OSTEOMYELITIS

DR SAGAR TOMAR

Llrm medical college,meerut,up

INTRODUCTION

Nelaton (1834) : coined osteomyelitis

The root words are

osteon (bone)

myelo (marrow)

these are combined with itis (inflammation) to

define the clinical state in which bone is infected

with microorganisms.

DEFINATION

Osteomyelitis is an inflammation of bone caused

by an infecting organism.

The infection may be limited to a single portion of

the bone or may involve numerous regions, such as

the marrow, cortex, periosteum, and the

surrounding soft tissue.

CLASSIFICATION

Attempts to classify are based on

(1) the duration and type of symptoms

(2)the mechanism of infection

(3)the type of host response

OSTEOMYELITIS

Acute: <2weeks Early acute

Late acute(4-5days)

Subacute: 2weeks—6weeks

Less virulent – more immune

Chronic: >6 weeks

Based on the duration and type of symptoms

CLASSIFIED ACCORDING TO MECHANISM

Osteomyelitis may be (waldvogel

classification)

1. Hematogenous (bacteremia)

2. contiguos (from adjacent root such

as open fracture or seeded implant)

3. chronic

BASED ON HOST RESPONSE

PYOGENIC

NON-PYOGENIC

ACUTE HEMATOGENOUS

OSTEOMYELITIS

Acute hematogenous osteomyelitis is the most

common type of bone infection and usually is seen

in children

It is caused by a bacteremia, which is a common

occurrence in childhood. Bacteriological seeding of

bone generally is associated with other factors such

as localized trauma, chronic illness, malnutrition, or

an inadequate immune system.

RISK FACTORS

Single pathogenic organism hematogenous osteomyelitis,

Multiple organisms direct inoculation or contiguous focus infection.

In infants:Staphylococcus

aureusStreptococcus

agalactiaeEscherichia coli

In children over one year of age:

Staphylococcus aureus, Streptococcus pyogenesHaemophilusinfluenzae1

adultsStaphylococcus aureus is

common organism isolated.

Etiology

Organism

Staphylococcus aureus

Coagulase-negative staphylococci or

Propionibacterium species

Enterobacteriaceae species

orPseudomonas aeruginosa

Streptococci or anaerobic bacteria

Salmonella species orStreptococcus

pneumoniae

Comments

Organism most often isolated in all types of

osteomyelitis

Foreign-body–associated infection

Common in nosocomial infections and punchured

wounds

Associated with bites, fist injuries caused by

contact with another person’s mouth, diabetic

foot lesions, decubitus ulcers

Sickle cell disease

Organisms Isolated in Bacterial Osteomyelitis

.

WHY STAPHYLOCOCCUS MOST COMMON?

S.aureus and S.epidermis ----- elements of normal skin flora

S.aureus -----increased affinity for host proteins (traumatised bone)

Enzymes (coagulase, surface factor A) ----- hampers hosts immuneresponse .

Inactive “L” forms ------dormant for years

“Biofilm” (polysaccharide “slime” layer) ---- increases bacterialadherence to any substrate .

Large variety of adhesive proteins and glycoproteins ----- mediatebinding with bone components.

BACTERIAL RESISTANCE BY BIOFILM

If a planktic bacteria (free floating bacteria )

encouters a suitable inert material such as dead or

necrotic tissue ,foreign bodies, or any avascular

body part either by direct contamination,contiguos

spreading or hematogenous apreading

It attaches itself via vander wall forces (irrevesible

crosslinks)

(devitalised bone devoid of periosteum presents

collagen matrix to which bacteia can attach

Bacteria now begin to produce

mucopolysaccharides layer over themselves

called BIOFILM OR SLIME

the bacteria begin to COLONISE

A colonised bacteria can remain viable: when(a) the inoculum is larger than threshold levels,

(b) host defense mechanisms are impaired,

(c) the tissue on which the bacteria colonize is traumatized (or necrotic),

(d) a foreign body is present, and

(e) the surface (or tissue) is acellular or inanimate (e.g., dead bone, cartilage,

and biomaterials)

After colonisation bacteria begin to develop into

mature colonies.these colonies are resistant to

antibiotics because

---antibiotics are unable to cross mucopolysaccaride layer

(glycocalyx)

---bacteria within slime are dormant or have decreased

metabolic rate and also undergo phenotypic changes active

process such as cell membrane formation which are targeted

by antibiotics would be decreased.

