infected non union

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INFECTED NON-UNION DR SAGAR TOMAR llrm medical college meerut,up

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INFECTED NON-UNION

DR SAGAR TOMAR

llrm medical college meerut,up

NON UNION

Definition

A state in which healing process comes to a halt

as judged by clinical & x-ray evidence, beyond

the stipulated period of healing for a particular

bone and fracture pattern due to mechanical or

biological failure

CAUSES OF NON UNION

BASED ON THE EXTENT OF INFECTION

NON-INFECTED NON-UNION

INFECTED NON-

UNION

CLASSIFICATION OF NON UNION

CLASSIFICATION OF NON-INFECTED NON-UNION

HYPERTROHIC NON

UNION

Hypervascular

nonunions have shown

uptake of strontium-85,

which indicates a rich

blood supply in the ends

of the fragments

ATROPHIC NON

UNION

strontium-85 uptake in

these nonunions

indicate a poor blood

supply in the ends of

the fragments

HYPERTRROPHIC NON-UNION

1 “Elephant foot” nonunions

These are hypertrophic and rich in callus. They result from insecure fixation, inadequate immobilization, or premature weight bearing in a reduced fracture with viable fragments.

2 “Horse hoof” nonunions

These are mildly hypertrophic and poor in callus. They typically occur after a moderately unstable fixation with plate and screws. The ends of the fragments show some callus, insufficient for union, and possibly a little sclerosis.

3 Oligotrophic nonunions

These are not hypertrophic, but are vascular, and callus is absent. They typically occur after major displacement of a fracture, distraction of the fragments, or internal fixation without accurate apposition of the fragments.

Hypervascular nonunions.

A, “Elephant foot” nonunion.

B, “Horse hoof” nonunion.

C, Oligotrophic nonunion

AVASCULAR NON-UNION 1 Torsion wedge nonunions

These are characterized by the presence of an intermediate fragment in which the blood supply is decreased or absent. The intermediate fragment has healed to one main fragment but not to the other.

2 Comminuted nonunions

These are characterized by the presence of one or more intermediate fragments that are necrotic. The radiographs show absence of any sign of callus formation.

3 Defect nonunions

These are characterized by the loss of a fragment of the diaphysis of a bone. The ends of the fragments are viable, but union across the defect is impossible. As time passes, the ends of the fragments become atrophic.

4 Atrophic nonunions

These usually are the final result when intermediate fragments are missing and scar tissue that lacks osteogenic potential is left in their place. The ends of the fragments have become osteoporotic and atrophic.

Avascular nonunions.

A, Torsion wedge nonunion.

B, Comminuted nonunion.

C, Defect nonunion.

D, Atrophic nonunion

Paley et al.classification of non-union

Type A nonunions(<1 cm of bone loss)

A1, lax (mobile)

A2, stiff (nonmobile)

A2-1, no deformity

A2-2, fixed deformity.

Type B nonunions(>1 cm of bone loss)

B1, bony defect, no shortening

B2, shortening, no bony defect;

B3, bony defect and shortening.

WEILAND CLASSIFICATION OF INFECTED NONUNION

Based on the extend of infection

type 1

characterised by open and exposed bone without

osseous infection but with soft tissue infection

type 2

characterised by circumferential cortical and

endostesl infection with often and invlocrum

surroundind a sequestrum

type 3

characterised by cortical-endosteal infection

associated with a segmental bone defect.

CIERNY MADAR CLASSIFICATION

Cierny and Mader developed a classification system for chronic osteomyelitis, based on physiological and anatomical criteria, to determine the stage of infection.

Based on host class A- NORMAL

class B- COMPROMISED

class C-PROHIBITIVE

Based on anatomytype 1-MEDULLARY

type 2-SUPERFICIAL

type 3-LOCALISED

type 4-DIFFUSE

pairing of these forms 12 clinical stages

Clinical Stage

(Type+ Class = Clinical Stage)

UMIAROV’S CLASSIFICATION OF

INFECTED NON-UNION

based on the viability of bone ends, the presence of

limb shortening, the presence of bone, and soft

tissue defect.

