Seminar on chronic osteomyelitis sch

CHRONIC OSTEOMYELITISCHRONIC OSTEOMYELITIS
Chair Person-Dr.C.V.MudgaDr.C.V.Mudgal
Speaker – Dr.S.C.Hiremath.
PG In orthopedics KIMS Hubli

IntroductionIntroduction
Definition:
“ A severe,persistent and incapacitating
infection of bone and bone marrow ”
 Chronic osteomyelitis is often defined as
the presence of ongoing bone infection for
longer than 1 month in the presence of
devitalized bone

OsteomyelitisOsteomyelitis
Nelaton (1834) : coined osteomyelitis


OsteomyelitisOsteomyelitis
Osteomyelitis (osteo- derived from the Greek
word osteon, meaning bone, myelo- meaning
marrow, and -itis meaning inflammation) simply
means an infection of the bone or bone marrow.
Infection mainly involves
- Marrow spaces
-Haversian canals
-Subperiosteal Spaces

Bone and joint infections pose a formidable
challenge to the Orthopaedic surgeon
The high success rate obtained with antibiotic
therapy in most bacterial diseases has not been
obtained in bone and joint infections because of
the physiological and anatomical characteristics of
bone

The mere presence of bacteria in bone, whether
from bacteremia or from direct inoculation, is
insufficient to produce osteomyelitis
Morrissy and Haynes have shown the relationship
of trauma to osteomyelitis. Illness, malnutrition,
and inadequacy of the immune system also can
cause bone and joint infections.

As in other parts of the body, bones and joints
produce inflammatory and immune responses to
infection.
Osteomyelitis occurs when an adequate number
of a sufficiently virulent organism overcomes the
host's natural defenses (inflammatory and immune
responses) and establishes a focus of infection, for
example; local skeletal factors also play a role in
the development of infection
The relative absence of phagocytic cells in the
metaphyses of bones in children may explain why
acute hematogenous osteomyelitis is more
common in this location

 The peculiarity of an abscess in bone is that it is contained
within a firm structure with little chance of tissue
expansion
 As infection progresses, purulent material works its way
through the haversian system and Volkmann canals and
lifts the periosteum off the surface of bone
 The combination of pus in the medullary cavity and in the
subperiosteal space causes necrosis of cortical bone.
 This necrotic cortical bone, known as a sequestrum, can
continue to harbor bacteria despite antibiotic treatment.
Antibiotics and inflammatory cells cannot adequately
access this avascular area, resulting in failure of medical
treatment of osteomyelitis

Hematogenous osteomyelitis ofHematogenous osteomyelitis of
Tubular bone in childTubular bone in child

Hairpin Bend vessels flow becomes considerably slower
and more turbulent

Steps in the progression ofSteps in the progression of
chronic osteomyelitischronic osteomyelitis

Factors That Turn Acute Bone InfectionFactors That Turn Acute Bone Infection
to Chronic Osteomyelitisto Chronic Osteomyelitis::
Trauma (orthopaedic surgery or open fracture)
Prosthetic orthopaedic device
Diabetes
Peripheral vascular disease
Chronic joint disease
Alcoholism
Intravenous drug abuse
Chronic steroid use
Immunosuppression
Tuberculosis
HIV and AIDS
Sickle cell disease
Presence of catheter-related blood stream infection.

CHRONIC OSTEOMYELITISCHRONIC OSTEOMYELITIS
The hallmark of chronic osteomyelitis is infected
dead bone within a compromised soft-tissue
envelope
The infected foci within the bone are surrounded
by sclerotic, relatively avascular bone covered by a
thickened periosteum and scarred muscle and
subcutaneous tissue.
This avascular envelope of scar tissue leaves
systemic antibiotics essentially ineffective

Factors responsible for chronicity
Local factors: Cavity, Sequestrum, Sinus, Foreign
body, Degree of bone necrosis
General: Nutritional status of the involved tissues,
vascular disease, DM, low immunity
Organism: Virulence
Treatment: Appropriateness and compliance
Risk factors: Penetrating trauma, prosthesis, Animal
bite

ETIOLOGYETIOLOGY
ORGANISM POSSIBLE PROBLEM
1)Staphylococcus aureus
Pressure ulcer, penetrating wound, open fracture,
orthopedic surgery, vascular insufficiency disorder
2)Staphylococcus epidermidis
Indwelling prosthetic device
3)Streptococcus viridans
Abscessed tooth, gingival disease
4)Escherichia coli
Urinary tract infection
5)Mycobacterium tuberculosis
Tuberculosis

6)Neisseria gonorrhoeae
Gonorrhea
7)Pseudomonas sp.
Puncture wounds, intravenous drugs
8)Salmonella sp.
Sickle cell disease
9)Fungi, mycobacteria
Immunocompromised host

According To Age
1)Infants < 1yr : Gr. B streptococci, S.
aureus, E.coli
2) 1-16 yrs : S. aureus, S. pyogens,
H.influenzae
3) > 16 yrs : S.aureus, S epidermidis, Gram
–ve Bacilli

Before the discussion of diagnosis and
treatment,it is vital to understand by which
infections occur.
Most infections encountered in orthopaedics
are related to biofilm(A coherent cluster of
bacterial cells imbedded in a matrix—which
are more tolerant to most antimicrobials and
the host defence than planktonic bacterial
cells forming bacteria.)

