CHRONIC OSTEOMYELITIS

NUR AINA BINTI AB KADIR

CONTENTS

Pathology

Intro-duction

Investigation

Treatment

Clinicalfeatures

Staging

INTRODUCTION Chronic pyogenic osteomyelitis Incidence is decline Other causes: tuberculosis, fungal

infections Types

Chronic osteomyelitis secondary to acute osteomyelitisGarre’s osteomyelitis

Brodie’s abscess

CHRONIC OSTEOMYELITIS Open fracture/operation Staphylococcus aureus Escherichia coli Streptococcus pyogenes Proteus mirabilis Pseudomonas aeruginosa Staphylococcus epidermidis (foreign

implants )

PREDISPOSING FACTORS COMMONEST: local trauma eg: open

fracture/ prolonged bone operation, foreign implant

Host defences: Scar formation Dead bone Blood vessel Bacteria covered in a protein-

polysaccharides slime (glycocalyx)

PREDISPOSING FACTORS Delayed and inadequate treatment Patient’s condition: Very old/debilitated Suffering from substance abuse Diabetes Peripheral vascular disease

PATHOLOGY Bone is destroyed or devitalized Cavities containing pus and pieces of dead

bone (sequestra) the result of chronic reactive new bone

formation – which may take the form of a distinct bony sheath (involucrum).

Sequestra act as substrates for bacterial adhesion

A sinus may seal off for weeks/ even months healing

CLINICAL FEATURES Pain,Pyrexia,Redness,Tenderness Discharging sinus Longstanding cases the tissues are

thickened and puckered or folded inwards where a scar or sinus adheres to the underlying bone.

Seropurulent discharge and excoriation of the surrounding skin.

Post-traumatic osteomyelitis: the bone may be deformed or ununited

IMAGING

X- ray Radio

Isotopescintigra

phy

CT scan MRI

IMAGING X-ray examination: bone resorption

patchy loss of density/frank excavation around an implant & thickening & sclerosis of the surrounding bone

Crudely thickened & mishappentumour Sinogram: help

IMAGING Radioisotope

scintigraphy Sensitive,not specific. 99mTc-HDP scans:

increased activity 67Ga-citrate or

111In-labelled leucocytes: specific for osteomyelitis hidden foci of infection.

CT and MRI the extent of bone destruction and reactive oedema, hidden abscesses sequestra.

Technetium Indium

INVESTIGATIONS Elevated CSR,ESR and WBC levels. Cultures of organisms- antibiotic

sensitivity- deep tissue Molecular technique- amplication of

bacterial DNA/RNA fragments(PCR), by gel electrophoresis

STAGING-ADULT

LESION TYPESTAGE 1 MEDULLARYSTAGE 2 SUPERFICIALSTAGE 3 LOCALIZEDSTAGE 4 DIFFUSE

TYPE A NORMALTYPE B COMPROMISED BY LOCAL/SYSTEMIC CONDITIONTYPE C SEVERELY COMPROMISED BY LOCAL AND SYSTEMIC

CONDITIONS

CATEGORY INTERPRETATION

Stage 1 or 2, Type A Least serious

Stage 1,2,3, Type B Have chance of recover

Type C Poor prognosis

Stage 4 Long term palliative care

TREATMENT

Antibiotic

Local treatment

Operation

ANTIBIOTIC To suppress the infection, prevent its

spread to healthy bone Control acute flares Choices: Microbiological studies Capable of penetration Non toxic for long-term use

ANTIBIOTIC Fusidic acid, clindamycin, cephalosporins Meticillin-resistant Stapyhlococcus aureus

infection (MRSA): vancomycin and teicoplanin

4-6 weeks –serum antibiotic concentration measurement

Surgical clearance failed continue for another 4w

Continuous collaboration with a microbiologist.

LOCAL TREATMENT Simple dressing Colostomy paste Acute abscess urgent incision &

drainage

OPERATION INDICATIONS chronic haematogenous infection intrusive symptoms failure of adequate antibiotic treatment evidence of a sequestrum post-traumatic and postoperative infections intractable wound and/or an infected

ununited fracture Presence of foreign implant

Debridement Dealing with the ‘dead space’ Soft tissue cover After care

Dealing with the ‘dead space’ Porous antibiotic-impregnated beads can

be laid in the cavityleft for 2/3 weeksreplaced with cancellous bone grafts.

