OSTEOMYELITIS

ACUTE & CHRONIC

I DEWA AYU RAINA KENOVITA ARDANI

DR JAFRI HASAN, SP.OT
112016322
OSTEOMYELITIS
•Inflammation of the bone caused by an infecting organism
•Timing classification
 acute
 within 2 weeks
 subacute
 within one to several months
 chronic
 after several months
ACUTE HEMATOGENOUS OSTEOMYELITIS
•Mainly disease of children (2 and 6 years)  adult resistance is lowered
•Causal organism:
•Staphylococcus aureus 70%
•Streptococcus pyogenes (gram +; Group A beta-haemolytic streptococcus) chronic
skin infection
•Group B streptococcus  especially on new-born babies
•S. Pneumoniae (A haemolytic diplococcus)
•Gram negative Escherichia coli, Pseudomonas aeruginosa, proteus mrabilis,
bacteriodes fragilis
 Minor skin abrasion
treading on a sharp object
an injection point, a septic tooth
the newborn infection from an infected umbilical cord

Blood stream is invaded

Adult urethral catheter, indwelling arterial line, dirty needle

and syringe
 In Childern

Usually start in the vascular metaphysis of a long bone, most often in the
proximal tibia or in the distal or proximal ends of the femur

In Adult

haematogenous  20% of cases  mostly affecting the vertebrae.

Staphylococcus aureus  commonest organism
Pseudomonas aeruginosa in patients using IV drugs.
Adults with diabetes, who are prone to soft-tissue infections of the foot, may develop
contiguous bone infection involving a variety of organisms.
PATHOLOGY
Characteristic progresion marked by:
•inflammation, suppuration, bone necrosis,
reactive new bone formation and,
ultimately, resolution and healing or else
intractable chronicity.
 CLINICAL FEATURES
Childern

>4years
Severe pain, Malaise, Fever
Recent history of infection
child looks ill and feverish; pulse >100,temperature raised.
acute tenderness near one of the larger joints
painful and joint movement is restricted (‘pseudoparalysis’).
Local redness, swelling, warmth, oedema later signs  pus has escaped from the interior of the bone.
Lymphadenopathy is common but non-specific
 Infant

< 1 years old (especially newborn)

the constitutional disturbance can be misleadingly mild
history of birth difficulties, umbilical artery catheterization or a site of infection (however mild) such as an inflamed
intravenous infusion point
Metaphyseal tenderness and resistance to joint movement
Look for other sites – multiple infection is not uncommon
Radionuclide bone scans may help to discover additional sites.
 Adult

The commonest site thoracolumbar spine.

history of some urological procedure followed by a mild fever and backache.
it may take weeks before x-ray signs appear confirmed fine-needle aspiration and bacteriological
culture
Other bones are occasionally involved diabetes, malnutrition, drug addiction, leukaemia,
immunosuppressive therapy or debility.

very elderly, those with systemic features are mild and the diagnosis is easily
immune deficiency missed.
 DIAGNOSTIC IMAGE
PLAIN X-RAY
first week  shows no abnormality
Displacement of the fat planes.
second week  faint extra-cortical outline
due to periosteal new bone formation
Later  periosteal thickening more obvious,
patchy rarefaction of the metaphysis, bone
destruction appear.
late sign  regional osteoporosis + localized
segment of apparently increased density.
 ULTRASONOGRAPHY
detect a subperiosteal collection of fluid in the early stages of osteomyelitis, but it cannot
distinguish between a haematoma and pus.

RADIONUCLIDE SCANNING
Radioscintigraphy with 99mTc-HDP reveals increased activity in both the perfusion phase
and the bone phase. This is a highly sensitive investigation, even in the very early stages,
but it has relatively low specificity and other inflammatory lesions can show similar
changes. In doubtful cases, scanning with 67Ga-citrate or 111In-labelled leucocytes may
be more revealing.
MAGNETIC RESONANCE IMAGING
Particularly in suspected infection of the axial skeleton. It is also the best method of
demonstrating bone marrow inflammation. It is extremely sensitive, even in the early
phase of bone infection, and can therefore assist in differentiating between softtissue
infection and osteomyelitis. However, specificity is too low to exclude other local
inflammatory lesions.
LABORATORY INVESTIGATIONS
The most certain way aspirate pus or fluid from the metaphyseal subperiosteal abscess, the
extraosseous soft tissues or an adjacent joint.
Even if no pus is found, a smear of the aspirate is examined immediately for cells and
organisms; a simple Gram stain  type of infection, initial choice of antibiotic.
CRP ↑ 12–24 hours, ESR ↑ 24–48 hours, WBC ↑, haemoglobin concentration may be
diminished.
Antistaphylococcal antibody titres ↑ useful where the diagnosis is in doubt.
unusual site or with an unusual organism  heroin addiction, sickle-cell disease, HIV
DIFFERENTIAL DIAGNOSIS

