Osteomyelitis

Osteomyelitis
by
DR. FARAN MAHMOOD
FCPS Ortho
1

Osteomyelitis
is an acute or chronic inflammatory process of bone,
bone marrow and its structure secondary to infection
with micro organisms.
2

CLASSIFICATION
Duration
- Acute / Subacute / Chronic
Mechanism
- Heamatogenous (tonsil , lungs , ear/ GIT)
- Exogenous (injection , open fractures)
Host response
- Pyogenic / Granulomatous
3

 Age : Infancy and childhood.
 Sex : Males predominate 4:1
 Location : Metaphysis of long bone.
 Poor nutrition, unhygienic
surroundings.
4
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

Pathophysiology
 Role 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.
8
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
9
ACUTE
OSTEOMYELITIS

Rare organisms Isolated in Bacterial
Osteomyelitis
Bartonella henselae
Pasteurella multocida or Eikenella
corrodens
Aspergillus species, Mycobacterium
avium-intracellulare or Candida
albicans
Mycobacterium tuberculosis
Brucella species, Coxiella burnetii
(cause of chronic Q fever) or other
fungi found in specific
geographic 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)
11
ACUTE
OSTEOMYELITIS

Pathogenesis
 Pre-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

CLINICAL FEATURES
 Fever (High Grade)
 Child refuses to use limb (pseudoparalysis)
 Local redness , swelling , warmth , oedema
 Newborn – failure to thrive , drowsy , irritable.
18
ACUTE
OSTEOMYELITIS

Laboratory Tests
 Elevations 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.
19
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

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.
22
ACUTE
OSTEOMYELITIS

Management of acute osteomyelitis.
ACUTE
OSTEOMYELITIS

Drainage technique of acute
Hematigenous Osteomyelitis of tibia
 Use 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.
24
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.
26
ACUTE
OSTEOMYELITIS

 Bone abscess
 Septic Arthritis
 Septicemia
 Fracture
 Growth arrest
 Overlying soft-tissue cellulitis
 Chronic infection
27
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
28

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)
29

Clinical Features
 Pain (several weeks / months)
 Limping
 Swelling & Local tenderness
 Muscle wasting
 Body temperature usually normal (no fever)
30

Radiological Finding
Brodie’s abscess
 A 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.
31

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)
 Biopsy
 Fluid aspiration & culture
 ESR raised
 WBC count may be normal
33

Treatment
Conservative :
a) Immobilization
b) Antibiotics (flucloxacillin + fusidic acid) for 6weeks
Surgical (if the diagnosis is in doubt / failed conservative
treatment) :
a) Open biopsy
b) Perform curettage on the lesion
34

Chronic Osteomyelitis
“ A severe, persistent and incapacitating infection of
bone and bone marrow ”
35
CHRONIC OSTEOMYELITIS

Aetiological Agents
Usual organisms (with time there is always a mixed
infection)
 Staph.aureus(commonest)
 Staph.pyogenes
 E.coli
 Pseudomonas
 Staph.epidermidis
(commonest in surgical implant)
 Animal bites – pasturella multocida
 Human bites – eikenella corrodens
36

Aetiology
 Inadequately treated acute osteomyelitis
 Haematogenous spread
 Iatrogenic
 Penetrating trauma
 Open fractures
37

Clinical Features
 Pain
 Pyrexia
 Redness
 Tenderness
 Discharging sinus
(seropurulent
discharge)
38

 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.

Pathogenesis
Inadequate treatment of acute OM /
Foreign implant /
Open fracture
Inflammatory process continues with time
together 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
40

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)
41

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.

SEQUESTRUM
PERIOSTEAL NEW BONE
FORMATION
INVOLUCRUM

INVOLUCRUM (the new bone)
46

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.
47

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. 49

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
50

Radiographic Findings
1) 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
53

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

MR
I
 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.
Acaseofchronicosteomylitisoffibula

Sinograph
y
•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

Treatmen
t
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)
65

Antibiotic
choice
 Guided by microbiology department
 Clindamycin (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
66

- 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]
67

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
68

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 technique
 Useful for bone deficiencies of less than 4cm
 (preferably autogenous) mixed with an antibiotic and fibrin
sealant
Vascularised bone graft
 Heals as a segmental fracture
 Indicated when defect is > 6cm
 Iliac crest for defects > 8cm
 Fibula 6-35cm can be bridged
Bypass graft
 Involves the establishment of a cross union between the fibula
70

75
- 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

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.

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?

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
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
osteomyelitis
2) 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.
83

Osteomyelitis

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