2. GENERAL ASPECTS OF INFECTION
– HOST SUSCEPTIBILITY
• Increased by local factors e.g scar tissue, poor circulation,
diminished sensibility, chronic bone or jt disease presence of
• 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.
Mainly a dx of children
Adults have lowered resistance
Trauma may determine the site of infection-
small hematoma or fluid collection in bone with
Incidence- reducing in the west
Higher in less affluent societies
6. • Organisms
– Staph aureus ->70%
– Gram positive cocci- group A beta hemolytic
– Group B streptococcus – newborn
– Alpha hemolytic diplococcus- s. pneumoniae
– 1-4 yrs;haemophilus influenza- h influenzae type b
– Kingella kingae
– Gram negative organisms- e-coli, p-aeruginosa,
8. How does infection reach
1. Direct introduction thro the skin; pinprick,
injection, stab wound, laceration, open # or
2. Direct spread from contiguous focus of
infection e.g. an adjacent cellulitis/ myositis
3. Indirect spread via blood stream from distant
sites such as nose/ mouth/ respiratory tract/
the bowel or gut.
The bloodstream is invaded through
– Minor skin abrasion
– Treading on a sharp object
– Injection point
– Septic tooth
– Infected umbilical cord in the newborn
– Adults: urethral catheter, indwelling arterial line,
dirty needle & syringe.
• 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
– In infants, metaphyseal & epiphyseal vessels anastomose so
infection can also reach the epiphysis.
– 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.
AHO shows a xtic progression marked by;
• bone necrosis
• reactive new bone formation
• resolution & healing intractable chronicity
• 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, &
• 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
• 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
• Bacterial toxins &leukocyte enzymes advancing tx
13. • With gradual ingrowth of granulation tissue the boundary
btn living & devitalized bone become defined.
• Pieces of dead bone= aka(sequestra); separates in varying
• 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.
• 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.
• 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.
CHILDREN OVER 4 YRS:
• Severe pain fever &malaise- in neglected cases, there is marked
• 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
• local redness warmth, & edema- later signs signify pus has escaped
from the interior of the bone.
17. • INFANTS;
• <1yr old/newborn
• Constitutional disturbance/ failure to thrive.
• Drowsy &irritable
• Metaphyseal tenderness & resistance of mvt.
• Multiple infxn are not common.
• 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/
18. DIAGNOSTIC IMAGING
• In the first week x-ray is normal
• 2nd week- periosteal new bone formation/
U/S may show sub periosteal abscess in the early
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
– 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.
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
• Septicemia & fever can cause severe DEH2O.
• For comfort
– Simple traction (in hip involvement prevent
• 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.
• Antibiotics may treat
• If features do not improve within 36 hours of starting
• Or if there are signs of deep pus (swelling, edema,
• 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
• Full weight bearing at 3-4 weeks
Delayed treatment or organisms insensitive to chosen antibiotics
1. Epiphyseal damage & altered bone growth
– 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