Biofilm bacteria exist in one of the two
states
1. Planktonic state
2. Stationary state

Planktonic state bacteria are free floating in
the extra cellular matrix and are isolated and
relatively small in quantity.
In this state,body host defences can easily
eradicate the organism through the usual
immunological mechanisms.
It is rare for planktonic bacteria to survive
long in the extra cellular matrix despite
numerous and repeat occurences of entry.

However,if the bacterial load is large and
sustained,they can overwhelm the host
defences and escape the effects of antibiotics.
Then they can invade tissue and
blood,leading to septicemia and death.
Planktonic bacteria are metabolically active
and reproductive.

This is important consideration for antibiotics
treatments that work by either interfering with
cellwall or protien synthesis or with
reproduction.
If planktonic bacteria encounter a suitable
inert surface such as dead or necrotic
tissue,foreign bodies or avascular body part by
either dircet contamination,contiguous
spreading or hematogenous seeding,they can
attach and began the process of colonisation.

Juxta position of the bacteria with a surface
or biomaterial is accomplished by vander
waal’s forces,which allow bacteria to
develop irreversible crosslinks with the
surface (adhesion-receptor interaction).
Following adhesion,bacteria begin to create
a mucopolysachharide layer called biofilm
or slime.
Then they develop into colonies.

These colonies exhibit remarkably resilient
behaviour.
In the early stages of colonisation,sessile
bacteria can be killed or neutralised by the
host defences.
However,some of these bacteria may ecape
destruction and potentially act as a nidus for
future infection.

Transition from colonisation to infection
usually requires other condition to exist.
This might occur if there was an inoculum
that was larger than threshold levels,impaired
host immune defence mechanisms,traumatised
or necrotic tissues,foreign bodies or an a
acellular or inanimate surface such as dead
bone,cartilage or biomaterials.

Damaged bone,being relatively acellular,acts as
a suitable surface for bacterial adhesion and
colonisation.
Devitalised bone divide of normal periosteum
presents a collagen matrix to which bacteria
can bind.
Moreover,it has been suggested that bone sialo
protein can act as a ligand for bacterial binding
to bone.

Biomaterials and other foreign bodies are
usually inert and susceptible to bacterial
colonisation because they are inanimate.
Following bacterial adherence and
colonisation,the resistance to antibiotics
appears to increase.
Bacterial colonies can undergo phenotypic
changes and appear to hybernate.

They can survive in a dormant state without
causing infection,and this can explain the
recovery of bacteria from asymptomatic
hardware removal.
So while colonisation is a necessary
antecedent for infection,colonisation alone
does not necessarily lead to infection.

Once colonisation occurs,body defences
continue to identify bacteria as foreign.
The subsequent collection of inflammatory
cells brought into wall off the bacteria via
chemotaxis manifest as purulence,which is a
symptom of host’s attempt to isolate and
destroy the infection.
The accute inflammatory cells will also release
a spectrum oxidative and enzymatic products
in an attempt to penetrate the glycocalyx.

These mediators and enzymes are nonspecific
and may be toxic to host tissues.
Increased host tissue damage can lead to
more surface substrate for local
bacteria,creating cycle of tissue damage,host
response,and exacerbation of infection.
The host tissues will eventually react to limit
the spread of infection macroscopically as
well as microscopically.

The clinical manifestation of a sequestered
infection is an abcess or involucrum.
Alternatively,if the infection grows and reaches
the skin or an internal epithealial surafce,a sinus
tract forms as a route to dispel detritus.
While the appearance of sinus tract is a
manifestation of a locally devastating disease
process and indicates severe underlying
infection,it should be remembered that it can
also prevent the accumulation of internal
collection which can lead to bacterimia and
septicimia.

Eventually the equilibrium may exist in the
form of chronic infection,which is what many
surgeons see in practice.
 There is usually history of intermittent
symptoms and drainage that has responded to
some type of antibiotic regimen.
Longstanding infections that were tolerated by
healthy individuals may suddenly become limb
or life threatening as the individual’s age.