Cellulitis
Streptococcal necrotizing
myositis
Acute suppurative arthritis
Acute rheumatism
Streptococcal necrotizing
myositis
Gaucher’s disease
Acute rheumatism
TREATMENT
•General Supportive treatment for pain and dehydration.
•Splintage of the affected part  prevent joint contractures, prevent dislocation
•Appropriate antimicrobial therapy.
•Surgical drainage.
 flucloxacillin plus a third-generation
Neonates and infants up to 6 months
cephalosporin like cefotaxime

combination IV flucloxacillin and

Children 6 months to 6 years
cefotaxime or cefuroxime.

Older children and previously fit intravenous flucloxacillin and fusidic acid
adults zylpenicillin

Elderly and previously unfit patients flucloxacillin and a second or third

generation cephalosporin.
 Chloramphenicol, third-generation
Patients with sickle-cell disease cephalosporin or a fluoroquinolone like
ciprofloxacin.

broad-spectrum antibiotic the third

Heroin addicts, immunocompromised
generation cephalosporins or a fluoro-
patients, unusual infections quinolone

Patients considered to be at risk of

Endemic IV vancomycin+ third
meticillin-resistant Staphylococcus
generation cephalosporin.
aureus (MRSA)
DRAINAGE
Antibiotics given early (first 48 hours)  often unnecessary
Clinical features do not improve within 36 hours of starting treatment, or if there are
signs of deep pus (swelling, oedema, fluctuation)
if pus is aspirated, the abscess should be drained by open operation under general
anaesthesia.
Extensive intramedullary abscess  drainage cutting a small window in the cortex
Signs of infection subside, movements are encouraged and the child is allowed to
walk with the aid of crutches Full weightbearing usually after 3–4 weeks.
COMPLICATIONS
Epiphyseal damage and altered
bone growth
Pathological fracture

Suppurative arthritis
Chronic osteomyelitis

Metastatic infection
 SUBACUTE HAEMATOGENOUS OSTEOMYELITIS
the distal femur and the proximal and distal tibia are the favourite sites.

Pathology

well-defined cavity in cancellous bone containing glairy seropurulent fluid (rarely pus).
The cavity is lined by granulation tissue  acute and chronic inflammatory cells, surrounding
bone trabeculae are often thickened.
The lesion sometimes encroaches on and erodes the bony cortex.
Occasionally it appears in the epiphysis and, in adults, in one of the vertebral bodies.
Clinical features

child or adolescent  pain near one of the larger joints for several weeks or even months.
limp and often there is slight swelling, local tenderness.
The temperature is usually normal and there is little to suggest an infection.
The WBC count and blood cultures usually show no abnormality,ESR is sometimes elevated.
Cavity

a circumscribed, round or oval 1–2 cm in diameter (tibial or femoral metaphysis)

surrounded by a halo of sclerosis (the classic Brodie’s abscess) well defined, extending into
the diaphysis.
Metaphyseal lesions cause little or no periosteal reaction; diaphyseal lesions may be
associated with periosteal new bone formation and marked cortical thickening.
If the cortex is eroded the lesion may be mistaken for a malignant tumour.
 Diagnosis
The clinical and x-ray appearances may resemble those of cystic tuberculosis, eosinophilic
granuloma or osteoid osteoma; mimic a malignant bone tumour like Ewing’s sarcoma.
Epiphyseal lesions are easily mistaken for chondroblastoma.
The diagnosis often remains in doubt until a biopsy is performed.
fluid bacteriological culture (+) half the cases, Staphylococcus aureus.

Treatment

Immobilization and antibiotics (flucloxacillin and fusidic acid) IV for 4 or 5 days  orally
for another 6 weeks -12 months.
If the diagnosis is in doubt open biopsy, lesion may be curetted at the same time.
Curettage x-ray shows no healing after conservative treatment further course of anti
biotics.
POST-TRAUMATIC OSTEOMYELITIS
Open fractures  prone to infection.
The combination of tissue injury, vascular damage, oedema, haematoma, dead bone
fragments and an open pathway to the atmosphere must invite bacterial invasion
even if the wound is not contaminated with particulate dirt.
Staphylococcus aureus is the usual pathogen,
Clinical features Microbiological investigation

feverish, pain and swelling over the fracture site;

the wound is inflamed, seropurulent discharge. Blood tests  ↑ CRP levels,
leucocytosis, ↑ ESR
MRI differentiating between bone and soft tissue infection less reliable in
distinguishing longstanding infection and bone destruction due to trauma.

