Acute Haematogenous Osteomyelitis

1. ACUTE HAEMATOGENOUS
OSTEOMYELITIS (AHO)

2. • Mainly disease of children
• Rarely happen in adult, usually when their resistance is lowered
• The incidence of acute haematogenous osteomyelitis in Western European
children is thought to have declined in recent years because improving social
conditions
• decrease surgical treatment related to earlier and more effective antibiotic
treatment

3. Etiology
• Staphylococcus aureus 70% of cases in both adults and children
• Gram positive cocci, group A beta-haemolytic (Streptococcus pyogenes) less often
– in chronic skin infection
• Group B streptococcus – especially in newborn babies
• 1 and 4 years age, gram negative Haemophilus influenzae fairly common
pathogen
• In recent years its Kingella kingae, mainly following upper respiratory infection in
young children.
• Other Gram-negative organisms (e.g. Escherichia coli, Pseudomonas aeruginosa,
Proteus mirabilis and the anaerobic Bacteroides fragilis) occasionally cause acute
bone infection.
• patients with sickle-cell disease are prone to infection by Salmonella typhi.

4. • In infants, in whom there are still anastomoses between metaphyseal and
epiphyseal blood vessels, infection can also reach the epiphysis
• In adults, haematogenous infection accounts for only about 20% of cases of
osteomyelitis. Staphylococcus aureus is the commonest organism but
Pseudomonas aeruginosa often appears in patients using intravenous drugs.
• Adults with diabetes and vascular disease, who are prone to soft-tissue infections
of the foot, may develop contiguous bone infection involving a variety of
organisms.

5. Pathogenesis
• The bloodstream is invaded from a minor skin abrasion (sharp object, an injection
point, a boil, a septic tooth or in the newborn from an infected umbilical cord.
• In adults, the source of infection may be a urethral catheter, an indwelling arterial
line or a contaminated needle and syringe.
• In children, the infection usually starts in the vascular metaphysis of a long bone,
most often in the proximal tibia or in the distal or proximal ends of the femur.
• The structure of the fine vessels in the hypertrophic zone of the physis may more
easily allow bacteria to pass through and adhere to type 1 collagen in that area

6. • Predilection for this site has traditionally 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 ; and
• consequent lowered oxygen tension are believed to
favour bacterial colonization.

7. ACUTE OSTEOMYELITIS IN CHILDREN
The ‘classical’ picture is seen in children between 2 and 6 years.
• metaphysis acute inflammatory reaction with vascular congestion
• exudation of fluid and infiltration by polymorphonuclear leucocytes rapidly
• The intraosseous pressure rises causing intense pain, obstruction to blood flow
and intravascular thrombosis.
• Bone tissue is threatened impending ischaemia
• Second or third day, pus forms within the bone and forces its way along the
Volkmann canals to the surface where it produces a subperiosteal abscess

8. • Increase intraosseous pressure, vascular stasis, small-vessel thrombosis and
periosteal stripping increasingly compromise the blood supply
• By the end of a week there is usually microscopic evidence of bone death.
• Bacterial toxins and leucocytic enzymes also may play their part in the advancing
tissue destruction.
• With the gradual ingrowth of granulation tissue the boundary between living and
devitalized bone becomes defined.
• Pieces of dead bone may separate as sequestra varying in size from mere spicules
to large necrotic segments of the cortex in neglected cases.

9. • Another feature of advancing acute osteomyelitis is new bone formation.
• Initially, the area around the infected zone is porotic (probably due to
hyperaemia and osteoclastic activity) but if the pus is not released, either
spontaneously or by surgical decompression, new bone starts forming on
viable surfaces in the bone and from the deep layers of the stripped
periosteum.
• New bone thickens to form a casement (involucrum) enclosing the
sequestrum and infected tissue.
• If the infection persists, pus and tiny sequestrated spicules of bone may
discharge through perforations (cloacae) in the involucrum and track by
sinuses to the skin surface

10. ACUTE OSTEOMYELITIS IN INFANTS
• During the first year of life, is the frequency with which the metaphyseal infection
spreads to the epiphysis and from there into the adjacent joint. In the process, the
physeal anlage may be irreparably damaged, further growth at that site is severely
retarded and the joint will be permanently deformed.
• During the first 6–9 months of life, small metaphyseal vessels penetrate the
physeal cartilage and this may permit the infection to spread into the cartilaginous
epiphysis,
• Sometimes bizarre new bone formation along the diaphysis;

11. ACUTE OSTEOMYELITIS IN ADULTS
• Bone infection in the adult usually follows an open injury, an operation or spread
from a contiguous focus of infection (e.g. a neuropathic ulcer or an infected
diabetic foot) in over 70% of the cases.
• A vertebral infection may spread through the end plate and the intervertebral disc
into an adjacent vertebral body. If a long bone is infected, the abscess is likely to
spread within the medullary cavity, eroding the cortex and extending into the
surrounding soft tissues.
• If the bone end becomes involved, there is also a risk of the infection spreading
into an adjacent joint.