Bacteria settle down in metaphysis
Primary focus in metaphysis (form abscess in
metaphysis)
Subperiosteal abscess
Sequestrum formation (dead bone )
Involucrum formation (new bone formed by
cambium layer of periosteum)
Pus eventually perforates periosteum and forms
abscess in soft tissues.
Ultimately abscess burst on surface and forms
discharging sinus

Necrosis.  stage of new bone formation
involucrum with sequestrum inside,
there will always be a persistent discharging
sinus.  pus from bone escapes through
multiple hole in involucrum (Cloacae)

Pus spreads into vascular channels
 Raising intraosseous pressure
Impairing blood flow -> Chronic
ischemic necrosis -> Separation of
large devascularized fragment -> New
bone formation ->(involucrum)

Chronic osteomylitis involving metaphysis ofChronic osteomylitis involving metaphysis of
tibiatibia

Discharging sinusDischarging sinus

SEQUESTRUMSEQUESTRUM
Dead piece of bone separated from living bone by
a layer of unhealthy granulation tissue and lying
freely in the cavity
Types
1) Tubular – in pyogenic infections below 2 yrs
2) Feathery – pyogenic infections
3) Course sandy – tuberculosis
4) Dense ivory – syphilis

5) Coloured ( Black) – in ulna & tibia
osteomyelitis
6) Ring – Amputation stump & pin track
infections
7) Bombay – Calcaneal OM
8) Corolliform – Pyogenic infections
9) Buttonhole – Pott’ puffy tumour,
Tuberculosis of skull bones

Sequestrum ExposedSequestrum Exposed

Sequestrum RemovedSequestrum Removed

CLASSIFICATIONCLASSIFICATION
Duration
Acute, Subacute , Chronic
Route of infection
Hematogenous or Exogenous
Host response
Pyogenic or Granulomatous

CLASSIFICATION OF CHRONICCLASSIFICATION OF CHRONIC
OSTEOMYELITISOSTEOMYELITIS
Cierny and Mader developed a
classification system for chronic
osteomyelitis, based on physiological and
anatomical criteria, to determine the stage
of infection
The physiological criteria are divided into
three classes based on three types of hosts

Class A hosts have a normal response to
infection and surgery
Class B hosts are compromised and have
deficient wound healing capabilities
When the results of treatment are
potentially more damaging than the
presenting condition, the patient is
considered a class C host

Anatomical criteria consist of four types
Type I, a medullary lesion, is characterized
by endosteal disease
In type II, superficial osteomyelitis is
limited to the surface of the bone, and
infection is secondary to a coverage defect

Type III is a localized infection involving a stable,
well-demarcated lesion characterized by full-
thickness cortical sequestration and cavitation (in
this type, complete débridement of the area would
not lead to instability)
Type IV is a diffuse osteomyelitic lesion that
creates mechanical instability, either at
presentation or after appropriate treatment

Cierney & Mader Class.Cierney & Mader Class.

StageStage CharacteristicCharacteristic FeaturesFeatures
II MedullaryMedullary Endosteal diseaseEndosteal disease
IIII SuperficialSuperficial Cortical surface infected because of coverageCortical surface infected because of coverage
defectdefect
IIIIII LocalisedLocalised Cortical sequestrum that can be excised withoutCortical sequestrum that can be excised without
compromising stabilitycompromising stability
IVIV DiffuseDiffuse I, II and III plus mechanical instability before orI, II and III plus mechanical instability before or
after debridement.after debridement.
Anatomical Type
Cierney and Mader staging system of
Chronic Osteomyelitis

ClassClass Host’s immuneHost’s immune
systemsystem
FeaturesFeatures
A hostA host NormalNormal Immunocompetent with good local vascularityImmunocompetent with good local vascularity
B hostB host CompromisedCompromised Local or systemic factors that compromiseLocal or systemic factors that compromise
immunity or healingimmunity or healing
C hostC host ProhibitiveProhibitive Minimal disability, prohibitive morbidityMinimal disability, prohibitive morbidity
anticipated, poor prognosis for cure, treatmentanticipated, poor prognosis for cure, treatment
worse than diseaseworse than disease
Physiological classification

Cierney and Mader staging system ofCierney and Mader staging system of
Chronic OsteomyelitisChronic Osteomyelitis
Anatomical typeAnatomical type

Clinical StagingClinical Staging
(Cierny-Mader, 1985)(Cierny-Mader, 1985)
Anatomic Type
+ CLINICAL STAGE
Physiologic Class
Example: IV B
S
tibial osteomyelitis = diffuse tibial lesion in a systemically compromised host

USE OF THIS CLASSIFICATION
- To decide whether treatment should be
1) Simple or Complex
2) Curative or Palliative
3) Limb sparing or Ablative

