This document provides information about osteomyelitis (bone infection). It discusses the causes of increased susceptibility to bone infections, including local factors, systemic illnesses, and immunosuppression. It describes how infections spread to the bones and the pathogenesis of acute hematogenous osteomyelitis. It covers the typical clinical features and stages of bone infection in children versus adults. Diagnostic testing including imaging, laboratory tests, and aspiration are outlined. Treatment involves antibiotics, splinting, and surgical drainage of pus in severe cases. Complications can include bone deformity, arthritis, metastatic spread, and chronic infection.

1. OSTEOMYELITIS
Dr.muthoka

2. GENERAL ASPECTS OF INFECTION
Define infection?
– HOST SUSCEPTIBILITY
• Increased by local factors e.g scar tissue, poor circulation,
diminished sensibility, chronic bone or jt disease presence of
f.b.
• SYSTEMIC FACTORS;- malnutrition, general illness, debility,
dm, rheumatoid arthritis, corticosteroid administration or all
forms of immunosuppression(acquired or induced).
• Bacterial colonization &resistance to antibiotics.
– How is pus formed?
– Lymphadenopathy & lymphagitis.
– Bacteremia vs septicemia.

3. CLASSIFICATION:
– Acute hematogenous osteomyelitis.
– Subacute.
– Chronic.

4. ACUTE HEMATOGENOUS OSTEOMYELITIS

5. AETIOLOGY
Mainly a dx of children
Adults have lowered resistance
Trauma may determine the site of infection-
small hematoma or fluid collection in bone with
concurrent bacteremia
Incidence- reducing in the west
Higher in less affluent societies

6. • Organisms
– Staph aureus ->70%
– Gram positive cocci- group A beta hemolytic
streptococcus pyogenes
– Group B streptococcus – newborn
– Alpha hemolytic diplococcus- s. pneumoniae
– 1-4 yrs;haemophilus influenza- h influenzae type b
vaccine
– Kingella kingae
– Gram negative organisms- e-coli, p-aeruginosa,
proteus mirabilis

7. • Anaerobic- bacteroides fragilis
• Sickle cell dx- salmonella typhi
• Mixed infection.

8. How does infection reach
musculoskeletal system?
1. Direct introduction thro the skin; pinprick,
injection, stab wound, laceration, open # or
operation
2. Direct spread from contiguous focus of
infection e.g. an adjacent cellulitis/ myositis
etc.
3. Indirect spread via blood stream from distant
sites such as nose/ mouth/ respiratory tract/
the bowel or gut.

9. pathogenesis
The bloodstream is invaded through
– Minor skin abrasion
– Treading on a sharp object
– Injection point
– Boil
– Septic tooth
– Infected umbilical cord in the newborn
– Adults: urethral catheter, indwelling arterial line,
dirty needle & syringe.

10. CHILDREN
• Infection begin in the vascular metaphysis of long bone in
the proximal tibia & distal end of femur.
• The following favour colonization:
– Hairpin loop of nutrient artery/ relative vascular stasis/ lowered
oxygen tension.
– In infants, metaphyseal & epiphyseal vessels anastomose so
infection can also reach the epiphysis.
ADULTS:
– Haematogenous infxn account for only about 20%.
– Mostly affect the vertebrae.
– Staph aureus.
– P. aeruginosa in pts using I.V. drugs.
– D.M commonly have a variety of organisms.

11. PATHOLOGY
AHO shows a xtic progression marked by;
• inflammation
• suppuration
• bone necrosis
• reactive new bone formation
• resolution & healing intractable chronicity
CHILDREN
• The classical picture is seen in children btn 2-8 years
• Earliest change in the metaphysis acute inflammatory rxn with vascular
congestion, exudation & infiltration of polymorphonuclear leukocytes.
• Intraosseous pressure rises rapidly causing intense pain, obstruction of
blood flow & intravascular thrombosis.
• Ischemia & resorption due to a combination of phagocytic activity, & the
local accumulation of cytokines, growth factors, prostaglandins, &
bacterial enzymes.
• By 2nd to 3rd day, pus forms- thro volkman canal to the surface where it
produces a sub periosteal abscess.

12. • More evident in children because they have a loose
periosteum than adults
• Pus spread along the shaft to re-enter the bone at another
level or burst into the surrounding soft tissues.
• The developing physis act as a barrier to spread towards
the epiphysis
• Where the metaphysis is intracapsular, pus may discharge
thro the periosteum into the jt.(hip, shoulder & elbow.)
• Rising intraosseous pressure, vascular stasis, small vessel
thrombosis & periosteal stripping increasingly compromise
the blood supply.
• By end of a week there is microscopic evidence of bone
death.
• Bacterial toxins &leukocyte enzymes advancing tx
destruction

13. • With gradual ingrowth of granulation tissue the boundary
btn living & devitalized bone become defined.
• Pieces of dead bone= aka(sequestra); separates in varying
sizes.
• Macrophages & leukocytes come in & remove debri by a
combination of phagocytosis & osteoclastic resorption
• New bone formation-deep layers of stripped periosteum &
viable surface in the bone
• New bone thickens to form a casement or involucrum
enclosing the sequestrum & infected tx.
• Pus & tiny spicules of bone may discharge thro the
perforations( cloacae) in the involucrum & track by sinuses
to the surface.
• If the infxn is controlled & intraosseous pressure released
at an early stage & dire process can be halted.
• Persistent infxn result in COM.