---antibiotic concentration of 1500 times normal is required to

penetrate both biofilm and bacterial cell wall

Illustration of the biofilm bacterial colonization process.

First, the bacteria need to find an inert surface (e.g., implant or

dead tissue). Implants or dead tissue that have been integrated by

the host with some type of surface are not inert and will resist

colonization. Then, the colonization process will continue until

mature colonies are formed. Once mature, the colonies can

change based on environmental signals or signals between

colonies.

PATHOLOGY:

the most common site is lower femoral metaphysis

Other sites- upper tibial

upper femoral

upper humeral metaphyis

PATHOGENESIS:

Direct inoculation of microorganisms into bone penetrating injuries and surgical contamination are most common causes

Hematogenous spreadusually involves themetaphysis of longbones in children or thevertebral bodies inadults

OsteomyelitisMicroorganisms in bone

Contiguous focus of infectionseen in patients with severevascular disease.

PATHOGENESIS

Whatever may be the inciting cause the bacteria reaches the

metaphysis of rapidly growing bone & provokes an inflammatory

response.

why metaphysis is involved

1. Infected embolus is trapped in U-shaped small end arteries located

predominantly in metaphyseal region

2. Relative lack of phagocytosis activity in metaphyseal region

3. Highly vascularised region ---minor trauma—hemorrhage ----locus

minoris resistantae---excellent culture medium

PATHOLOGY:

– sharp hairpin turns

– flow becomes considerably slower and

more turbulent

-- relatively fewer phagocytic cells than

physis and metaphysis

Medullary artery

Medullary vein

Hair pin

arrangemaent

PATHOLOGYThese are end-artery branches of the nutrient artery

Obstruction

Avascular necrosis of bone

tissue necrosis, breakdown of bone

acute inflammatory response due to infection

Squestra formation

Chronic osteomyelitis

THE INFLAMMATORY RESPONSE TO OSTEOMYELITIS:

Prostaglandin-E production has been shown to be five to thirty fold

higher in infected bone than in normal bone

postulated to be responsible for bone resorption and sequestrum

formation

Effective phagocytosis is defense in patients with osteomyelitis

Intramedullary oxygen tensions important for phagocytic function

oxygen tensions of <30 mm Hg impair normal phagocytic function

PATHOLOGY:

Pathologic features of chronic osteomyelitis are :

SEQUESTRUM is a devitalized avascular segment of bone, surrounded, by pus /infected granulation tissue and is more dense than surrounding bone .Because of avascularity , sequestrum does not decalcify , is more radio opaque and heavy , so sinks in waterIts outer surface is usually jagged / irregular due to erosive process by proteolytic enzymes in granulation tissue

Features: Dead piece of bone Pale Inner smooth ,outer rough Surrounded by infected granulation tissue trying to eat it Types-

ring(external fixator) tubular/match-stick(sickle) coke and rice grain(TB) Feathery(syphilis) Colored(fungal) Annular(amputation stumps)

PATHOLOGY:

Involucrum :is derived from the word “volvere” i.e. to wrap .It is

the result of reactive new bone formed by periosteal

reaction , in an attempt to wall off the infection by

forming a thick tense wall ,effectively sealing it off the blood stream just like a wall of abscess.

