osteomyelitis
DESCRIPTION
A BRIEF OVERVIEW OF BACTERIAL BONE INFECTIONTRANSCRIPT
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Osteomyelitis
byDR. FARAN MAHMOOD
FCPS Ortho
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Osteomyelitis is an acute or chronic inflammatory process of bone, bone marrow and its structure secondary to infection with micro organisms.
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CLASSIFICATION
Duration - Acute / Subacute / Chronic
Mechanism - Heamatogenous (tonsil , lungs , ear/
GIT) - Exogenous (injection , open fractures)
Host response - Pyogenic / Granulomatous
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Age : Infancy and childhood.Sex : Males predominate 4:1Location : Metaphysis of long
bone.Poor nutrition, unhygienic
surroundings.
ACUTE OSTEOMYELITIS
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– sharp hairpin turns in metaphyseal capillaries
– flow becomes considerably slower and more turbulent
ACUTE OSTEOMYELITIS
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Pathophysiology
Infection◦ Starts in Metaphysis
- Arteriole Loop / Venous Lakes◦ Spread via Volkman’s canal / Haversian
system◦ Endothelium Leaks
ACUTE OSTEOMYELITIS
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PathophysiologyRole of growth plate
◦ Over 18/12◦ Impermeable to spread◦ Under 18/12 infection crosses growth plate
ACUTE OSTEOMYELITIS
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Acute Osteomyelitis Infants
Joint involvement is common
Nutrient metaphyseal capillaries perforate the epiphyseal growth plate, particularly in the hip, shoulder, and knee.
ACUTE OSTEOMYELITIS
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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
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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
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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
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Pathogenesis: Host Factors
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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
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Hyperemia and immobilization causes decalcification.
Proteolytic enzymes destroy bacteria and medullary elements.
The debris increase and intramedullary pressure increases.
ACUTE OSTEOMYELITIS
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Follows paths of least resistance.
Passes through Haversian canal and Volkmann canal.
Local cortical necrosis.
ACUTE OSTEOMYELITIS
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Enter subperiosteal space.
Strips periosteum.
Perforation of periosteum / reach joint by piercing capsule.
Enters soft tissue and may drain out
ACUTE OSTEOMYELITIS
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Development of Osteomyelitis
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CLINICAL FEATURESFever (High Grade)
Child refuses to use limb (pseudoparalysis)
Local redness , swelling , warmth , oedema
Newborn – failure to thrive , drowsy , irritable.
ACUTE OSTEOMYELITIS
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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
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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
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ACUTE OSTEOMYELITIS
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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
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Management of acute osteomyelitis.ACUTE OSTEOMYELITIS
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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
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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
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Complications of acute osteomyelitis
Bone abscessSeptic ArthritisSepticemiaFractureGrowth arrestOverlying soft-tissue cellulitisChronic infection
ACUTE OSTEOMYELITIS
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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
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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)
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Clinical Features
Pain (several weeks / months)LimpingSwelling & Local tendernessMuscle wastingBody temperature usually normal (no fever)
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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.
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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.
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Investigations
X-ray (may resemble osteoid osteoma / malignant bone tumour)
BiopsyFluid aspiration & cultureESR raisedWBC count may be normal
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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
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Chronic Osteomyelitis
“ A severe, persistent and incapacitating infection of bone and bone marrow ”
CHRONIC OSTEOMYELITIS
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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
CHRONIC OSTEOMYELITIS
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Aetiology
Inadequately treated acute osteomyelitisHaematogenous spread IatrogenicPenetrating traumaOpen fractures
CHRONIC OSTEOMYELITIS
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Clinical Features
Pain Pyrexia Redness Tenderness Discharging sinus (seropurulent
discharge)
CHRONIC OSTEOMYELITIS
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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.
CHRONIC OSTEOMYELITIS
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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
CHRONIC OSTEOMYELITIS
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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)
CHRONIC OSTEOMYELITIS
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CHRONIC OSTEOMYELITIS
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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.
CHRONIC OSTEOMYELITIS
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SEQUESTRUM
PERIOSTEAL NEW BONEFORMATION
INVOLUCRUM
CHRONIC OSTEOMYELITIS
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INVOLUCRUM (the new bone)
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CHRONIC OSTEOMYELITIS
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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.
CHRONIC OSTEOMYELITIS
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CHRONIC OSTEOMYELITIS
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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.
CHRONIC OSTEOMYELITIS
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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
CHRONIC OSTEOMYELITIS
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CHRONIC OSTEOMYELITIS
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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
CHRONIC OSTEOMYELITIS
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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)
CHRONIC OSTEOMYELITIS
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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.
CHRONIC OSTEOMYELITIS
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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
CHRONIC OSTEOMYELITIS
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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
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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
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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
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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)
CHRONIC OSTEOMYELITIS
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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
CHRONIC OSTEOMYELITIS
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- 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]
CHRONIC OSTEOMYELITIS
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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
CHRONIC OSTEOMYELITIS
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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.
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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
CHRONIC OSTEOMYELITIS
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CHRONIC OSTEOMYELITIS
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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
CHRONIC OSTEOMYELITIS
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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.
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Treatment algorithm of Cierny-Mader Stages-3 and 4 long-bone osteomyelitis.
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OSEOMYELITIS & IMPLANT
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OSEOMYELITIS & IMPLANT
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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
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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
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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.
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