14. INFANTS-SPECIAL:
• Metaphyseal infxn may spread to the
epiphysis & jt.
• The growth plate may be irreparably damaged
& further growth @that site is severely
retarded & jt is permanently deformed.
• Exuberant periosteal rxn.

15. ADULTS`
• Bone infection in adults usually follow an open
surgery, operation or spread from a contiguous
infection(neuropathic ulcer or diabetic foot)
• True hematogenous O.M is uncommon & it
affects the vertebra e.g. following a pelvic infxn
or a small cuboidal bone.
• May spread through endplate & intervertebral
discs to adjacent vertebra.
• Long bone may be affected.
• No exuberant new bone formation.

16. C/FS
CHILDREN OVER 4 YRS:
• Severe pain fever &malaise- in neglected cases, there is marked
toxaemia
• Refusal to use a limb, handled or touched.
• h/o infxn, septic toe, boil sore throat or discharge from the ear.
• Ill & feverish
• Raised p.r >100per min. Increased temp.
• Limb is held still. Acute tenderness near a large joint.
• Manipulation is painful & joint movement is
restricted(pseudoparalysis)
• local redness warmth, & edema- later signs signify pus has escaped
from the interior of the bone.
• Lymphadenopathy.

17. • INFANTS;
• <1yr old/newborn
• Constitutional disturbance/ failure to thrive.
• Drowsy &irritable
• Metaphyseal tenderness & resistance of mvt.
• Multiple infxn are not common.
• ADULTS
• Commonest site is thoracolumbar spine.
• Urological procedure followed by fever &backache.
• Local tenderness is not marked.
• It may take weeks be4 x-ray signs appear.
• Confirm by FNA & bacteriologic culture.
• Other bones are affected in DM, malnutrition, drug addiction,
leukemia, immunosuppressive therapy or debility( elderly/
immunodeficiency)

18. DIAGNOSTIC IMAGING
XRAYS;
• In the first week x-ray is normal
• 2nd week- periosteal new bone formation/
regional osteoporosis
U/S may show sub periosteal abscess in the early
stages? Haematoma.
Radionuclide scanning/radioscintigraphy-reveal
increased activity/ sensitive in early stages.
MRI- sensitive in early phase.

19. LABORATORY INVESTIGATIONS
• The most certain way to confirm diagnosis is to aspirate pus from
metaphyseal subperiosteal abscess/ extraosseous soft txs or
adjacent joint.
– Gram stain
– Microbiologic exam &sensitivity
– Tx aspirate give +ve results in over 60%of cases
• Blood cultures are +ve in less than half the cases
• Crp/ esr values are usually elevated within 24 hours.
• Elevated WBC & low Hb.
• Antistaphylococcal ab titre may be raised
• Om in an unusual site or with unusual organism should alert one of
the possibility of heroin addiction, sickle cell disease,or deficit in
host defense mechanisms eg HIV.

20. DDX
• Cellulitis
• Acute suppurative arthritis
• Streptoccocal necritizing myositis
• Acute rheumatism-
• Sickle cell crisis
• Gauchers disease

21. RX
4 important aspects
1. Supportive rx for pain & deh2o
2. splintage of affected part
3. Appropriate antimicrobial therapy
4. Surgical drainage.

22. GENERAL SUPPORTIVE RX;
• Distressed child needs to be comforted and rxd
for pain.
• Septicemia & fever can cause severe DEH2O.
SPLINTAGE.
• For comfort
• Methods
– Simple traction (in hip involvement prevent
dislocation)
• Plaster slab
• Half cylinder cast.

23. • ANTIBIOTICS
• Blood & aspirate material are sent for culture.
• Start antibiotics immediately as you wait for
results “best guess”
• Staph aureus is most common at all ages.
• factors on choice
– Patients age/ general state of resistance/ renal
fxn/ degree of toxaemia & allergy.

24. • Neonates &infants- flucloxacillin + 3rd
generation cephalosporins eg. cefotaxime.
– Flucloxacillin+ benzylpenincillin + gentamycin
• 6 months to 6 years; -flucloxacillin+
cefotaxime or cefuroxime
• Adults; - flucloxacillin+ fusidic acid.
• Sickle cell- chlomphenicol + 3rd generation
cephalosporins + fluoroquiunolones.
• Methicillin resistant staph aureus:-
vancomycin.

25. drainage
• Antibiotics may treat
• If features do not improve within 36 hours of starting
antibiotics
• Or if there are signs of deep pus (swelling, edema,
fluctuation)
• If pus aspirated- abscess is drained thro open
operation under general anesthesia
• Then drill a few holes in different directions
• When signs of infection subside the child is encouraged
to walk
• Full weight bearing at 3-4 weeks

26. COMPLICATIONS
Delayed treatment or organisms insensitive to chosen antibiotics
1. Epiphyseal damage & altered bone growth
– Length/
– Pseudoarthrosis/ limp
2. Suppurative arthritis
a) Young infants in whom the growth disc is not an important barrier
b) Where metaphysis is intracapsular eg. upper femur
3. Metastatic infection- may involve other jts, bones, serous cavities,
brain or lung
4. Pathological #s
5. Chronic om- sometimes AHO fail to resolve weeks or months after
onset of acute infection