It is jagged on its inner surface but

smooth on its outer surface

Cloacae are single or multiple openings in involucrum and

are caused by rupture of periosteum due to pus

under tension .Exudates , sequestra are extruded

through the cloacae on the surface

CLINICAL FEATURES

calor, rubor, dolor, tumor

Heat, red, pain or tenderness, swelling

Initially, the lesion is within the medually cavity, there isno swelling, soft tissue is also normal.

The merely sign is deep tenderness.

Localized finger-tip tenderness is felt over or around themetaphysis.

it is necessary to palpate carefully all metaphysic areasto determine local tenderness,

DIAGNOSIS OF ACUTE OSTEOMYELITIS

PELTOLA AND VAHVANEN’S CRITERIA (if 2/4

are found)

1. Purulent material on aspiration of the affected

bone

2. Positive finding s of bone tissue or blood culture

3. Localised classic physical findings

a. bonny tenderness

b. overlying soft tissue edema ,erythema

4 Positive radiological imaging

DIAGNOSIS

LABORATORY DIAGNOSIS

Include - complete blood count

- erythrocyte sedimentation rate (ESR)

- C- reactive protein (CRP)

The white blood cell count will show a marked

leucocytosis as high as 20,000 or more

Peak elevation of the ESR occurs at 3 to 5 days

after infection and returns to normal approximately

3 weeks after treatment is begun.

ERYTHROCYTE SEDIMENTATION RATE

The ESR becomes elevated when infection is

present

Fractures or other underlying diseases can cause

elevation of the ESR.

The ESR also is unreliable in neonates, patients

with sickle cell disease, patients taking

corticosteroids, and patients whose symptoms have

been present for less than 48 hours

C-REACTIVE PROTEIN

CRP, synthesized by the liver in response to

infection, is a better way to follow the response of

infection to treatment.

CRP increases within 6 hours of infection, reaches

a peak elevation 2 days after infection, and returns

to normal within 1 week after adequate treatment

has begun

PLAIN RADIOGRAPH

The earliest changes are swelling of the soft tissue, periosteal thickening and/or elevation, and focal osteopenia.

The more diagnostic lytic changes are delayed and are associated with subacute and chronic osteomyelitis.

Osteoporosis is a feature of metabolically

active living bone; the segment that fails to

become osteoporotic is metablically inactive

and possibly dead.

Soft tissue swelling--- 1-3 days

Periosteal reaction---10-12 daysOsteomyelitis of the tibia of a

young child. Numerous

abscesses in the bone show as

radiolucency.

SINOGRAPHY:

Sinography can be performed if a sinus track

is present

Roentgenograms made in two planes after

injection of radiopaque liquid into sinus.

Helpful in locating focus of infection in

chronic osteomyelitis.

A valuable adjunct to surgical planning

RADIONUCLEOTIDE SCAN

The most common is 99mTc phosphate, which can

detect osteomyelitis within 48 hours after clinical

onset of infection.

The uptake of this compound is related primarily to

osteoblastic activity, although regional blood flow

also plays a role in skeletal uptake.

The three-phase bone scan consists of images

taken in

(1) the flow phase,

(2) the immediate or equilibrium phase

(3) the delayed phase

RADIONUCLEOTIDE SCAN

Flow phase- shows blood flow

Immediate or equilibrium - shows relative flow

and distribution of radio isotope into extracellular

matrix

Delayed phase-shows osteoblastic activity

Osteomyelitis shows increase uptake in all three

phase

MRI

MRI has very high sensitivity and specificity for the

diagnosis of osteomyelitis.

three types of images

T1 image- shows fat as a high bright signal

T2 image- shows water as a bright signal

STIR image – produced by suppressing the fat

signal

The classic findings of osteomyelitis on MRI are a

decrease in the normally high marrow signal on T1

images and a normal or increased signal on T2

images

MRI

The reported abnormal images reflect an increase

in water content, resulting from edema in the

marrow cavity. Marrow fat is replaced by edema

and cellular infiltrates that are lower in signal than

fat on T1 images and higher in signal than fat on T2

and STIR image

ULTRASONOGRAPHY

may detect a subperiosteal collection of fluid in

early stages of osteomyelitis.