12. Clinical features
• IN CHILDREN
• a child over 4 years, presents with severe pain, malaise and a
fever, toxaemia
• refuses to use one limb or to allow it to be handled or even
touched
• recent history of infection looks ill and feverish
• the pulse rate is likely to be over 100 and the temperature is
raised.
• Local redness, swelling, warmth and oedema are later signs and
signify that pus has escaped from the interior of the bone
• Lymphadenopathy is common but non-specific.

13. • IN INFANTS
• In children under 1 year old, and especially in the newborn fails to thrive and
is drowsy but irritable.
• Metaphyseal tenderness and resistance to joint movement can signify either
osteomyelitis or septic arthritis;
• history of birth difficulties, umbilical artery catheterization or a site of
infection

14. • IN ADULTS
• A common site for haematogenous infection is the thoracolumbar spine
• mild fever and backache
• Local tenderness is not very marked

15. Cierny Mader Classification

16. Diagnostic imaging
• PLAIN X-RAY
• the first week after the onset of symptoms, the plain radiograph shows no
abnormality
• By the second week there may be a faint extracortical outline due to periosteal
new bone formation; this is the classic X-ray sign of early pyogenic
osteomyelitis,
• ULTRASONOGRAPHY
• may detect a subperiosteal collection of fluid in the early stages of
osteomyelitis, but it cannot distinguish between a haematoma and pus.

17. • SPECT/CT
• Increasingly used in musculoskeletal infections.
• Excellent differentiation between soft-tissue and bone infections, assessment
of suspected infected sites with underlying structural bone alterations, and
clear definition of infective foci within complex anatomical locations.

18. • MAGNETIC RESONANCE IMAGING (MRI)
• helpful in cases of doubtful diagnosis, and particularly in suspected infection
of the axial skeleton
• the best method of demonstrating bone marrow inflammation.
• extremely sensitive, even in the early phase of bone infection
• assist in differentiating between soft-tissue infection and osteomyelitis.

19. CT
• The advantage of planar bone definition, including bone destruction and soft
tissue mass, such as an abscess, within or surrounding bone.
RADIONUCLIDE SCANNING
• 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.

20. Laboratory investigations
• The most certain way to confirm the clinical diagnosis is o aspirate pus or fluid
from the metaphyseal subperiosteal abscess, the extraosseous soft tissues or an
adjacent joint.
• best done using a 16- or 18-gauge trocar needle
• Blood cultures should be obtained if fever above 38 °C is detected
• C-reactive protein (CRP) values are usually elevated within 12–24 hours
• the erythrocyte sedimentation rate (ESR) within 24–48 hours after the onset of
symptoms
• The white blood cell (WBC) count rises and the haemoglobin concentration may
be diminished
• Anti-staphylococcal antibody titres may be raised

21. Treatment
• Treatment started immediately without waiting for final confirmation of the
diagnosis.
• ANTIBIOTICS : intravenous administration of antibiotics is so vital that
treatment should not await the result.
• Staphylococcus aureus is the most common at all ages,

22. • Neonates and infants up to 6 months of age : Staphylococcus aureus, Group B
streptococcus and Gram-negative organisms.
• flucloxacillin plus a third-generation cephalosporin such as cefotaxime.
• Children 6 months to 6 years of age : Empirical treatment in this age group
should include cover against Haemophilus influenzae
• combination of intravenous flucloxacillin and cefotaxime or cefuroxime.
• Older children and previously fit adults : The vast majority in this group will
have a staphylococcal infection and can be started on intravenous flucloxacillin
and fusidic acid.

23. • Elderly and previously unfit patients : combination of flucloxacillin and a
second- or third-generation cephalosporin.
• Patients with sickle-cell disease : third-generation cephalosporin or a
fluoroquinolone such as ciprofloxacin.
• Heroin addicts and immunocompromised patients : best treated empirically with
a broad-spectrum antibiotic such as one of the third-generation cephalosporins or
a fluoroquinolone preparation, depending on the results of sensitivity tests.
• Patients considered to be at risk of methicillinresistant Staphylococcus aureus
(MRSA) infection : intravenous vancomycin (or other glucopeptide such as
teicoplanin) together with a third- generation cephalosporin.

24. Cephalosporin

25. • appropriate antimicrobial therapy (first empirical, then specific)
• surgical drainage if required
• splintage and rest of the affected part
• supportive treatment for pain and dehydration.

26. Complications
• Epiphyseal damage and altered bone growth
• Suppurative arthritis
• Metastatic infection
• Pathological fracture
• Chronic osteomyelitis

27. TERIMA KASIH