- type 1 the nonunion is normotrophic without

shortening

- type 2 the nonunion is hypertrophic with shortening

- type 3 the nonunion is atrophic with shortening

- type 4 the nonunion is atrophic with bone and soft

tissue defect, in general as a result of an

open

fracture

G.S KULKARNI CLASSIFICATION OF

INFECTED NON UNION

Severity of infection

Apposition of fragments

Presence or absence of deformity.

G.S KULKARNI CLASSIFICATION OF

INFECTED NON UNION

TYPE I:

fragments in apposition with mild infection and with or with out implant

TYPE II:

Fragments in apposition with severe infection with large or small wound.

TYPE III:

Severe infection with a gap or deformity or shortening.

3A defect with loss of full circumference

3B defect in > 1/3 of cortex

3C infected nonunion with deformity.

GORDON’S CLASSIFICATION

TYPE A

Tibial defects and non unions without significant

bone

loss

TYPE B

tibial defects greater than 3 cm with an intact fibula

TYPE C

tibial defect greater than 3 cm without intact fibula

MAY’S CLASSIFICATION

-it focuses on the status of tibia after bone and soft tissue

debridement

-it helps to estimate the length of rehabilitation period before

ambulation

NON-DRAINING/

DRY/QUIESCENT

-- nondraining for at least

3 months

-- requires 1 stage

treatment

DRAINING/ACTIVE

--drainig with abscess and

fever

-- Requires 2 stage

treatment

-- stage 2 after a period

of 10-20 days

How infection causes non union??

1. Dissection of pus through planes and periosteum-

devascularising th ends

2. Fragmentation and dissolution of fracture

haematoma

3. Inflammatory mediators promotes fibrous tissue

formation

4. If fixation was done then implant failure occurs

destabilization the fragments

5. Increase catabolic response at # ends

PATHOGENESIS

OSTEOMYELITIS

thrombosis of blood vessel of haversian canals

bone sclerosis and dead bone.

Butterfly fragments become sequestrii, isolated & devitalized by pus & INFECTED GRANULATION TISSUE

Infection granulation tissue

OSTEOLYIS

GAP NON UNION

Osteolysis occurs around the implants loosening instability of fixation nonunion.

DIAGNOSIS OF INFECTED NON UNION

1. Pain and mobility at fracture site

2. Raised local temperature

3. Discharging sinus

4. Scar healed by secondary intension with

“puckering”

5. Irregularity of bone showing osteomyelitis

INVESTIGATIONS

Include - complete blood count

- erythrocyte sedimentation rate (ESR)

- C- reactive protein (CRP)

Plain radiogarphy

Sinography

Radionucleotide scan

MRI

CT-scan

Culture sensitivity

usg

goals

Treatment of Infected non-union…

ERADICATE INFECTION

ACHIEVE UNION

SOLVE:soft tissue problem,deformity,joint

stiffness

GOAL 1

GOAL 2

GOAL 3

GOAL 1 : ERADICATE INFECTION

INCREASE HOST RESISTANCE :

Correct host morbidity

-control blood sugar level in diabetic

-smoking cessation

-treatment of liver or renal malfunction

-optimising nutrition

-treatment of chronic disease

Antibiotic therapy according to culture sensitivity

reports.

- systemic antibiotic therapy

LOCAL CONTROL OF INFECTION

DECREASE INFECTION LOAD:

• thorough debridement of dead and necrotic tissue

• closed suction antibiotic ingress and egress irrigation systems.

• negative suction drainage system.

INCREASE LOCAL HOST RESISTANCE:

• PMMA antibiotics beads

• biodegradable antibiotic delivery system

GOAL 2 : TO ACHIEVE UNION

• ADDING BIOLOGY

– Aspirated stem cells (with or without expansion)

– Demineralized Bone Matrix

– Autogenous Cancellous Graft

– Growth Factors

• Platelet derived

• Recombinant BMPs

• Gene Therapy

EXTERNAL STIMULI

-low intensity ultrasound therapy

-electric and electromegnetic therapy

• Aspirated iliac crest stem cells has been shown to enhance the activity of osteoconductive grafts.

