OSTEOMYELITIS IN PAEDIATRIC AGE GROUP

1. Dr chiranjeevi ortho pg
RMC , KAKINADA
ACUTE HEMATOGENOUS
OSTEOMYELITIS IN CHILDREN

2. ACUTE OSTEOMYELITIS
INTRODUCTION
 Coined by Nelaton
 Greek word – osteon:- bone
myelo:-marrow
itis :- inflammation
 primarily marrow spaces, haversion
canals, sub periosteal spaces are involved
Auguste Nélaton was a French
physician and surgeon

3. Aetiology

4. Predisposing factors
 Common in active bone growth
 M:F – 1:4
 Site; metaphysis
 Poor nutrition
 Trauma
 Infections: skin, dental, resp, GIT, UTI
 Burns
 Iv drug abusers
 Scar
 Immuno compromised state
 Old age

5. Host susceptability
Local factors systemic factors
• trauma,
• scar tissue,
• poor circulation,
• diminished sensibility,
• chronic bone or joint
disease
• presence of foreign
bodies
• malnutrition,
• general illness,
• debility,
• diabetes,
• rheumatoid disease,
• corticosteroid
• all forms of
immunosuppression

6. Bacterial colonisation/Rn
 Avascular bone surfaces/ foreign material
 Protein polysacharide slime layer
 Increased ability to adhere by microbes

7. Microbial pattern in AHO
 M/C organism– staph. Aureus
 Vertebrae– GNB
 IV drug abusers– pseudomonas
 SCA– salmonella
 Chronic ill pt on IV drugs – fungal
 Infants– staph.aureus
 LBW infants– S.A, GNB
 Children 6m to 4yrs – H. influenza

8. Classification
1) The duration - acute, subacute and
chronic
2) Mechanism of infection –
exogenous or hematogenous
3) The type of host response -
pyogenic or non pyogenic

9. Route of transfer
Hematogenous( metaphyses of long bone)
Direct innoculation
 Bone penetrating injury
 Surgical contamonation
Contaguos focus(vascular dx)
microbe osteomyelit
is

10. AHO
 M/Cly Seen in children
 Bimodal age distribution < 2yrs, 8 – 12 yrs
 M> F
 WHAT IS M/C SITE INVOLVED…….?
Metaphysis…?

13. Pathophysiology
 a/c inflammation of marrow
 Spread of exudates in marrow space
 Thrombosis of vessels due to compression
 Lack of blood supply-- necrosis of bone
 Liquifarction of necrotic tissue
 Lifting of periosteum-- further necrosis
 Abscess formation (increased)
 Rise in intramedullary pressure
 Cortical ischemia
 Purulent material escapes from cortex into
subperiosteal space
 Subperiosteal abscess develops

16. IN CHILDREN < 2 YRS
 blood vessels cross the physis, thus epiphysis
may be involved
 Limb shortening or angular deformity may
occur
 Joint may be involved in some cases- hip joint
most common,
 Especially for intraarticular physes- proximal
humerus,radial neck, distal fibula
 Metaphysis has relatively fewer phagocytic
cells than the physis or diaphysis, hence more
infection here.

17. Intra articular metaphyses

18.  In children >2 years
 The physis effectively acts as a barrier to the
spread of a metaphyseal abscess
 Metaphyseal cortex thicker, hence diaphysis
more at risk
 After physes are closed acute hematogenous
osteomyelitis is much less common

19. After the physes are closed,
 infection can extend directly from the
metaphysis into the epiphysis and involve the
joint
 Septic arthritis resulting from acute
hematogenous osteomyelitis generally is seen
only in infants and adults.

20. Clinical features
 History and physical examination
Fever and malaise
Pain and local tenderness
Sweliing
Compartment syndrome in children
m/c in lower extremiteis
Femur>tibia>humerus

21. Investigations
Elevated acute phase reactants
 WBC: >11000cell/mm3
 ESR : rise slowly, peaks 3-4 days, decline over
3wks
helps in standard appropriate treatment
duration
 CRP: rapidly rises, useful in monitoring dx
normalizes in 7days after initiation of
treatment
 Aspiration of abscess: culture and Sn
 Blood culture:+ve in 30% cases

22.  BIOPSY:
NECROTIC BONE ;
 Loss of osteocytes from
lacunae
 Peripheral resorption
 Bacterial colanisation
 a/c inflammatory
infiltrates(
palymarphonuclear cells)

23. Radiology
 Plain radiographs
 Soft tissue swelling(
initial finding)
 Periosteal reaction
 Bony destruction (10-
12 days)

24. Bone scan
Can confirm diagnosis
24-48 hrs after
onset

25. USG
 may demonstrate deep soft tissue swelling earlier
 Joint effusion
 Abscess
 DVT

26. CT
 Sn 66%, Sp 97%
 Limited role
 Gave details about sequestrum and large
abscess
 Useful in treatment monitoring
MRI
 ioc
 can identify marrow inflammation
 great utility in initial screening test

28. MANAGEMENT
ANTIBIOTICS:
 Alone can cure
 Based on highest bacteriological activity, least
toxicity,lowest cast
 Initiate empherical treatment
 Change after culture report
 6wks of iv

29. Surgical treatment
 INDICATION
Abscess drainage
Failure of medical management(48-72hrs)
 OBJECTIVE
 Removal of all dead tissue
 Subperiosteal abscess ; small drill holes into
medullary canal
 Intramedullary pus:window of bone removed
 Splint the limb
 Fallowup for 1 yr

30. NADE’S 5 PRINCIPLES OF
TREATMENT
1. An appropriate antibiotic is effective
before pus formation
2. Antibiotics do not sterilize avascular
tissues or abscesses and such areas
require surgical removal
3. If such removal is effective, antibiotics
should prevent their reformation and
primary wound closure should be safe
4. Surgery should not damage already
ischaemic bone and soft tissue
5. Antibiotics should be continued after

31. COMPLICATIONS
Epiphyseal damage and
altered bone growth --1.8%
Supparative arthritis
Metastatic infection-- rare
Pathological fracture--1.7%
Chronic osteomyelitis-- 1.7%
Reccurent infection-- 6.8%
DVT – 0.4 to 6%

32. Subacute osteomyelits
 Described by Brodie
 More difficult to diagnose bcz lock of
charecteristic signs and symptoms
 Mild symptoms may be present for > 2wks before
medication
 Lab findings are normal or mildly elevated
 Radigraphic features often suggest benign /
malignant tumors
 m/c/c staph.aureus
 Diaphysis and epiphysis involve more than
metaphysis
 Avg age is 7.5 yrs ( older than AHO)

33. Brodies abscess
Pathophysiology
 Decresed bacterial
virulance/increased
host resistance
 Secondary to
inadequate treatment
of AHO
 Only local
inflammation
develops lead to local
bone destruction

34. Radiographic classification of SOM, based on
anatomic location,response of sorounding tissue
to infection, similarity to benign / mallignant tumor
GLEDHILL EXTENDED 6 PART CLASSIFICATION

36.  Biopsy and culture helps in differentiation from
bone tumors
 6 wks course of antibiotics after biopsy report
COMPLICATION
Primary chronic sclerosic OM
Chronic reccurent multifocal OM

37. THANK
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