Osteomyelitis

Osteomyelitis

byDR. FARAN MAHMOOD

FCPS Ortho

Osteomyelitis is an acute or chronic inflammatory process of bone, bone marrow and its structure secondary to infection with micro organisms.

CLASSIFICATION

Duration - Acute / Subacute / Chronic

Mechanism - Heamatogenous (tonsil , lungs , ear/

GIT) - Exogenous (injection , open fractures)

Host response - Pyogenic / Granulomatous

Age : Infancy and childhood.Sex : Males predominate 4:1Location : Metaphysis of long

bone.Poor nutrition, unhygienic

surroundings.

ACUTE OSTEOMYELITIS

– sharp hairpin turns in metaphyseal capillaries

– flow becomes considerably slower and more turbulent

ACUTE OSTEOMYELITIS

Pathophysiology

Infection◦ Starts in Metaphysis

- Arteriole Loop / Venous Lakes◦ Spread via Volkman’s canal / Haversian

system◦ Endothelium Leaks

ACUTE OSTEOMYELITIS

PathophysiologyRole of growth plate

◦ Over 18/12◦ Impermeable to spread◦ Under 18/12 infection crosses growth plate

ACUTE OSTEOMYELITIS

Acute Osteomyelitis Infants

Joint involvement is common

Nutrient metaphyseal capillaries perforate the epiphyseal growth plate, particularly in the hip, shoulder, and knee.

ACUTE OSTEOMYELITIS

Etiological Agents Infants < 1 year – Group B streptococci Staph aureus E.coli

1- 16 years – S. aureus , S. pyogens , H. Influenza

> 16 years – S.aureus , S.epidermidis ,

Gram –ve bacteria

ACUTE OSTEOMYELITIS

Rare organisms Isolated in Bacterial Osteomyelitis

Bartonella henselae

Pasteurella multocida or Eikenella corrodens

Aspergillus species, Mycobacterium avium-intracellulare or Candidaalbicans

Mycobacterium tuberculosis

Brucella species, Coxiella burnetii(cause of chronic Q fever) or otherfungi found in specificgeographic areas

Human immunodeficiency virus infection

Human or animal bites

Immunocompromised patients

Populations in which tuberculosis is prevalent.

Population in which these pathogens are endemic

Pathogenesis

Introduction of bacteria from :

Outside through a wound or continuity from a neighboring soft tissue infection

Hematogenous spread from a pre existing focus (most common route of infection)

ACUTE OSTEOMYELITIS

Pathogenesis: Host Factors

PathogenesisPre-existing focus / Exogenous Infection

Infective embolus enters nutrient artery

Trapped in a vessel of small caliber(metaphysis) Blocks the vessel

Active hyperemia + PMN cells exudate

ACUTE OSTEOMYELITIS

Hyperemia and immobilization causes decalcification.

Proteolytic enzymes destroy bacteria and medullary elements.

The debris increase and intramedullary pressure increases.

ACUTE OSTEOMYELITIS

Follows paths of least resistance.

Passes through Haversian canal and Volkmann canal.

Local cortical necrosis.

ACUTE OSTEOMYELITIS

Enter subperiosteal space.

Strips periosteum.

Perforation of periosteum / reach joint by piercing capsule.

Enters soft tissue and may drain out

ACUTE OSTEOMYELITIS

Development of Osteomyelitis

CLINICAL FEATURESFever (High Grade)

Child refuses to use limb (pseudoparalysis)

Local redness , swelling , warmth , oedema

Newborn – failure to thrive , drowsy , irritable.

ACUTE OSTEOMYELITIS

Laboratory TestsElevations in the peripheral white blood cell

count (WBC),

Erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) in children with hematogenous osteomyelitis are variable and nonspecific.

Blood culture is positive in half of cases.

ACUTE OSTEOMYELITIS

X-ray findings

It takes from 10 to 21 days for an osseous lesion to become visible conventional radiography, because a 30–50% reduction of bone density must occur before radiographic change is apparent

ACUTE OSTEOMYELITIS

ACUTE OSTEOMYELITIS

Differential Diagnosis

Rheumatic fever : Onset is more gradual, pain and tenderness are less intense. Involvement is polyarticular. Response to salicylates and ACTH is dramatic.

Acute suppurative arthritis : Pain and tenderness are , limted to the joint, joint movements is greatly restricted, muscle spasm is intense, and aspiration reveals purulent synovial fluid.

ACUTE OSTEOMYELITIS

Management of acute osteomyelitis.ACUTE OSTEOMYELITIS

Drainage technique of acute Hematigenous Osteomyelitis of

tibiaUse tourniquet whenever possibe.Make an anteromedial incision 5 – 7.5 cm long

over the affected part of tibia. Incise periosteum longitudinally, gently elevate

the periostum 1.5 cm on each side. Drill several holes 4mm in diameter through the

cortex into the medullary cannal. If pus escapes through these holes, use drill to outline a corticle window 1.3 × 2.5 cm and remove the cortex with osteotome.