• There are few commercially available Recombinant BMP proved to be effective treating nonunions.

Bone grafting in infected non union

Onlay bone grafting: graft applied or laid on the surface

of a bone

Inlay bone grafting: By the inlay technique a slot or

rectangular defect is created in the

cortex of the host bone, usually A graft

the same size or slightly smaller is then

fitted

into the defect.

Single onlay dual onlay

Cancellous

Insert graft

Papinaeu method of bone grafting

Stage I: Radical debridement

Stage II: bone grafting

Stage III: skin coverage.

HARMONS’ POSTEROLATERAL GRAFT

Bone grafting on the

interosseous membrane

to obtain a long

synostosis with fibula,

spanning the tibial

defect.

Free vascularised bone transfer

Rib, fibula, iliac crest.

Isolation of a segment

of contra lateral fibula

with attached nutrient

artery and vein.

Length of graft should

be 4 cm longer than

defect to allow 2 cm

overlap at the proximal

and distal ends.

ULTRASOUND THERAPY

it cause increases in cellular activity at osteotomy

sites and increases in mineralization of the bone and

metabolic activity.

It promotes bone healing because it stimulates the

genes involved in inflammation and bone

regeneration.

It increases blood flow through dilation of capillaries

and enhancement of angiogenesis, increasing the

flow of nutrients to the fracture site.

Used : for 20 min / day

ELECTRICAL AND ELECTROMAGNETIC

STIMULATION

used for 3 or more hours per day has been

successful in healing nonunions of long and short

bones, open or closed fractures, long-standing

nonunions, infected nonunions, and those with

fracture gaps up to 1 cm.

The three methods of administering electric stimulation are shown in this diagram.

(a) Direct current (DC): A cathode is implanted at the fracture site which is attached to either a subcutaneous power source or an external power source to generate an electric field at the fracture site.

(b) Capacitive coupling(CC): Two capacitive coupled electrodes are situated on the skin on either sides of the fracture site. An external power source is then attached to the electrodes, which induces an electric field at the fracture site.

(c) Inductive coupling (IC): An electromagnetic current carrying coil is placed on the skin overlying the fracture site, which is attached to an external power source. The coil generates a magnetic field, which induces an electrical field at the fracture site.

GOAL NO.3

SOFT TISSUE PROBLEMS:

The transfer of vascularized muscle tissue improves

the local biological environment by bringing in a

blood supply that is important in the host's defense

mechanisms and for antibiotic delivery and osseous

and soft tissue healing

DEFORMITY AND SHORTENING:

- Ilizarov is the gold standard treatment to correct

deformity and shortening and eradicate infection at

the same time

TREATMENT PROTOCOL (AO BASED)

queiscent nonunion

use of short term antibiotic prophylaxis

excise dead bone and scarred ,non vascularised soft tissue

remove loose hardware

correct alignment

perform cancellous bone grafting if required

stabilise using plate or intramedullary devise or external

fixator

mobilise adjacent joints by physiotherapy

QUEISCENT NON

UNION

ACTIVE NON UNION

STAGE 1

thorough debridement

- excise and debride

- drain using closed suction irrigation

- antibiotics beads and i.v. antibiotics

- stabilize with external fixator

STAGE 2 after 10-20 days

shingling and cancellous bone auto graft.

STAGE 3

additional bone graft ,muscle or skin pedicle flap can be used

Shingling and cancellous bone

grafting

Shingling Cancellous bone graft

Shingling:a process by which ends of the fracture

Fragments are decorticated subperiosteally forming many

Small osteoperiosteal flaps.

ELIMINATION OF INFECTION IN ILIZAROV

METHOD

Resection of infected bone and subsequent

intercalary bone lengthening

gradual bone transport of one wall of the cavity

Controlled osteogenesis, filling of cavities by newly

formed tissue

A corticotomy is performed to fracture the bone into two segments, and the two bone ends of the bone are gradually moved apart during the distraction phase, allowing new bone to form in the gap. When the desired or possible length is reached, a consolidation phase follows in which the bone is allowed to keep healing.

CONCLUSION : general approach to

infection

Thank you