Treatment
prophylaxis: cleansing and debridement of open fractures drainage leaving the
wound open, immobilization of the fracture, antibiotics (flucloxacillin+benzylpenicillin)
6-hourly for 48 hours. Clearly contaminated metronidazole for 4 or 5 days
Treatment calls for regular wound dressing and repeated excision of all dead and
infected tissue.
recommended that stable implants (fixation plates and medullary nails) should be left
in place until the fracture had united, the wound remains accessible for dressings and
superficial debridement.
 CHRONIC OSTEOMYELITIS
The usual organisms Staphylococcus aureus, Escherichia coli, Streptococcus pyogenes, Proteus
mirabilis and Pseudomonas aeruginosa

Predisposing factors

Acute haematogenous osteomyelitis, Inadequately treated,

local trauma open fracture or prolonged bone operationespecially use of a foreign
implant.
greater risk very old or debilitated, suffering from substance abuse, diabetes, peripheral
vascular disease, skin infections, malnutrition, lupus erythematosus or immune deficiency.
 PATHOLOGY
Bone destroyed/devitalized Cavities containing pus, dead bone (sequestra) surrounded
by vascular tissue, areas of sclerosismform of a distinct bony sheath (involucrum).
Worst cases diaphysis may be devitalized and encased in a thick involucrum.
Sequestra actpersistence of infection until they are removed through perforations in the
involucrum and sinuses that drain to the skin
Bone destruction, and the increasingly brittle sclerosis, sometimes results in a pathological
fracture.
The histological picture is one of chronic inflamma- tory cell infiltration around areas of
acellular bone or microscopic sequestra.

X frank excavation around an implant, thickening
Clinical features
pain, pyrexia, redness and tenderness (a ‘flare’), discharging
sinus. tissues are thickened and often puckered or folded
inwards where a scar or sinus adheres to the underlying bone
Seropurulent discharge,excoriation of the surrounding skin.
In post-traumatic osteomyelitis the bone may be deformed or
un- united.
Imaging
bone resorptionpatchy loss of density or as
and sclerosis of the surrounding bone.
localized loss of trabeculation, or an area of
osteoporosis, or periosteal thickening;
sequestra show up as unnaturally dense
fragments,
Contrast surrounding osteopaenic bone
bone crudely thickened and misshapen,
resembling a tumour.
A sinogram  localize the site of infection.
Radioisotope scintigraphy
99mTc-HDP scans ↑activity perfusion
phase and the bone phase.
67Ga-citrate or 111In-labelled leucocytes 
more specificshowing hidden foci of infection.
CT and MRI  the extent of bone destruction and
reactive oedema, hidden abscesses and sequestra.
INVESTIGATIONS
Acute flares CSR, ESR and WBC levels ↑
Organisms cultured from discharging sinuses should be tested repeatedly for
antibiotic sensitivitysampling from deeper tissues is important.
Standard bacterial cultures negative results 20% of cases of overt infection.
Type B compromised by a few
local or systemic factors, if the
infection is localized and the
bone still in continuity and stable
(Stage 1–3) they have a
reasonable chance of recovery.
Type C severely
compromisedprognosis is poor.
Stage 4 operative treatment
contraindicated, the best
optionlong-term palliative
treatment may have to advise
amputation.
TREATMENT Fusidic acid, clindamycin and the cephalosporins
Vancomycin and teicoplanin MRSA
ANTIBIOTICS
4–6 weeks (starting from the beginning of treatment or the last
debride- ment) before considering operative treatment.
If surgical clearance failsantibiotics should be continued for another
4 weeks before considering another attempt at full debridement.

Sinus dressing to protect the clothing.

LOCAL TREATMENT Colostomy paste can be used to stop excoriation of the skin.
Acute abscessurgent incision and drainage
OPERATION
indication for radical surgery: for chronic haematogenous infections, post-traumatic
infections, postoperative infection
foreign implantfurther incentive to operate

Debridement Porous antibiotic-impregnated beads

Dealing with the ‘dead space’ cancellous bone grafts

Muscle flap transfer
A free vascularized bone graft
closed irrigation
filled by vascular granulation tissueThe tubes removed Ilizarov method
when cultures remain negative in three consecutive fluid
samples and the cavity is obliterated
Soft-tissue cover

Prognosis
Local trauma must be avoided and any recurrence of symptoms,
Aftercare however slight, should be taken seriously and investigated
The watchword is ‘cautious optimism’ – a ‘probable cure’ is better
than no cure at all.
THANK YOU