ACUTE OSTEOMYELITIS

Evavuate the intramedullary pus and remove the necrotic tissue.

Irrigate the cavity with at least 3 L of saline with a pulsatile lavage system.

Close the skin loosely over drains.Limb is splinted in neutral position.Generally 6 weeks course of antibiotics is

given.

ACUTE OSTEOMYELITIS

Complications of acute osteomyelitis

Bone abscessSeptic ArthritisSepticemiaFractureGrowth arrestOverlying soft-tissue cellulitisChronic infection

ACUTE OSTEOMYELITIS

Subacute Osteomyelitis

It has an insidious onset, mild symptoms, lack of systemic reaction

Its relative mildness is due to: a) Organism being less virulent

OR b) Patient more resistant OR

c) (Both)Most common site: Distal femur, Proximal &

Distal Tibia

Causative Organism

a) Staphyloccocus aureus (30-60%)b) Others (Streptococcus, Pseudomonas,

Haemophilus influenzae)c) Pseudomonas aeruginosa (IV drug user)d) Salmonella (patient with sickle cell

anaemia)

Clinical Features

Pain (several weeks / months)LimpingSwelling & Local tendernessMuscle wastingBody temperature usually normal (no fever)

Radiological Finding

Brodie’s abscessA circumscribed, round/oval cavity containing pus

and pieces of dead bone (sequestra) surrounded by sclerosis.

Most commonly seen in tibial / femoral metaphysis.

May occur in epiphysis / cuboidal bone (eg: calcaneum).

Metaphyseal lesion cause no / little periosteal reaction.

Diaphyseal lesion may be associated with periosteal new bone formation and marked cortical thickening.

A circumscribed, oval cavity surrounded by a zone of sclerosis at the proximal tibia (Brodie’s abscess)

This is a lateral view X-ray of left tibia and fibula. There is a marked periosteal reaction at the diaphysis.

Investigations

X-ray (may resemble osteoid osteoma / malignant bone tumour)

BiopsyFluid aspiration & cultureESR raisedWBC count may be normal

TreatmentConservative :a) Immobilizationb) Antibiotics (flucloxacillin + fusidic acid) for

6weeks

Surgical (if the diagnosis is in doubt / failed conservative treatment) :

c) Open biopsyd) Perform curettage on the lesion

Chronic Osteomyelitis

“ A severe, persistent and incapacitating infection of bone and bone marrow ”

CHRONIC OSTEOMYELITIS

Aetiological AgentsUsual organisms (with time there is always a

mixed infection)Staph.aureus(commonest)Staph.pyogenesE.coliPseudomonasStaph.epidermidis(commonest in surgical implant)Animal bites – pasturella multocidaHuman bites – eikenella corrodens


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Aetiology

Inadequately treated acute osteomyelitisHaematogenous spread IatrogenicPenetrating traumaOpen fractures


Clinical Features

Pain Pyrexia Redness Tenderness Discharging sinus (seropurulent

discharge)


Incidence of infection increases with increase in grade of open fractures (Guistilo, Anderson) :

◦ Approx. 2% for type I and type II◦ Approx. 10% to 50% for type III

The tibia most common site for infection.


PathogenesisInadequate treatment of acute OM /

Foreign implant /Open fracture

Inflammatory process continues with timetogether with persistent infection by

Staphylococcus aureus

Persistent infection in the bone leads to increase in intramedullary pressure due to

inflammatory exudates (pus)stripping the periosteum


Vascular thrombosis

Bone necrosis (Sequestrum formation)

New bone formation occur (Involucrum)

Multiple openings appear in this involucrum, through which exudates & debris from the

sequestrum pass via the sinuses(Sinus formation)



The involucrum is the sheath of reactive, new, immature, subperiosteal bone that forms around the sequestrum, effectively sealing it off the blood stream just like a wall of abscess.

The involucrum is irregular and is often perforated by openings.

The involucrum may gradually increase in density and thickness to form part or all of a new diaphysis.


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SEQUESTRUM

PERIOSTEAL NEW BONEFORMATION

INVOLUCRUM


INVOLUCRUM (the new bone)

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Staging Of Osteomyelitis:

The Cierny-Mader staging system.

It is determined by the status of the disease process.

It takes into account the state of the bone, the patient's overall condition and factors affecting the development of osteomyelitis.



The Cierny-Mader Classification

Medullary Osteomyelitis -

Infection confined to medullary cavity.

Superficial Osteomyelitis Contiguous type of infection. Confined to surface of bone.

Localized Osteomyelitis - Full-thickness cortical sequestration which can easily be removed surgically.

Diffuse Osteomyelitis -Loss of bone stability, even after surgical debridement.