Papineau technique: the entire cavity is packed with small cancellous chips mixed with an antibiotic and a fibrin sealantarea is covered by adjacent muscle & the skin wound is sutured without tension

Dealing with the ‘dead space’ Radical excision of all avascular and infected

tissue followed by closed irrigation and suction drainage of the bed using double-lumen tubes and an appropriate antibiotic solution in high concentration.

The spaces is gradually filled by vascular granulation tissue

Tubes is removedculture negative Refractory caseexcise the infected and/or

devitalized segment of bone completely and then close the gap by the Ilizarov method

DIFFERENTIAL DIAGNOSISTubercular

osteomyelitis •Thin& watery discharge•Often multifocal

Soft tissueinfection

•Absence of thickening of underlying bone•Absence of sinus fixed to the bone

Ewing’s sarcoma •Sudden onset of pain & swelling•Biopsy

GARRE’S SCLEROSING OSTEOMYELITIS

GARRE’S SCLEROSING OTEOMYELITIS

Rare form of non-suppurative osteomyelitis Marked sclerosis, cortical thickening No abscess, diffuse enlargement of the

bone at the affected site Adolescent and young adult Long history of aching and slight swelling

over the bone Recurrent attack of acute pain with malaise

and slight fever

X-RAY increased bone density and cortical

thickening some cases the marrow cavity is

completelly obliterated. There is no abscess cavity. Diaphysis and mandible

DIAGNOSIS If a small segment of bone is

involvedosteoid osteoma. If there is marked periosteal layering of

new boneEwing’s sarcoma. Biopsy: low-grade inflammatory lesion

with reactive bone formation Micro-organism culture: staphylococal

infection

TREATMENT Operation: the abnormal area is excised and the

exposed surface thoroughly curetted. Bone grafts, bone transport or free bone

transfer may be needed.

Also know as SUBACUTE HAEMATOGENOUS OSTEOMYELITIS

BRODIE’S ABSCESS

PATHOLOGY

well-defined cavity in cancellous bone – usually in the tibial metaphysis – containing glairy seropurulent fluid (rarely pus).

The cavity is lined by granulation tissue containing a mixture of acute and chronic inflammatory cells.

The surrounding bone trabeculae are often thickened.

The lesion sometimes encroaches on and erodes the bony cortex.

CLINICAL FEATURES

child or adolescent had pain near one of the larger joints for

several weeks or even months. Limp,slight swelling, muscle wasting and

local tenderness. The temperature is usually normal and there is little to suggest an infection. The WBC count and blood cultures usually

show no abnormality but the ESR is sometimes elevated

IMAGING

lesion is a circumscribed, round or oval radiolucent ‘cavity’ 1–2 cm in diameter. tibial or femoral metaphysis, but it may occur in the

epiphysis or in one of the cuboidal bones (e.g. the calcaneum).

Sometimes the ‘cavity’ is surrounded by a halo of sclerosis extending into the diaphysis.

Metaphyseal lesions cause little or no periosteal reaction; diaphyseal lesions may be associated with periosteal new bone formation and marked cortical thickening.

If the cortex malignant tumour.

DIAGNOSIS Clinical and x ray appearances may

resembles osteoid osteoma,cystic tuberculosis, eosinophilic granuloma

Biopsy If fluid is encountered: bacteriological

culture

TREATMENT Conservative Immobilization Antibiotic (flucloxacillin & fusidic acid) IV for 4-5 days Oral 6 weeks Diagnosis in doubt: open biopsy +

curettage Curettage: x-ray shows no healing after

conservative treatment

Apley’s System of Orthopaedics and Fracture ,11th edition, page 36-41

Essential orthopaedics by Maheshwari http://

reference.medscape.com/features/slideshow/osteomyelitis#page=7

http://radiopaedia.org/articles/osteomyelitis

REFERENCES