GI, GU or respiratory tracts entered electively, no spillage or unusual contamination

• Minor break in sterile technique occurred• Endogenous flora involved• Risk of infection: <10 %• Eg: appendicectomy, bowel resection

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Class III: Contaminated

• Non-purulent inflammation• Gross spillage from GIT, entry into GU or biliary

tract in the presence of infected bile/urine.• Major break in technique• Penetrating trauma < 4hrs old• Chronic open wounds• Risk of infection: 20%• Eg: GSW, rectal surgery

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Class IV : Dirty

• Purulent inflammation (abscess)• Pre-operative perforation of GI, GU, biliary or

respiratory tract• Penetrating trauma > 4 hrs• Existing acute bacterial infection or a

perforated viscera is encountered (clean tissue is transected to gain access to pus).

• Risk of infection: 40%

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Signs of Infection

• The cardinal points of acute inflammationI. CalorII. RuborIII. DolorIV. TumourV. Functio Laesa

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Signs of Infection

• Patient may be systemically unwell↑ TempTachycardicHypotensionWound breakdownWound dischargeWarm peripheriesSeptic shock

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Prevention

• Aseptic technique• Good technique• Prophylactic antibiotics where appropriate• Microbiology input• Clean operating theatre• Elective surgery• Good post op care

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Conclusion

• Fracture and wound healing is influenced by many variables including mechanical stability, electrical environment, biochemical factors and blood flow etc…

• Our ability to enhance fracture and wound healing will increase as we better understand the interaction between these variables.

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