CLINICAL FEATURESCLINICAL FEATURES
DURING THE PERIOD OF
INACTIVITY
- Usually no symptoms
- Skin over the focus is dusky, thin,
scarred, poorly nourished
- Break in the skin causes ulceration that
heals slowly
- Muscles are scarred & leads to
contractures of the adjacent joints

DURING ACUTE EXACERBATION
- Aching pain worsening at night, overlying
soft tissue becomes edematous, warm
redddened & tender
- patient is febrile
- As infection progresses, sinus may open
up & drain extruding small sequestrum at
intervals

- Intervals between flare ups may be months
or years
- Flare ups may be due to poor general
condition & lowered resistance
- Recurrent toxemia will eventually cause
debilitary & sometimes fatal amyloidosis

DIAGNOSISDIAGNOSIS
The diagnosis of chronic osteomyelitis is
based on CLINICAL, LABORATORY &
IMAGING studies

POSSIBLE CLINICAL FINDINGS
- Asymptomatic
- Pain
- Fever
- Tenderness

- Erythema
- Swelling
- Sinus Tract
- Limp
- Drainage

 LAB. INVESTIGATIONS
- Nonspecific
- Gives no indication of severity of infection
1) Raised ESR & CRP
2) Raised WBC ( Raised Lymphocytes) in 35%
patients
3) Biopsy with Culture & Sensitivity (Gold
Standard)

IMAGINGIMAGING
For confirmation of the diagnosis
To prepare for surgical treatment
However no technique can absolutely
confirm or exclude the presence of
osteomyelitis

1) It takes from 10 to 21 days for an osseous lesion to
become visible on conventional radiography, because a
30–50% reduction of bone density must occur before
radiographic change is apparent
- earliest radiographic changes appears after 8 to 10 days
- In early stages, bone appears moth eaten & osteoporotic
due to CORTICAL DESTRUCTION with sclerotic
areas
- PERIOSTEUM IS ELEVATED by subperiostel
laminations of new bone
-grdually each necrotic dense area becomes surrounded by
white ring representing new bone formation, the
INVOLCRUM

Ssequestrum with normal structuralSsequestrum with normal structural
involucrum of a proximal humerus.involucrum of a proximal humerus.

Radiographs of a distal femur highlighting the features ofRadiographs of a distal femur highlighting the features of
diffuse osteomyelitis peripheral sclerosis, sequestrum, anddiffuse osteomyelitis peripheral sclerosis, sequestrum, and
involucrum.involucrum.

SEQUESTRUM
PERIOSTEAL NEW BONE
FORMATION
INVOLUCRUM

SINOGRAPHYSINOGRAPHY
 Helpful if the sinus is present in locating
focus of the infection in chronic
osteomyelitis

A) Anteroposterior view of the right femur demonstrates severalA) Anteroposterior view of the right femur demonstrates several
radiodense, sharply marginated foci within lucent cavities suggestive ofradiodense, sharply marginated foci within lucent cavities suggestive of
sequestrationsequestration (B) Oblique view showing retrograde(B) Oblique view showing retrograde
opacification of a sinus tract defining the course and extent of the fistula andopacification of a sinus tract defining the course and extent of the fistula and
confirming the communication with an abscess inconfirming the communication with an abscess in
the bone.the bone.

ScintigraphyScintigraphy
Radio nucleotide
TC 99m Poly Phosphate scan
Gallium citrate scan
Indium
Sensitivity (84 to 100 percent) and specific
(70 to 96 percent)

1)99M
Tc Scan
- Action
binds to hydroxyapetite crystals
- Shows increased uptake in the areas of
increased blood flow or oseoblastic
activity
- lacks specificity

2) 67
Ga Scan
- shows increased uptake in areas where
leucocytes or bacteria accumulate
- normal Ga scan excludes presence of
osteomyelitis
- useful as follow up examination after
surgery

3) 111
Indium leucocyte scan
- more sensitive than Tc or Ga scans
- especially useful in differentiating
chronic osteomyelitis from
neuropathic arthropathy like diabetic
foot

These leukocytelabeledThese leukocytelabeled
images suggest multiple areasimages suggest multiple areas
of bilateral pedal osteomyelitis.of bilateral pedal osteomyelitis.

Various combinations of aforementioned
scintigraphic method remain the gold
standard diagnostic method in post
traumatic infections.
This is especially true because the presence
of metallic implants limits the usefullness of
MRI scanning.
Flourodeoxy glucose (FDG)-PET scan
enables noninvasive detection and
demonstration of the chronic osteomyelitis
with 97% accuracy.