To establish if joint effusion is present

To localise needle aspiration

CT SCAN

detecting smaller areas of cortical destruction,

Small foci of gas or foreign bodies,

sequestra formation (areas of necrotic bone separated by granulation tissue from living bone)

involucra (a layer ofliving bone that has formed along the sequestrum),

cloacae (an opening in the involucrum through which the sequestrum and granulation tissue may be discharged)

surrounding soft-tissue abscesses and

the replacement of the normal bone marrow fat with pus.

CULTURAL STUDIES

Key to the successful management of osteomyelitisis the isolation of the involved pathogens before the initiation of antibiotics in order to tailor optimal antimicrobial therapy

Cultures of superficial wounds or sinus tracks should not be relied on because they have been shown to be poor indicators of deep infection and usually are polymicrobial.

The preferred specimen in most bacterial and yeast infections is aspirated fluid (joint or purulent fluid). A deep wound biopsy or a curetted specimen after cleaning the wound is acceptable.

TREATMENT

1. General treatment: nutritional therapy or

general supportive treatment by intaking

enough caloric, protein, vitamin etc.

2. Antibiotic therapy

3. Surgical treatment

4. Immobilization

TREATMENT

NADE’S PRINCIPLES

1. an appropriate antibiotic will b effective before pus formation

2. Antibiotics will not sterilize avascular tissues or abscess and

such areas require surgical removal

3. If such removal is effective, antibiotics should prevent there

reformation and therefore primary wound closure should be

safe.

4. Surgery should not further damage already ischeamic bone

and soft tissue.

5. Antibiotics should be continued after surgery.

ANTIBIOTICS THERAPY

PATHOGEN FIRST LINE DRUG SECOND OPTIONS

OPERATIVE INDICATIONS

1. The presence of an abscess requiring drainage

2. Failure of the patient to improve despite

appropriate intravenous antibiotic treatment

COMPLICATIONS

Chronic osteomyelitis- 2% in >3wks, 19% in < 3wks

Septic arthritis

Growth disturbance

Septicemia

DVT

Pulmonary embolism

SUBACUTE OSTEOMYELITIS

This has a more incidious in onset and lacks the

severity of symptoms

Duration between 2-6 weeks

The indolent course of subacute osteomyelitis is

thought to be the result of increased host

resistance, decreased bacterial virulence, or the

administration of antibiotics before the onset of

symptoms

SUB ACUTE OSTEOMYELITIS CLASSIFICATION

Type Gledhill Classification Robert et al. Classification

I Solitary localized zone of

radiolucency surrounded by

reactive new bone formation

Ia—Punched-out radiolucency

Ib—Punched-out radiolucent

lesion with sclerotic margin

II Metaphyseal radiolucencies with

cortical erosion

—

III Cortical hyperostosis in diaphysis;

no onion skinning

Localized cortical and periosteal

reaction

IV Subperiosteal new bone and onion

skin layering

Onion skin periosteal reaction

V — Central radiolucency in epiphysis

VI — Destructive process involving

vertebral body

Anatomical type 1, central metaphyseal

lesion;

type 2, eccentric metaphyseallesion with cortical erosion;

type 3, diaphyseal cortical lesion;

type 4, diaphyseal lesion with periosteal new bone formation, but without definite bony lesion;

type 5, primary subacuteepiphyseal osteomyelitis; and

type 6, subacute osteomyelitiscrossing physis to involve metaphysis and epiphysis

TREATMENT

biopsy and curettage folllowed by treatment with

appropriate antibiotics

BRODIE’S ABSCESS

A Brodie abscess is a localized form of subacute

osteomyelitis that occurs most often in the long

bones of the lower extremities of young adult

Organisms of low virulence are believed to cause

the lesion. S. aureus is cultured in 50% of patients;

in 20%, the culture is negative.

The WBC count and blood culture usually shows no

abnormality but the ESR is sometimes elevated.

