BONE AND JOINT

INFECTIONS
 BONE AND JOINT
INFECTIONS
EXOGENOUS

OPEN FRACTURES

POST-OPERATIVE
HAEMATOGENOUS

SPECIFIC( TB,…)
NON-SPECIFIC
IN BONES 
OSTEOMYELITIS (OM)
IN JOINTS 
SYNOVITIS … ARTHRITIS
 ACUTE
HEMATOGENOUS
OSTEOMYELITIS
 ACUTE HEMATOGENOUS OSTEOMYELITIS

Age group:

Acute hematogenous osteomyelitis

is almost a disease of
children.
When adults are affected it is usually because of
defective immunity
by debility, disease or drugs, e.g. Diabetes mellitus,AIDS,…
.
Trauma
may determinethe site of infection , possibly by
causing a fluid collection or a small hematoma
Causative organisms:
1)Staph aureus…. Most common
2)Strept pyogenes
3)Strept pneumonaie
4)Haemophilus influenzae(5-50% in children under 4 years)
5)Salmonella (common in patients with Sickle cell anaemia)
6)Others ; gram negative and anaerobic organisms)

Source and Route of infection:

In children,blood stream may be invaded from a minor skin
abrasion, boil, a septic tooth or infected umbilical cord.
In adults entry could be through an indwelling catheter,
arterial line or contaminated syringe.
Sites of infection:
Usually in the metaphysis,
mostly in proximal tibia or distal
and proximal ends of femur.
This predilection to the metaphysis is
due to its peculiar vascular pattern:
the non- ananstmosing terminal
branches of the nutrient artery twist
back in hair –pin loops
before entering the sinusoidal veins
causing relative vascular stasis.

In adults, hematogemous infection is

more common in vertebrae than in
long bones.
PATHOLOGIC STAGES OF
OSTEOMYELITISM
*ACUTE
*SUBACUTE
*CHRONIC
Pathology :
ACUTE
1)Inflammation
2)Suppuration :
Intra-osseous abscess
Sub-periosteal abscess
3)Resolution(with ttt)
or  Subacute
CHRONIC
1)Bone necrosis 
Sequestrum
2)New bone
formation 
Involucrum
3)Cavity,discharging
sinus  Cloaca
Clinical picture of acute OM:
General :
Typically the child looks ill
feverish.
Pulse>100
Infants fail to thrive, drowsy but irritable.
In neglected cases, toxemia may be
marked.
Local :
The limb is held still(Pseudo-paralysis)
there is acute tenderness near a major joint;
joint movement becomes restricted.
Local swelling and redness are late signs and
indicate that pus escaped from the interior of the bone.
Diagnostic imaging:
Plain X-ray
- Shows no abnormality of the bone before the second week
- After 2 weeks,there may be a faint extra cortical line due
to periosteal new bone formation.
- An important late sign is a combination of regional
osteoporosis with a localized segment of increased density.
U.S:
- may detect subperiosteal collection but cannot differntiate
between pus and hematoma
MRI
- is extremely sensitive even in the early phases of bone infection
RADIOACTIVE ISOTOPE SCAN
- sensitive even in the early phases of bone infection  Hot spot
Investigations:

1)The most certain way is to aspirate pus from the

metaphyseal subperiosteal abscess or adjacent joint

2)Elevated WBC count, C reactive protein and ESR

3)Blood culture: +ve in 50% of cases

N.B: osteomyelitis in an unusual site or unusual

organism should alert to the possibility of
heroin addiction, deficient immunity or sickle
cell anaemia.
Differential diagnosis:

1)Cellulitis .

2) Acute suppurative arthritis.

3) Acute rheumatic arthritis.

4) Sickle cell crisis .

5) Streptococcal necrotizing myositis.

