Infecti ON: Acute, Subacute and Chronic Osteomyelitis
Infecti ON: Acute, Subacute and Chronic Osteomyelitis
Infecti ON: Acute, Subacute and Chronic Osteomyelitis
ON
Micro-organisms
enter the bones and
joints :
: a break in
the skin (a pinprick, a
stab wound, a
laceration, an open
fracture or an
operation)
indirectly via the blood
stream from a distant
site:
the nose or mouth, the
respiratory tract, the
bowel or the genitourinary tract.
directly
Chronic infection
follow
Host Response:
Age
Local Factors :
damaged
ACUTE HAEMATOGENOUS
OSTEOMYELITIS
Acute osteomyelitis is almost invariably a disease
of children.
This predilection for the metaphysis has been
attributed to the peculiar arrangement of the
blood vessels in that area: the non-anastomosing
terminal branches of the nutrient artery twist
back in hairpin loops before entering the large
network of sinusoidal veins; the relative vascular
stasis favours bacterial colonization.
In young infants, in
whom there is still a
free anastomosis
between metaphyseal
and epiphyseal blood
vessels, infection can
just as easily lodge in
the epiphysis
In adults,
haematogenous
infection is more
common in the
vertebrae than in the
long bones.
PATHOLOGY OF
ACUTE OSTEMYELITIS
Inflammation
acute inflammatory reaction,
vascular congestion, exudation of
fluid, infiltration of PMN, increase of
intraosseus pressure
Suppuration
Subperiosteal abscess, end plate and
intervertebral disc infection
Necrosis
avascular necrosis of growth
plate in infant. Bacterial toxins
and leucocytic enzymes also may
play their part in the advancing
tissue destruction.
RESOLUTION
CLINICAL FEATURES
INVESTIGATIONS
The most certain way to confirm the clinical
diagnosis is to aspirate pus from the metaphyseal
subperiosteal abscess or the adjacent joint.
The white cell count and C-reactive protein
values are usually high and the haemoglobin
concentration diminished; the ESR also rises but
it may take several days to do so and it often
remains elevated even after the infection
subsides.
Blood culture is positive in only about half the
cases of proven infection.
DIFFERENTIAL DIAGNOSIS
Cellulitis
Streptococcal necrotizing myositis
Acute suppurative arthritis
Acute rheumatism
Sickle-cell crisis
Gaucher's disease
TREATMENT
Supportive treatment for pain and dehydration;
Splintage of the affected part;
Antibiotic therapy 3 6 weeks; and
Surgical drainage
ANTIBIOTIK TREATMENT
SUBACUTE OSTEOMYELITIS
Relative mildness
The organism being less
virulent (Staphylococcus
aureusor ) and the
patient more resistance
(or both);
More variable in skeletal
distribution than acute
osteomyelitis
The Distal femur and the
proximal and distal tibia
are favorite sites.
PATHOLOGY
Well defined cavity in cancellous bone glairy
seropurulent fluid (rare pus)
Cavity is lined by granulation tissue of mixture of
acute and chronic inflammatory cells.
The surrounding bone trabeculae are often
thickened
CLINICAL FEATURES
The patient : child or adolescent
Pain near one of the larger joints for several
weeks or even months
A limp or slight swelling, muscle wasting and
local tenderness
Normal temperature to slight higher
White cell count may be normal but ESR is
raised
IMAGING
Plain X-Ray
A
Radioisotope scan
DIAGNOSIS
Differential diagnosis : Osteoid osteoma with
appearance as malignant bone tumour
Certain examination by Biopsy for bacteriological
culture.
TREATMENT
Conservative
Immobilization and antibiotics (flucloxacillin and
fusidic acid) for 6 weeks than thereafter for 6
12 months
Curretage; indicate for lesion after biopsy and
also for the case with no healing with
conservative treatment. Antibiotics
CHRONIC
OSTEOMYELITIS
PATHOLOGY
Bone is destroyed or devitalized in a discrete area
at the focus of infection or more diffusely along
the surface of a foreign implant.
Cavities containing pus and pieces of dead bone
(sequestra) are surrounded by vascular tissue,
and beyond that by areas of sclerosis -the result
of chronic reactive new bone formation. The
sequestra act as substrates
The histological picture is one of chronic
inflammatory cell infiltration around areas of
acellular bone or microscopic sequestra.
CLINICAL FEATURES
The patient presents because pain, pyrexia,
redness and tenderness have recurred (a 'flare'),
or with a discharging sinus.
In long-standing cases the tissues are thickened
and often puckered or folded in where a scar or
sinus is attached to the underlying bone.
There may be a sero-purulent discharge and
excoriation of the surrounding skin.
In post-traumatic osteomyelitis the bone may be
deformed or non-united.
IMAGING
X-ray examination
Bone resorption with thickening and sclerosis of
surrounding bone, loss of trabeculation, area osteoporosis,
periosteal thickening, sequestra, or the bone crudely
thickened and misshapen
Radioisotope scintigraphy
Sensitive but not specific. Using 99m Tc-HDP for showing
increased activity of perfusion and bone phase and 67 GaCitrate or In-labelled leucocytes for showing hidden foci of
infection
CT and MRI
Show the extent of bone destruction and reactive edema,
hidden abscess and sequestra
INVESTIGATIONS
ESR and blood white cell
count may be increased;
are helpful in assessing the
progress of bone infection but
they are not for diagnostic.
Organisms cultured from
discharging sinuses should be
tested repeatedly for
antibiotic sensitivity; with
time, they often change their
characteristics and become
resistant to treatment.
TREATMENT
Antibiotics ; Fucidic acid,
clindamycin and
cephalosporins
Local treatment : incision
and drainage
Operation
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