18
FDG PET Scan
Meta-analysis showed –Fluorodeoxyglucose
positron emission tomography has the
highest accuracy for confirming or excluding
the diagnosis of Chr OM

CT SCAN
- Provides excellent difinition of cortical
bone
- especially useful in identification of
Sequestra

MRI SCAN
- more sensitive than nuclear studies
- reveals a well defined rim of high signal
intensity surrounding the focus of active
disease ( RIM SIGN)

This MRI scan demonstrates extensiveThis MRI scan demonstrates extensive
intramedullary involvement as well as surrounding soft tissueintramedullary involvement as well as surrounding soft tissue
edema in aedema in a
patient with post-traumatic osteomyelitis of the right femoralpatient with post-traumatic osteomyelitis of the right femoral
diaphysis.diaphysis.

A case of chronic osteomylitis of fibulaA case of chronic osteomylitis of fibula

MR images chronic osteomyelitis of rightMR images chronic osteomyelitis of right
distal femur.distal femur.

MOLECULAR DIAGNOSTICSMOLECULAR DIAGNOSTICS
Identification procedures based on molecular
analysis and RNA or DNA typing are currently in
development to facilitate diagnosis in osteomyelitis.
The most commonly used method is PCR
technique.
Unfortunately,PCR cannot easily delineate between
nuclear materials from living or dead bacteria.
This increases likelihood of false positive results.

TREATMENTTREATMENT
To wait is to invite disaster.

Chronic OM generally cannot be eradicated
without surgical treatment
Surgery for Chronic OM consists of
sequestrectomy & resection of scarred &
infected bone & soft tissue

THE GOALS OF SURGERY
- Eradication of infection by achieving a
viable & vascular environment
- Radical debridement
- Prevent recurrences

SEQUESTRECTOMY & CURETTAGESEQUESTRECTOMY & CURETTAGE
1) All sinus tracts are excised completely
along with sequestra, purulent material &
scarred and necrotic tissue
if sclerosis bone seals off a cavity within the
medullary canal, it is opened into the canal
in both directions to allow blood vessels
to grow into the cavity

When medullary canal is infected
intramedullary reaming as a debridement
technique has shown favourable results in
the treatment of medullary osteomyelitis.

Sequestrectomy and curettage, A, Affected bone is
exposed, and sequestrum is removed, B, All infected
matter is removed,C, , Wound is either packed open or
closed loosely over drains.

AFTER TREATMENT
- Limb is splinted until the wound is healed & then
it is protected to prevent pahological fracture
- prolonged antibiotic therapy is given usually for 6
weeks
- bony & soft tissue defects must be filled to reduce
chances of continued infection & loss of function

METHODS TO ELIMINATE THIS DEAD
SPACE
1) Bone grafting with primary or secondary closure
2) use of PMMA beads
3) local muscle flaps & skin grafting with or
without bone grafting
4) microvascular transfer of muscle, myocutaneos,
osseous & osteocutaneous flaps
5) use of bone transport( Ilizarov’s technique)

Four basic methods of immediate, biological management of dead space using living
tissue or cancellous bone grafts.

 OPEN BONE GRAFTING( PAPINEAU
TECHNIQUE)
This procedure is based on the following principles:
- granulation tissue markedly resists infection
- autogenous cancellous bone grafts are rapidly
revascularized and are resistant to infection
-the infected area is completely excised
-adequate drainage is provided
-adequate immobilization is provided
-antibiotics are used for prolonged periods

DONE IN 3 STAGES
1)Excision of infected tissue without or with
stabilization using an external fixator or an
intramedullary rod
2) Cancellous autografting
3) skin closure

A, Chronic osteomyelitis B, After débridement and
development of granulation tissue C, Open bone graft D,
Blood clot in place

 PMMA BEAD CHAINS
-The rationale for this treatment is to deliver levels of
antibiotics locally in concentrations that exceed the
minimal inhibitory concentrations
-The antibiotic is leached from the PMMA beads into the
postoperative wound hematoma and secretion, which act
as a transport medium
-Aminoglycosides are the most commonly employed
antibiotics for use with PMMA beads
-most commercially available bone cements have a
prepackaged form available with GENTAMICIN or
VANCOMYCIN
- In short-term implantation, the beads are removed within
10 days and in long-term implantation, they may be left for
80 days

Preparation of antibiotic beads

BIODEGRADABLE ANTIBIOTIC
DELIVERY SYSTEMS
-Biodegradable substrates contain osteoconductive
and osteoinductive materials, which can be used
to promote new bone formation
- Bioabsorbable substrates (calcium sulfate or
calcium phosphate) that can be mixed with
antibiotics ( Vancomycin or Tobramycin)
-These beads typically resorb by about 8 weeks
after surgery

Polymethylmethacrylate (PMMA) beads connectedPolymethylmethacrylate (PMMA) beads connected
together in a chain are the most widely used drugtogether in a chain are the most widely used drug
delivery system.delivery system.

