ETIOLOGY

acute hematogenous osteomyelitis

subacute osteomyelitis
chronic osteomyelitis

osteomyelitis
Osteomyelitis may occur at any age.
Most common in ages 3-12 years.
It affected boys twice frequently as girls .
A microbial ethiology is confirmed in three
fourth of osteomyelitis and two thirds of
cases of septic joint

pathogenesis

1. Hematogenous
2. Direct spread from a contiguous focus of
infection.
Osteomylitis in children is most often the
consequence of bacterremia.

Pathogenesis

(con)

involves growing bone . Particularly the

metaphyses of the long bone .
Femur and tibia are equally and together almost
half of the all cases .
(distal femur , proximal tibia ,distal humerus ,
distal radius)

Pathogenesis

(con)

Bacteria lodge in nutrient arteries supplying the

growth plates of bones.
Blood in the large sinusoidal veins flows slowly
No phagocytic cells present in this area.
Obstruction of flow by bacterial microemboli
produces small areas of avascular necrosis and
metaphyseal abscess .

1. Bacteria lodge in nutrient arteries supplying the

growth plates of bones.
2. Blood in the large sinusoidal veins flows slowly.
No phagocytic cells present in this area.
3. obstruction of flow by bacterial microemboli
produces small areas of avascular necrosis and
metaphyseal abscess .

pathogenesis

(con)

Trauma often is noted before the onset of

osteomyelitis. (in about one third)

Chronic osteomyelitis
Involucrum:
Infected periosteum calcify into a shell of new bone
around the infected portion of the shaft .
Brodie abscess: a subacute intraosseous
abscess that does not drain into the subperiosteal
space and is classically located in the distal tibia

Sequestrum:

portions of avascular bone that have

separated from adjacent bone, frequenrly are covered
with a thickened sheat

Contiguous osteomyelitis

Less common in children

Usually occur after the spread of cellulitis as a
result of Infected wound .
osteomyelitis also may result from direct
inoculation of a penetrating wound

Primary viral infection of bones or joints are rare

etiology
S.aureus is responsible for most infections in
all age groups.
Group B ( neonate) or other streptococci(A)
and pneumococcus , anaerobic
microorganism , gram-negative entric bacteria,
M,tuberculosis .
furunculosis , infected burns ,varicella, trauma,
drug abuse ,prolong IV or central parenteral
alimentation

etiology
Sickle cell anemia :
( salmonella , staphylococcus and less common
S.pneumonia)
Cat or dog bite ( pasteurella multocida)
Puncture wounds ,IV drug abuse (pseudomonas)
H,influ type b account for more than half of all case
but is rarely seen in an immunized population .

Clinical manifestations
Hematogenous osteomylitis usually involves a
single bone.
The most common presenting complaints are
focal pain, exquisite point tenderness over the
bone, warmth, erythema, swelling, and
decreased use of the affected extremity.
Fever, anorexia, irritability, and lethargy may
accompany the focal findings.

Clinical manifestations
Weight bearing and spontaneous or requested
motion are refused .( pseudoparalysis)
Hematogenous vertebral osteomyelitis is
insidious onset. With little fever or systemic
toxicity.
Pelvic osteomyelitis present with limp
,abdominal, hip ,groin ,pain and fever

Clinical manifestations
Neonate 40% multiple site

1-24 mo

2-20 yr

long bones
involve joints

local edema
reduced limb motion
joint effusion (60-70)
pseudoparalysis
fever,limp

metaphysis of
focal pain+ fever (90%)
long bones
focal tenderness (70%)
rarely vertebral joint effusion (20%)
pelvis

GBS,E coli
S,aureus

S,aureus
GBS

S,aureus(60-90%)
strep(10%)

diagnosis
Marked tenderness over the involved site.
leukocytosis may be present , ESR , CRP
Blood culture ( 60% positive).
Cultures of aspirated cellulitis or priosteal space
before antibiotic therapy.

diagnosis
Radiography :
finding of acute systemic osteomyelitis, at about 9 days, is
loss of the periosteal fat line
Periosteal elevation and periosteal destruction are later
findings
technetium 99m bone scans .
MRI is particularly useful for extended of infection or
when infection is a complication of trauma , surgery, sickle
cell anemia

treatment
Initial IV antibiotic should be based on result of
Gram stain of bone aspiration ,blood culture, age
associated disease.
Initial IV antibiotic should cover S.aureus
(oxacillin,nafcillin methicillin, clindamycin)
Possibility of methicilin resistant staph should
be considered .
Gram- negative organism if wound contamination
or IV drug abuse .

treatment ( con)
sickle cell anemia S.aureus and salmonell must be
covered (cefotaxim ,ceftriaxon)
The response to appropriate IV antibiotic usually
occur in 48 hr .
Lack of improvement in fever and pain after this
time indicates that surgical drainage may be
necessary or an unusual pathogen may be present .

Treatment ( con)
surgical drainage may be appropriate at earlier
time if :
1.
sequestrum is present
2.
disease is chronic or atypical
3.
the hip joint is involved
4.
Presence of spinal cord compression.
standard therapy usually consist of antibiotic for 4-6 weeks

 After initial inpatient treatment and a

good clinical response, including
decreases in CRP or ESR,
consideration may be given for home
therapy with IV antibiotics or oral
antibiotics,

o.M distal radius

O.M forearm salmonella type C