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Classification (Cierny)

Type I Medullary cortical de-roofing and medullary debridement

Type II Superficial shallow decortication back to bleeding bone

Type III Localised saucerisation and debridement

Type IV Diffuse infected area excised en-bloc and stabilised with ex-fix


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Radiographic Findings1) X-ray examination- Usually show bone resorption (patchy loss of density /

osteolytic lesion)- Thickening & sclerosis around the bone (involucrum)- Presence of sequestra

2) Radioisotope scintigraphy- Sensitive but not specific- Technetium labelled hydroxymethylene diphosphonate

(99mTc-HDP) may show increased activity in both perfusion phase and bone phase

3) CT scan & MRI- Show the extent of bone destruction, reactive oedema,

hidden abscess and sequestra


Radiology

Plain xray◦ Specificity 75-83%◦ Sensitivity 43-75%

Soft tissue swelling 48hrs

Periosteal reaction 5-7d

Osteolysis 10d to 2 wks ◦ (need 50% bone loss)


AP & lateral view of the left wrist show a lobulated osteolytic lesion with well-defined borders and surrounding sclerosis at the distal radius. Minimal expansion, mild periosteal reaction and soft tissue swelling are present.


Bone scan Radioisotopic bone scanning is valuable in early

localization (within 48 hrs) of bone infection. The specificity of radioactive isotopic imaging

techniques have improved in the evaluation of musculoskeletal infection.

Technitium-99m imaging is very sensitive , it is the choice for acute hematogenous osteomyelitis, the overall accuracy being 92%.

Bone scan revealing hot spot in right tibia


MRI

Has very high sensitivity and specificity.

Advantage:◦ Useful for

differentiating between bone and soft-tissue infection.

◦ Helpful in surgical planning.

Disadvantage:◦ A metallic implant in

the region of interest may produce focal artifacts.

◦ False positives in tumors and healing fractures.

Plain film and MR images chronic osteomyelitis of right distal femur.

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f fibula

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

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 - Antibiotics

- Chronic infection is seldom eradicated by antibiotics alone.

- Bactericidal drugs are important to: a) Stop the spread of infection to healthy

bone b) Control acute flares

- Antibiotics used in treating chronic osteomyelitis

(Fusidic acid, Clindamycin, Vancomycin, Cefazolin)


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Antibiotic choice

Guided by microbiology departmentClindamycin (98% serum level) and

vancomycin(14% serum level) have good bone penetration

Minimum length 6 weeks with 3 months being the standard treatment course

May need to treat for 6-12 months


- Antibiotic (IV route) is given for 10 days prior to surgery.

- After the major debridement surgery, antibiotic is continued for another 6 weeks (min) but usually >3months.

[treat until inflammatory parameters (ESR) are normal]


Surgical Treatment

- After 10 days of antibiotic administration, debridement is done to remove:

a) All the infected tissue

b) Dead / devitalised bone (Sequestrectomy)

c) Sinus tract


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.

Closure of dead space- After debridement is done, a large dead space is left in

the bone- Among the methods of managing dead space:Open cancellous grafting – Papineau techniqueUseful for bone deficiencies of less than 4cm (preferably autogenous) mixed with an antibiotic and

fibrin sealantVascularised bone graftHeals as a segmental fracture Indicated when defect is > 6cm Iliac crest for defects > 8cmFibula 6-35cm can be bridgedBypass graft Involves the establishment of a cross union between the

fibula and tibia proximally and distally to the defect which has been debrided and bone grafted


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- Primary closure with transferred tissue: In muscle flap transfer, a suitable large wad of muscle with its blood supply intact can be mobilized and laid into the cavity. The surface is later closed with a split-skin graft

- Primary closure with antibiotic impregnated beads: Porous gentamicin-impregnated beads are used to sterilize the cavity. It is easier but less successful. Furthermore, they are extremely difficult to be removed if not taken out by 2-3 weeks


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A 46-year-old man with chronic osteomyelitis. The patient was treated with debridement followed by insertion of aminoglycoside-

impregnated methylmethacrylate beads and a local muscle flap.

Treatment algorithm of Cierny-Mader Stages-3 and 4 long-bone osteomyelitis.

OSEOMYELITIS & IMPLANT

OSEOMYELITIS & IMPLANT

In either case it is critical to preserve the involucrum preferable to wait at least 3-6 months before performing a sequestrectomy

Early sequestrectomy- Eradicate infection-Better environment for

periosteum to respond

Delayed sequestrectomy

Wait till sufficient involucrum has formed before doing a sequestrectomy to mimimize the risk of fracture, deformity & segmental loss

When to do sequestrectomy? CHRONIC OSTEOMYELITIS

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

ADEQUACY OF

INVOLUCRUM

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


Complications

1) Pathological Fracture- This occurs in the bone weakened by

chronic osteomyelitis2) Deformity

– In children the focus of osteomyelitis destroys part of the epiphysis growth plate.

3) Shortening/ lengthening- Destruction of growth plate arrest growth.- Stimulation of growth plate due to

hyperemia.


Osteomyelitis

Health & Medicine

turbulent acute osteomyelitis

apparent acute osteomyelitis

hematogenous osteomyelitis

subacute osteomyelitis

development of osteomyelitis

acute suppurative arthritis

pathophysiology infection

common route of infection