Advantages
- 2nd
procedure is not required to remove the
implant
- Calcium in the substrate can be used in new bone
formation
- as the beads resorb, they are slowly replaced by
new bone & soft tissue & this process may
decrease the need for further reconstructive or
coverage procedure

CLOSED IRRIGATION & SUCTION
-For resistant focal infections, topical instillation of
solution containing mild detergent ( eg. Alevaire)
& one or more antibiotic seems to be effective
- detergent inhibits the formation of penicillinase
- so penicillins used with detergents becomes
effective against resistant, bacterial strains

-Closed suction antibiotic ingress and egress high-
volume irrigation systems(Lautenbach continuous
irrigation method) can be used over 3 to 21 days
- the material collected through suction tube is
cultured every day when 3 successive negative
cultures are obtained, the antibiotic detergent
solution is discontinued

Detergents or soaps have been showed to
be the only irrigation solutions that remove
additional bacteria beyond the affect of
mechanical irrigation alone.
Castille soap has recently been reported to
be useful in this situation.

SOFT TISSUE TRANSFER
- Soft-tissue transfers to fill dead space left behind
after extensive debridement may range from a
localized muscle flap on a vascular pedicle to
microvascular free tissue transfer
- 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.

- Most commonly, a local muscle flap is used in the
treatment of chronic osteomyelitis of the tibia
- The gastrocnemius muscle is used for defects
around the proximal third of the tibia
- the soleus muscle is used for defects around the
middle third
- A microvascular free muscle transfer is required
for defects around the distal third of the tibia

- When a microvascular free muscle flap is used,
and segmental bone loss has occurred, autogenous
cancellous bone grafting can be done about 6
weeks after the initial free flap transfer
- free fibular graft can be used for segmental bone
loss of the tibia
- If chronic osteomyelitis involves segmental bone
loss of the tibia and the fibula, the results of a free
fibular graft are not good, and amputation or
reconstruction by the Ilizarov technique is advised

 ILIZAROV’S TECHNIQUE
- The Ilizarov technique has been helpful in the treatment
of chronic osteomyelitis and infected nonunions
- This technique allows radical resection of the infected
bone
- A corticotomy is performed through normal bone
proximal and distal to the area of disease. The bone is
transported until union is achieved
- Disadvantages of this technique include the time required
to achieve a solid union and the high incidence of
associated complications
-

Mr. J.S. bow hunting with his IlizarovMr. J.S. bow hunting with his Ilizarov
external fixator frame in place illustrates that patients areexternal fixator frame in place illustrates that patients are
able to remainable to remain active during their treatmentactive during their treatment..

BELFAST TECHNIQUE
2 Stage Technique
- in 1st
stage, all necrotic & infected tissues
are debrided & is covered with soft tissue
transfer
- in 2nd
stage , at later time autogenous
cancellous grfating is done after infection
has been completely subsided

SILVER IONTOPHORESIS
- Electrically generated silver ions have been
shown to have antibacterial properties
- can be used as adjuvent treatment in
management of chronic osteomyelitis

Ionophorosis Delivary of silver IonsIonophorosis Delivary of silver Ions

HYPERBARIC OXYGEN THERAPYHYPERBARIC OXYGEN THERAPY
Used as adjuvent to other methods of
treatment

HYPERBARIC OXYGEN THERAPYHYPERBARIC OXYGEN THERAPY
ChamberChamber

HBO enhances oxygen-dependent
leukocyte killing through the production of
hydrogen peroxide and superoxide by
providing increased oxygen tension in the
hypoxic tissue.
Secondly, optimal tissue oxygen tension
enhances osteogenesis and
neovascularizationnto fill the dead space
with new bone and soft tissues.

HBO has also been shown to enhance
osteoclastic activity to remove bony debris.
Finally, HBO also potentiates the
antimicrobial effects of aminoglycosides,
and possibly sulpha drugs and vancomycin,
in the killing of susceptible bacteria
Patients with osteomyelitis are usually
treated at 2.0-2.5 ATA for 90-120 min per
day and typically receive 20-40 treatments

AMPUTATION FOR CHRONIC
OSTEOMYELITIS
- Malignant change of sinus tract
- Madura Mycosis
- Joint contractures & stiffness

COMPLICATIONSCOMPLICATIONS
Growth disturbances
Pathological fractures
Muscle contractures
Secondary septicemia
Epithelioma
Malignant changes( Squamous cell ca,Reticulum
cell ca, Fibrosarcoma)
Joint stiffness
Amyloidosis

Novel techniques underdevelopment include
the use of compounds that promote
detachment of stationary colonised bacteria
into the planktonic state,where they are easier
to eradicate.
The techniques include surface treatments
that inhibit colonisation and the use of light
activated dye that destroys ceratain bacteria
in wounds.