BRODIE’S ABSCESS

Bone abscess containing pus or jelly like granulation tissuesurrounded by a zone of sclerosis

Age 11-20 yrs, metaphyseal area, usually upper tibia or lowerfemur

Deep boring pain, worse at night, relieved by rest

On xray-Circular or oval luscency surrounded

by zone of sclerosis

Treatment:

Conservative if no doubt - rest + antibiotic for 6 wks.

if no response – surgical evacuation & curettage,

if large cavity - packed with cancellous bone graft

BRODIE’S ABSCESS

Brodie abscess. (A) AP radiograph of the femur

showing a lucent area (arrow) with cortical thickening

and sclerosis. (B) Axial CT image showing a central

sequestrum (arrowhead) and sinus tract (cloaca)

(arrows) leading through the thickened cortex.

CHRONIC OSTEOMYELITIS

Duration > 6 weeks

The hallmark of chronic osteomyelitis is infected

dead bone within a compromised soft tissue

envelope.(sequestrum)

The infected foci within the bone are surrounded by

sclerotic, relatively avascular bone covered by a

thickened periosteum (involcrum) and scarred

muscle and subcutaneous tissue.

This avascular envelope of scar tissue leaves

systemic antibiotics essentially ineffective

CIERNY AND MADER 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)

CLASSIFICATION

Cierny et al -

Includes four anatomic stages

Stage-1, or medullary,osteomyelitis is confined to themedullary cavity of the bone.

Stage-2, or superficial,osteomyelitis involves only thecortical bone.

Stage-3, or localized,osteomyelitis usually involvesboth cortical and medullary bonebut does not involve the entirediameter of the bone.

Stage-4, or diffuse, osteomyelitisinvolves the entire thickness ofthe bone, with loss of stability.

CLASSIFICATION

With this system, a patient with osteomyelitis is classified as an A, B,or C host.

An “A” host has no systemic or local compromising factors. Theyhave a normal response to infection and surgery.

A “B” host is affected by one or more compromising factors.

Bs-systemic compromise

Bl-local compromise

Bls-both sys and local compromise

are compromised and have deficient wound healing capabilities.

A “C” host is so severely compromised that the radical treatmentnecessary would have an unacceptable risk-benefit ratio

DIAGNOSIS

The diagnosis of chronic osteomyelitis is based on clinical, laboratory, and imaging studies.

The “gold standard” is to obtain a biopsy specimen for histological and microbiological evaluation of the infected bone.

Investigations

x ray

ct scan

sinogram

usg

mri

radionucleotide scan

TREATMENT

Involves

Antibiotic suppression

Surgical debridement

Reconstruction

Correct host morbidity

-control blood sugar level in diabetic

-smoking cessation

-treatment of liver or renal malfunction

-optimising nutrition

-treatment of chronic disease

SURGICAL INTERVENTION

Debridement-

- it includes sequestrectomy and curettage

- Removal of all sequestra ,purulent material,and scarred and necrotic tissue until the

PAPRIKA SIGN ( active punctate bleeding bone)

-

- It results in the formation of DEAD SPACE

- methods described to eliminate this dead space are

- (1) bone grafting with primary or secondary closure;

- (2) use of antibiotic PMMA beads as a temporary filler of the dead space before

reconstruction;

- (3) local muscle flaps and skin grafting with or without bone grafting;

- (4) microvascular transfer of muscle, myocutaneous, osseous, and osteocutaneous

flaps; and

- (5) the use of bone transport (Ilizarov technique).

SEQUETRECTOMY AND CURRETTAGE

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.

