INFECTI

ON

APLEYS SYSTEM OF ORTHOPAEDICS AND FRACTURES

8TH EDITION

TEAM IV : IK, JS, TS, SF

ACUTE, SUBACUTE AND

CHRONIC OSTEOMYELITIS

GENERAL ASPECT OF INFECTION

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

GENERAL ASPECTS OF INFECTION

Acute pyogenic infections are characterized by:

The

formation of pus or abscess (Local effect)

a concentrate of defunct leucocytes, dead and dying
bacteria and tissue debris.
Spread further afield via lymphatics or via the
bloodstream (systemic effect)
causing lymphangitis and lymphadenopathy,
bacteraemia and septicaemia, with systemic reaction :
vatigue, mild pyrexia, severe illness, fever, toxaemia
and shock.

GENERAL ASPECT OF INFECTION

Chronic infection
follow

on acute infection or start from beginning

The formation of granulation tissue (a combination of
fibroblastic and vascular proliferation) fibrosis.

Host Response:
Age

of patient (very young or too old is more

resistance),
state of malnutrition,
immuno-supresan
other disease like diabetes

Local Factors :
damaged

muscle and foreign bodies

bone structure itself consist of collection of rigid
compartment make it more susceptible for vascular
damage and cell death..

GENERAL ASPECT OF INFECTION

The principles of treatment are:

(1)

to provide analgesia and general supportive

measures;
(2) to rest the affected part;
(3) effective antibiotic or chemotherapy; and
(4) surgical eradication of infected and necrotic
tissue.
For acute infections, the timing of surgery is allimportant: in the early stages, antibiotics should be
given a chance and the clinical condition carefully
monitored to detect signs of improvement or
deterioration; if there is pus, it must be let out and
the sooner the better.

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.

reactive new bone formation

resolution and healing.

NEW BONE FORMATION

New bone forms from the deep layers of the
stripped periosteum.
This is typical of pyogenic infection and is usually
obvious by the end of the second week. With rime
the new bone thickens to form an involucrum
enclosing the infected tissue and sequestra.
If the infection persists, pus and tiny
sequestrated splcules of bone may continue to
discharge through perforations (cloacae) in the
involucrum and track by sinuses to the skin
surfaces; the condition is now established as a
chronic osteomyelitis.

(A) INFECTION IN THE METAPHYSIS MAY SPREAD COWARDS THE

SURFACE, TO FORM A SUBPERIOSTEAL ABSCESS (B). SOME OF THE BONE
MAY DIE, AND IS ENCASED IN PERIO STEAL NEW BONE AS A
SEQUESTRUM (C).THE ENCASING INVOLUCRUM IS SOMETIMES
PERFORATED BY SINUSES.

RESOLUTION

Once common, chronic osteomyelitis following on

acute is nowadays seldom seen. If infection is
controlled and intraosseous pressure released at
an early stage, this dire progress can be aborted.
The bone around the zone of infection is at first
osteoporotic (probably due to hypcraemia).

CLINICAL FEATURES

The patient, usually a child,

presents with severe pain,
malaise and a fever; in
neglected cases, toxaemia
may be marked.
X-RAYS NORMAL DURING
FIRST 10 DAYS
Ultrasound may detect a
subperiosteal collection of
fluid in the early stages of
osteomyelitis, but it cannot
distinguish between a
haematoma and pus.

Radioscintigrapby with 99mTc-HDP reveals

increased activity in both the perfusion phase
and the bone phase.. It has relatively low
specificity and other inflammatory lesions can
show similar changes.
In doubtful cases, scanning with Ga-citrate or In
labelled leucocytes may be more revealing.
MRI is extremely sensitive, even in the early
phase of bone infection, and can help to
differentiate between soft-tissue infection and
osteomyelitis.
The most typical feature is a reduced intensity
signal in T1-weighted images.

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

Older children and fit adult : Staphylococcus

group
Flucloxacillin

and fusidic acid i.v 1 2 weeks

Orally antibiotics 3 6 weeks

Children < 4 years ; Haemophilus group and

gram negatife organisms
Cephalosporins

(cefuroxime or cefotaxime) i.v or orally

Amoxicillin-clavulanic acid combination (coamoxiclav, a -lactamase inhibitor)

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

circumscribed, oval or round cavity 1 2 cm in

diameter on tibia or femoral metaphysis or in
epiphysis or in cuboidal bone (calcaneus)
Cavity surrounded by halo of sclerosis (the classic
Brodies abscess)
Metaphysis lesion little or no periosteal reaction
Diaphysial lesion periosteal new bone formation
and cortical thickening

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

The usual organisms (and with time there is

always a mixed infection) are Staph. aureus, E.
coti, S. pyogenes, Proteus and Pseudomonas;
In the presence of foreign implants Staph.
cpidermidis, which is normally non-pathogenic, is
the commonest of all.

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.

CHRONIC OSTEOMYELITIS CHRONIC BONE INFECTION,

WITH A PERSISTENT SEQUESTRUM, MAY BE A SEQUEL TO
ACUTE OSTEOMYELITIS (A). MORE OFTEN IT FOLLOWS AN
OPEN FRACTURE OR OPERATION (B). OCCASIONALLY IT
PRESENTS AS A BRODIE'S ABSCESS (C).

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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YOU