In this technique indocyanine green,which is
a harmless dye,is placed into the wound and
activated with near infrared light.
The light resulsts in the dye releasing
molecules that are toxic to the MRSA.
The mechanism of action is varied and
unlike standard antibiotics that development
of resistence is unlikely.
These and other methods under
development may provide novel adjunctive
treatments to help treat osteomyelitis.

PROPHYLAXISPROPHYLAXIS
Prevention is always better than cure.
Prophylactic antibiotics have an important
role in the treatment of closed fractures,the
use of which will reduce post operative
osteomyelitis in elective cases.
Antibiotic administration is not a substitute
for proper aseptic technique,but it is a
validated additional measure to reduce post
operative infection.

The current recommendation is that
antibiotic should be administered 30-60
mins befor the incision is made.

MISCELLANEOUS CONDITIONSMISCELLANEOUS CONDITIONS
SCLEROSING OM OF GARRE
- Idiopathic cortical sclerosis
- mc site Tibia
-chronic form of disease in which the bone is
thickened and distended, but abscesses and
sequestra are absent
-affects children and young adults
-cause is unknown, but it is thought to be an
infection caused by a low-grade, possibly
anaerobic bacterium

CLINICAL FEATURES
- Intermittent pain
- Swelling & Tenderness over affected bone

INVESTIGATIONS
- ESR : slightly raised
- C/S : usually negative
- X Ray : expanded bone with generalised
sclerosis
- Biopsy : chronic low grade non specific
OM

DIFFERTIAL DIAGNOSIS
- Paget’s disease
- Osteoid osteoma

TREATMENT
- Fenestration of sclerotic bone
- Antibiotics

RESIDUAL STAGE OFRESIDUAL STAGE OF
- characterized by a complete absence of the signs and
symptoms of infection, including drainage
-The bone is sclerotic, and its blood supply and strength are
normal
-During this stage of osteomyelitis, the bone bears the same
relation to normal bone that scar tissue bears to normal
connective tissue
-Adhesions of skin to bone are more common if the bone is
subcutaneous
-Injury to such tissues frequently causes skin breakdown and
even recurrence of infection

TREATMENT
-correcting leg-length inequality or angular
and joint deformities
-contracted scars must be released
-adherent scars must be replaced by
myocutaneous flaps

PATHOLOGICAL FRACTURE INPATHOLOGICAL FRACTURE IN
-Because the involucrum is sometimes insufficient, the shaft
of a long bone may fracture during the acute or subacute
stage of osteomyelitis before immobilization has been
started
-all operations necessary to combat the infection should be
carried out thoroughly, and bone fragments are then
realigned and immobilized as with any other fracture
-External fixation or cast immobilization usually is preferred
-If bone loss is significant, the defect can be filled with
autogenous bone graft, a vascularized osseous graft, or
bone transport using the Ilizarov technique

Osteomyelitis of Right Femur withOsteomyelitis of Right Femur with
pathological fracturepathological fracture

CHRONIC RECURRENTCHRONIC RECURRENT
MULTIFOCAL OSTEOMYELITISMULTIFOCAL OSTEOMYELITIS
CRMO was first described by Giedion and
colleagues in 1972
Inflammatory bone disease characterized by
an insidious onset of mild-to-moderate pain
with signs of inflammation over the
affected parts, which tend to recur
often affects the metaphysis of long bones,
especially the tibia, femur, and clavicle

ETIOLOGICAL FACTORS
- Infectious disease : Propiobacterium acne
- Autoimmune Diseases : Psoriasis & IBD
- Genetic Predisposition : LPIN2 gene

- Nonspecific : pain, swelling, restricted
mobility
- Duration : from days to several years

INVETIGATIONS
- raised ESR & CRP with normal WBC
count
- Cultures : negative
- Biopsy : may be useful

PATHOLOGICAL CONDITIONSPATHOLOGICAL CONDITIONS
ASSO. WITH CRMOASSO. WITH CRMO
• - Palmoplantar pustulosis
• - Psoriasis
• -IBD ( Crohn’s disease & Ulcerative colitis)
• - SAPHO Syndrome( Synovitis, Acne,
Pustulosis, Hyperostosis, osteitis)
• - Majeed syndrome-( CRMO,Cong.
Dyserythropoetic anaemia, inflammatory
dermatosis)

- Wegner’s granulomatosis
- Takayasu’s arteritis
- Pyoderma gangrenosum
- Sweet syndrome(Febrile neutrophilic
dermatoses)
- Acne fulminans
-Spondyloarthropathy