POST SEQUESTRECTOMY

NO STABLISATION IS

NECESSARY WHEN 70% OF

THE ORIGINAL CORTEX

REMAINS INTACT

If >70% cortical volume has

been retained—protect by cast

Greater bone loss-Ext fix

Focal bone loss-open

cancellous BG/conventional

BG

Seg. bone loss—BG/Bone

transport/other devices

Radiologically if cortical

continuity of the involucrum is

50% of the over all cortical

diameter on 2 orthogonal views

then the involucrum is

structurally adequate

SAUCERIZATION

Extension of surgical

debridement

Debrided wounds left open

widely through excision of

overhanging soft tissue and

bone

Wounds drain freely

Abscesses do not form

Limited to areas where it causes

acceptable loss of function e.g.

Tibia and femur

May require stabilization

saucerisation

BASIC METODS TO COVER DEAD SPACE

OPEN BONE GRAFTING

The Papineau technique involves local debridement

followed by a period of open management until a

healthy granulation tissue covers the wound base,

after which fresh autogenous cancellous graft is

packed into the defect, followed by frequent

dressing changes until the graft becomes

incorporated

THREE STAGE OPERATIONStage I: Débridement and Stabilization

Stage II: Grafting

Stage III: Wound Coverage

POLYMETHYLMETHACRYLATE ANTIBIOTIC BEAD

CHAINS

The antibiotic concentrationare 200 times higher

than levels achieved by systemic (I v)

administration

Advantage of achieving high local concentration

and while low serum concentration and low toxicity.

Short term implantation of 10 days to long term

implantation of 80 days as required

Aminoglycosides most commonly used , others are

penicillin, cephalosporins and clindamycin

Antibiotic

beads

BIODEGRADABLE ANTIBIOTIC DELIVERY

SYSTEM

Advantage over PMMA beads is that a secondary

procedure is not required to remove the implant.

Antibiotics are mixed with biodegradable substance

such as calcium sulfate or calcium phosphate to

produce reabsorbable beads or injectable filler

Reasobed in 8 weeks

CLOSED SUCTION DRAIN

Success rates of approximately 85% have been reported for the modified Lautenbach method of closed suction antibiotic ingress and egress irrigation systems

A more recent wound closure technique is negative pressure wound therapy (NPWT), which consists of a pump that generates a vacuum and is capable of creating a negative pressure environment within a sealed wound, dressing material used to pack and seal the wound, tubing for fluid removal from the wound area, and a container to collect waste materials removed from the wound

SOFT TISSUE TRANSFER

Soft tissue transfers to fill dead space left behind

after extensive débridement may range from a

localized muscle flap on a vascular pedicle to

microvascular free tissue transfer

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

ILIZAROV METHOD-

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.

ILIZAROV TECHNIQUE

A case of infected non-union of both bone leg managed by

ilizarov fixator application ,after bone transport the bone union is

acheived

HYPERBARIC OXYGEN THERAPY-HBO

- enhances oxygen-dependent leukocyte killing

through the production of hydrogen peroxide and

superoxide

- optimal tissue oxygen tension enhances

osteogenesis and neovascularization

Most wound healing patients receive one treatment

per day (20 MIN /DAY) for 20 – 30 days.

HYPERBARIC OXYGEN THERAPY

CHAMBER USED FOR HYPERBARIC OXYGEN

THERAPY

Culture Blood ± bone

Initial antibiotic selection

Change or confirm d/o culture results

Poor response

Operative treatment unroofing ,abscess

drainage, IM reaming

4 wks antibiotics

Failure

Retreat as

above

Arrest

Good response

Continue 2 wks parenteral & 4 wks

Oral antibiotics

Treatment algorithm of

Cierny-Mader Stage-1, or

hematogenous, long-

bone osteomyelitis.