Treatment :
Once osteomyelitis is suspected,
blood and fluid samples should be taken,
then treatment is started immediately before
confirmation of the diagnosis.
Patient should be admitted to hospital
1)Supportive treatment: Antipyretics –analgesics
2)Splintage : Rest – prevent joint contracture
3)Antibiotics : Start imperically then according to lab
investigations. Start with parentral (I.V.) treatment till
CRP returns to normal values,then continue oral
therapy for 3-6 weeks
4)Drainage : If clinical features don’t improve within
36 hours of starting treatment or even earlier if
there are signs of deep pus (redness-
hotness-swelling)
Follow-up
Once signs of inflammation subside,
movements are encouraged.
Full weight bearing is possible after 3-4
weeks.
Complications :
1)Metastatic infection:
Involving others bones, joints, serous cavities,
brain or lung.
2)Suppurative arthritis:
A-In young patients before closure of the epiphysis
B-Intracapsular metaphysis;e.g. head of femur
C-Metastatic infection
3)Altered bone growth:
In infants with physeal damage
4)Chronic osteomyelitis:
In neglected cases or immune-compromised
patients.
Subacute hematogenous osteomyelitis
Age :
Usually childhood and adolescence.
Pathology :
- Common sites include metaphyseal areas of distal
femur and proximal and distal tibia.
-There is a well defined cavity in the cancellous bone,
containing sero-purulent fluid (rarely pus).
-The cavity is lined by granulation tissue containing a
mixture of acute and chronic inflammatory cells.
-The surrounding bone trabeculae are often thickened.
Clinical picture:
Patient complains of pain near one of the big joints for
several weeks.
There may be a limp, slight swelling, muscle wasting
and local tenderness.
Patient may present with pathological fracture

Imaging :
Well circumscribed round or oval cavity,1-2 cm in
diameter.
Sometimes surrounded by a halo of sclerosis
[Brodie’s abscess];
Metaphyseal lesions cause little or no periosteal
reaction , yet diaphyseal lesions may be associated with
periosteal reaction and marked cortical thickening
Investigations :
WBC count may be normal, but ESR and CRP are
often elevated.

Treatment :
Immobilization and antibiotics for 6 weeks.
If diagnosis is doubtful or there is no response to
conservative treatment , open biopsy and curettage is
done, followed by a further course of antibiotics.
 Chronic osteomyelitis
Used to be a dreaded sequel to acute hematogenous
osteomyelitis, nowadays more frequently follows an open
fracture or operation.
Causative organisms:
1)Staph aureus.
2)E coli.
3)Strept pyogenes.
4)Proteus .
5)Pseudomonas .
6)Strept epidermidis (esp. with implants)
Pathology:
Affected bone is destroyed or
devitalized with cavities containing
pus and pieces of dead bone
(sequestrum), •New bone
surrounded by vascular tissue, and formation 
beyond that by areas of sclerosis. Involucrum
Sequestra act as substrates for •Bone
bacterial adhesion causing necrosis 
persistence of the infection until Sequestrum
removed or discharged through
draining sinuses. •Cavity,disch-
Sinuses may close arging sinus
spontaneously then reopen when  Cloaca
tissue tension rises.
Pathological fracture may
develop.
Clinical picture:
- Patient may present with pain, pyrexia, redness and
tenderness.
- There may be a discharging sinus.
- In long standing cases, tissues are thickened and even
folded in, where a scar or sinus is attached to the underlying
bone.
- There may be seropurulent discharge and excoriation of the
surrounding skin.
- Patient may present with pathological fracture .
Imaging :
X-ray
shows bone resorption
with thickening and
sclerosis of the Involucrum
surrounding bone.
Sequestra seen as Sequestrum
unnaturally dense
fragments in contrast with
the surrounding
vascularized bone.
Sometimes the bone
is crudely thickened and
misshapen resembling a
bone tumour,involucrum.
Imaging :
CT and MRI
are invaluable in
planning operative
treatment, showing
extent of bone
destruction, reactive
edema, hidden
abscesses, and
sequestra.