TREATMENTTREATMENT
No effective treatment for CRMO available
Cases of disease remission after treatment with
IFN gamma have been reported
Resolution of symptoms followed by recurrence
months later is characteristic of this disease
Generally, the symptoms continue to recur over 2
years, and the disease generally is self-limiting
The long-term prognosis seems to be good

OSTEOMYELITIS AFTEROSTEOMYELITIS AFTER
PUNCTURE WOUND OF THEPUNCTURE WOUND OF THE
FOOTFOOT
Association of Pseudomonas osteomyelitis
with puncture wounds to the foot
Treatment consists of surgical drainage,
curettage when indicated, and appropriate
antibiotic treatment

OSTEOMYELITIS OF SPECIFICOSTEOMYELITIS OF SPECIFIC
REGIONSREGIONS
1) CALCANEUM
- Cancellous bone with thin periosteum
firmly adherent to the bone
- Periosteum is usually perforated
- destruction of the cortex is not extensive
-sequestrum formation is minimal

TREATMENT
- Gaenslen’s approach: through plantar
surface of heel

2) SPINE
• Commonly affects lumbar spine > thoracic
spine > cervical spine
• Usual site : vertebral bodies
• Simultaneous involvement of the 2 adjacent
vertebral end plates with intervening discs

ETIOLOGY
- richly vascular metaphyseal bone near
anterior longitudinal ligament
- avascular disc
- end arterial supply of interosseous artery in
adults

X Ray Findings
- disc space narrowing with end plate erosion
with vertebral body destruction
- vertebral end plate sclerosis with increased
density in subchondral bone
- spinal fusion

TREATMENT
- IV Antibiotics
- Rest
- Spinal immobilisation
- Surgery

3) DISTAL THIRD FEMUR
-Chronic osteomyelitis of the distal third of the
femur is difficult to treat. Because the periosteum
may become completely separated posteriorly by a
subperiosteal abscess, this part of the bone may
lose most of its blood supply, and sinuses often
persist
- A mass of scar tissue forms that interferes with
revascularization of the bone; the scar tissue is
relatively inaccessible surgically because of the
proximity of large vessels and nerves

4) ILIUM
1) Treatment during Acute Phase
-large subperiosteal abscesses develop on the medial and
lateral cortices
-Early symptoms may suggest acute appendicitis or pyogenic
arthritis of the hip joint
-Ghahremani reported a relatively high incidence of
osteomyelitis of the ilium in patients with Crohn disease
(granulomatous enteritis and colitis)
-He found it was necessary to resect the involved bowel
before the osteomyelitis could be cured

2) Treatment during chronic phase
-the entire bone often is involved
-infection is so diffuse that it is impossible to
remove the individual sequestra and drain all the
abscesses
-Because most of the iliac wing can be removed
without causing significant disability, resecting it
usually is preferable to less radical operations

4) ISCHIUM & PUBIS
-an abscess develops either beneath the external or internal
obturator muscles or in the ischiorectal fossa
-Osteomyelitis of the ischial tuberosity is common in
bedridden and paraplegic patients who develop pressure
sores with secondary infection, necrosis, and osteomyelitis
-Effective treatment requires debridement of all necrotic
tissue and infected bone, and a soft-tissue transfer usually
is required to close the defect

SPECIFIC TYPESSPECIFIC TYPES
TUBERCULOUS OM
- chronic granulomatous infection caused by
AFB
- usually secondary to primary elsewhere
- commonly involving metaphysis in children
& epiphysis in adults

- Tubercle follicle is formed of epitheloid cells,
lymphocytes, langhans giant cells with central
caseation necrosis with peripheral fibrosis by
fibroblasts in central portion of shaft
- Caseated pus extends peripherally forms
subperiosteal absces, enters soft tissue planes with
least resistance to infection as cold abscess

-swelling
- local tenderness
- muscle spasm
- cold abscess with chronic discharging sinus

INVESTIGATIONS
- Tubeculin test
- Biopsy :typical tubercles
- Blood : lymphocytosis
- X Ray: osteoporosis, loss of outline of
articular cortex, granular foci

TREATMENT
- Sinuses with sequestra : curretage &
excision
- AKT

To conclude the treatment of chronic
osteomyelitis should be in collaboration with
other specialities like infectious
disease,psychiatry,medicine,micro vascular
surgery,social work and physical and
occupational therapy.
However,even with access to these experts
and appropriate surgery,the success rate for
treatment of osteomyelitis is still significantly
less than 100%.
There is no doubt that prevention remains
the best overall strategy.

Seminar on chronic osteomyelitis sch

Seminar on chronic osteomyelitis sch

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