Hardware removal

Bone stable

DEBRIDEMENT

INTRAMEDULLARY REAMING

AntibioticsContinue 2 wks

parenteral & 4 wks Oral

Failure

Retreat as above

Arrest

Bone unstable

Suppressive antibiotic treatment until stabilisation

Treatment algorithm of

Cierny-Mader Stage-1

long-bone

osteomyelitis

associated with

infection at the site of

hardware

Superficial debridement

Biopsy & culture

Initial antibiotic selection

Change or confirm based on culture results

Continue antibiotics for 2 wks

± Local MUSCLE

coverage

Treatment

algorithm of

Cierny-Mader

Stage-2 long-bone

osteomyelitis

Biopsy & Culture

Initial antibiotic selection

Change or confirm d/o culture results

6wks antibiotics after major operative

debridement

Failure

Retreat as above

Arrest

Debridement

Hardware removal

Dead space management, beads, bone grafts, & muscle

flaps

Stabilisation

external fixation

Ilizarov technique

Soft tissue coverage

Treatment

algorithm of

Cierny-Mader

Stages-3 and 4

long-bone

osteomyelitis.

OSTEOMYELITIS RELATED TO IMPLANT

FIRST CASE

HARDWARE REMOVAL

retain hardware

continue antibiotics until healed

HARDWARE STABLE

BONE NOT HEALED

IMPLANT RELATED OSTEOMYELITIS

SECOND CASE

remove hardware, antibiotics, temporary stabilization, spacer, and reconstruction when clean

Hardware unstable + bone not healed =

THIRD CASE

remove hardware, debride with effort not to destabilize, control

dead space, and antibiotics

Hardware stable + bone healed

FOURTH CASE

remove hardware, temporary stabilization, spacer, antibi-otics, and

reconstruction when able.

Hardware stable + bone not healed + systemic effects

Consider amputation if unsuitable hostConsider amputation if unsuitable host

CHRONIC MULTIFOCAL OSTEOMYELITIS

In the 1970s it was noted that a number of children

presented with a low-grade form of bone disease that

behaved clinically like an acute osteomyelitis.

Typically it affected the long bones and went on to a

sclerotic reaction. The first episode would settle and

some months or even a few years later there would

be recurrence at another site.

No organisms are grown and the course of the

disease becomes chronic and relapsing.

The clinical importance is to avoid repeated

biopsy once the relapsing nature of the

condition has been recognized.

Plain radiographs are essential to recognize the

bone infection.

Skeletal scintigraphy is a good method of

screening for other lesions

whilst MRI is the best means of judging extent

and activity

SCLEROSING OSTEOMYELITIS OF GARRÉ

A rare type of osteomyelitis occuring in children and

young adults presenting with insidious onset of

pain, pyrexia and swelling.

Symptoms recur at intervals for several years and

subside graudlly . .

Radiological appearance is of intense sclerosis

resulting in thickned bone.

There is predilection for involvement of mandible

and shaft of long bones.

SALMONELLA OSTEOMYELITIS

Subacute form

More commonly in children with sickle cell anaemia

Occurs during the convalescent phase after an

attack of typhoid fever

Mutiple bones are affected ,bilaterally symmetrical

Radiologically- diaphyseal sclerosis

Salmonella osteomyelitis

Bone destruction of radial shaft and dense sequestrum (arrow)

TUBERCULOUS OSTEOMYELITIS

Tuberculous bone infection occurs secondarily

as a resolt of hematogenous spread from a

primary source such as lung or genitourinary

tract.

Bone infection is most typically slow growing

and indolent. Tuberculous ‘caries’ is seen where

the margin of the bone is scalloped and eaten

away. Large ‘cold’ abscesses occur. This means

that the patient is surprisingly well given the

size of the collection

Little or no surrounding reactive bone with presence of

osteopenia

Affects epiphysis, metaphysis and diaphysis.

Eccentric area of osteolysis is seen in metaphysic

Transepiphyseal spread of lytic lesion

No sequestrum formation is seen.

Occasionally, destruction in the mid diaphysis of a short

tubular bone of the hand or foot(tuberculous dactylitis)

may produce a fusiform enlargement of the entire

diaphysis is called as spina vetosa.

M. tuberculosis. Sagittal T1-weighted (A) and T2-weighted (B) MR

images showing bone erosions and a large inhomogeneous

posterior soft tissue abscess

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