Bone scan
is sensitive but not
specific.
Investigations :
ESR , CRP and WBC count are
elevated in acute flares.
Organisms cultured from the
discharging sinuses should be tested
repeatedly for antibiotic sensitivity.
.Treatment :
Antibiotics :seldom
eradicate infection alone, yet
given to prevent local spread of
the infection and to control
acute flares(C&S to be done).
Operative treatment:
saucerization & sequestrectomy.
External fixator may be appliied to avoid
fracture
In refractory cases it may
possible to excise the infected
segment and perform segment
transfer using Ilizarov
technique.
 JOINT INFECTION
PATHOLOGIC STAGES OF JOINT INFECTION
*ACUTE :
SYNOVITIS
ARTHRITIS
*CHRONIC
SYNOVITIS
ARTHRITIS
CLINICAL PRESENTATION OF JOINT INFECTION
*ACUTE :
SYNOVITIS
ARTHRITIS
*CHRONIC
SYNOVITIS
ARTHRITIS
ASPIRATION
 Septic Arthritis
Aetiology:
Organisms: S.aureus, streptococcus or E.coli
in adults and H. influenza in infants.
Route of infection: either haematogenous
spread or direct spread from penetrating
wound, injection or after surgery or from
adjacent osteomyelitis.
P.F.: septic focus, trauma, R.A. and immuno-
compromised patient.
 Pathology of Septic Arthritis
Synovitis; serous, then seropurulent,
then purulent exudates.
Joint subluxation and/or dislocation.
Progressive damage of articular
cartilage.
Destruction of bony ends with reactive
new bone formation later.
Fibrous or bony ankylosis.
 Diagnosis
Symptoms: fever, pain, inability to
move the joint or weight bear.
Signs: high fever, tachycardia,
tenderness, deformity and loss of all
passive and active movement.
Discharging sinus in late cases.
Laboratory: leukocytosis, elevated ESR
and CRP.
 Diagnosis
Radiology:
X-ray: irregular and reduced joint space,
sclerosis of subchondral bone, bony
destruction, subluxation or dislocation and
finally bony ankylosis.
U.S.: to detect amount and type of fluid.
Aspiration: to obtain fluid for culture and
sensetivity.
 Differential Diagnosis

Trauma.

Rheumatic fever.

Gout.

Acute osteomyelitis.

T.B. arthritis.
INVESTIGATIONS OF JOINT INFECTION
*ACUTE :
SYNOVITIS
ARTHRITIS
*CHRONIC
SYNOVITIS
ARTHRITIS
LAB TESTS
RADIOGRAPHY
SONOGRAPHY
SCIETIGRAPHY
PARACETHESIS(Aspiration)
 Treatment
Rest and immobilization (traction or spica).
Supportive treatment.
Antibiotics for 4 weeks starting with I.V.
antibiotics for 5-7 days.
Surgical drainage must be done early to save
the articular cartilage and may be done by
arthroscopy or arthrotomy.
Arthrodesis may be required to achieve
fusion in the position of function.
TREATMENT OF JOINT
INFECTION
*ACUTE :
SYNOVITIS
ARTHRITIS
*CHRONIC
SYNOVITIS
ARTHRITIS
ASPIRATION
ARTHROTOMY
SYNOVECTOMY
EXCISION ARTHROPLASTY
(ARTHRODESIS(FUSION
CHRONIC SPECIFIC INFECTIONS
Tuberculosis of The Hip Joint

Aetiology:

Always secondary T.B.

Organism: mycobacterium T.B.

Predisposing factor: poor nutrition and health

conditions, D.M., and immuno-compromise.
Pathology of T.B. of the hip
Osseous type (common): focus at upper
part of the acetabulum or inferior part of
the head of the femur (Babcok’s
triangle).
Synovial type (rare): granulation tissue
causes hypertrophy of synovial
membrane followed by destruction of
articular cartilage.
Wandering acetabulum and path.
dislocation.
Cold abscess formation.
 T.B. of the Spine
.( (Pott’s Disease
Pathology:
Usually starts in the vertebral body and very
rarely in the vertebral arch.
Vertebral body is destroyed and replaced by
necrotic caseous material.
Early involvement of the disc and adjacent
vertebra leading to kyphosis and cold
abscess formation.
Paraplegia may develop due to cord
compression.
 Diagnosis
Tuberculous toxaemia and weakness.
Pain local or reffered.
Tenderness.
Angular kyphus deformity
Limited movements of te spine.
Cold abscess formation (psoas
abscess).
Varying degrees of neurological deficit.
 Pott’s Paraplegia
Occurs in about 10% of cases.
It may result from compression of the
thoracic spine due to, cold abscess
formation, granulation tissue,
inflammatory oedema, progressive
kyphus deformity, and thrombosis of
vessels of the cord.
It is usually spastic and it may
progress to be flaccid at the end.