Acute and subacute osteomyelitis Dr Kuldeep singh Resident doctor Aiims Bhopal

1. ACUTE AND SUBACUTE
OSTEOMYELITIS
Dr. Kuldeep Singh
Resident doctor
Department of orthopaedics
Aiims Bhopal

2. Introduction
• Osteomyelitis is defined as infection of bone or bone marrow
by an infecting organism.
• It may remain localized, or it may spread through the bone to
involve the marrow, cortex, periosteum, and soft tissue
surrounding the bone.

3. Classification
Classification is based on
1. Timing of the onset
2. Method of spread.

4. Timing of onset
1. Acute OM: <2week of duration
2. Subacute OM: 2weeks—6weeks of duration
3. Chronic OM: >6 weeks of duration

5. Method of spreads
1.Exogenously :-
 trauma
 surgery (iatrogenic)
 contiguous infection
2. Hematogenous (bacteremia)

6. Hematogenous osteomyelitis:
 occurs in children < 15 years of age
 occurs in the metaphysis of the long bones-
 Decreased activity of macrophages
 Frequent trauma
 Precarious blood supply

7. Diaphyseal osteomyelitis :
 Begins in metaphysis, but due to growth becomes diaphyseal -
 Mostly in children.
 Or direct trauma to diaphysis
 Tubercular

8. Pathophysiology:
• Metaphysis - highly
vascularized zones.
• Vessels are arranged in hair pin
arrangement resulting in
“sluggish flow” of blood,
• leading to bacterial
enlodgement

9. Pathogenesis
• M/c route- hematogenous
• Appendicular skeleton > Axial skeleton
• Most common bone involved in OM-
 Overall- metaphysis of distal femur > tibia
 Infant/children- metaphysis of distal femur
 Adults- vertebral body

10. Development of osteomyelitis

11. Most common cause of
Acute Hematogenous OM -
• Adult :- S.aureus is the commonest cause
• SCA(sickle cell anemia) patient:- Salmonella is the usual cause
• Intravenous drug abusers:-Pseudomonas aeruginosa and
S.epidermidis.

12. Why staphylococcus most
common?
 S.aureus and S.epidermis ----- elements of normal skin flora
 S.aureus -----increased affinity for host proteins (traumatised
bone)
 Enzymes (coagulase, surface factor A) ----- hosts immune
response .

13. Why staphylococcus most
common
 Inactive “L” forms ------dormant for years
 “Biofilm” (polysaccharide “slime” layer) ---- increases bacterial
adherence to any substrate
 Large variety of adhesive proteins and glycoproteins -----
mediate binding with bone components.

14. Causes
General factors
 Anemia
 Infection
 Poor nutrition
 Poor immune status
Local factors
 Hair pin bend vessels
 Metaphyseal haemorrhage
 Defective Phagocytosis
 Vasospasm

15. Pathogenesis
Host factors
 Chronic steroid use
 Diabetes
 Peripheral vascular disease
 Intravenous drug abuse
 Immunosuppression (HIV
and AIDS)
 Tuberculosis
 Sickle cell disease

16. Acute Osteomyelitis
• Clinical findings
 Rapid presentation of pain,
 Raised temperature,
 Redness

17. Diagnosis of acute osteomyelitis
• PELTOLA AND VAHVANEN’S CRITERIA (if 2/4
are found)
1. Purulent material on aspiration of the affected bone
2. Positive findings of bone tissue or blood culture
3. Localised classic physical findings
a. bonny tenderness
b. overlying soft tissue edema ,erythema
4 Positive radiological imaging
Principles And Practice Of Pediatrics Infectious Disease( 5th edition) by Sarah S. Long
MD , Charles G. Prober MD , Marc Fischer MD

18. Acute Osteomyelitis
• lab reports-
 Inflammatory markers will be raised
 CRP-most sensitive marker
short half-life
decreases about a week after effective treatment.

19. Plain radiographs shows
• Ist week: soft tissue shadow/lucency appear within
48hrs- first/ earliest x-ray sign (but not appreciable).
• 2nd week : Faint extra cortical outline due to
periosteal new bone formation ( classic x-ray sign of
early pyogenic osteomyelitis-first appreciable sign)

20. Plain radiographs shows
• 3 to 6 weeks : elevation of periosteum and layered new bone
formation .
• 3-8 weeks :The dead bone (i.e. sequestrum formation) occurs

21. ULTRASOUND
• Sub periosteal collection of fluid in the early stage of
osteomyelitis
• But cannot distinguish between hematoma and pus.

22. CT
• To detect early osseous erosion
• To document the presence of sequestrum, foreign body, or
gas formation

23. M.R.I.
• It is highly sensitive for detecting osteomyelitis as early as 3 to
5 days after the onset of infection [ Marrow edema within
24hr].
• It is best method of demonstrating bone marrow
inflammation.
• It helps to differentiate between soft tissue infection and
osteomyelitis.

25. Three phase bone scan
99mTc-MDP
• Components of a three-phase technetium
bone scan-
(A) Initial dynamic [ angiographic ] phase
(B) Blood pool phase
(c) Delayed [ bone] phase

26. Bone scan
I) Three phase bone scan
99mTc-MDP
i) Increased uptake in all 3 phases of
scan
ii) Highly sensitive(95%) in acute
infection.
II) Gallium scan and indium-111
labelled leukocyte scan used
in conjugation with technetium
scanning

27. Differential Diagnosis
1. Cellulitis
2. Acute suppurative arthritis
3. Tuberculosis
4. Sickle cell crisis
5. Streptococcal necrotising myositis

28. Treatment
1.General treatment: Analgesics, nutrition
general supportive treatment by intaking
enough caloric, protein, vitamin etc.
2. Antibiotic therapy
3. Surgical treatment
4. Immobilization
• Splintage of affected part

29. Nade’s principles of treatment of acute
OM.
1)An appropriate antibiotic is effective before pus formation.
2)Antibiotics do not sterilize avascular tissues or abscesses, such
areas require surgical removal.
3)If such removal is effective antibiotics should prevent their
reformation and primary wound closure should be safe.
General Principles Of Orthopedics And Trauma[ K. Mohan Iyer]-2nd edition

30. Nade’s principles of treatment of acute
OM.
4)Surgery should not damage further already ischemic bone and
soft tissues
5)Antibiotics to be continued after surgery.
General Principles Of Orthopedics And Trauma[ K. Mohan Iyer]-2nd edition

31. Prerequisites for Antibiotics
• Drug which penetrates infected tissues and attains sufficient
levels in bone and pus.
• If abscess not found, IV antibiotics to be started based on
gram stain.
• The antibiotic dosage for OM is usually 2x to 3x the standard
dose to ensure a peak serum bactericidal titer of 1:8 or
greater
• Parenteral antibiotic continued till appropriate clinical/lab
response has occurred.

32. Antibiotics
• Under most circumstances
most appropriate antibiotic
is semi synthetic
penicillin(oxacillin/naficilllin
) or 1st gen.cephalosporins.
• If allergic, clindamycin
because of good intra
osseous penetration

33. End point of treatment

34. Nade’s indications for surgery
1. Abscess
2. Severely ill & moribund child with features of acute
osteomyelitis
3. Failure to respond to IV antibiotics for >48 hrs
General principles of orthopedics and trauma[ K. Mohan Iyer]- 2nd edition

35. Technique for drainage of acute OM
TIBIA
• Tourniquet applied whenever possible, don’t exsanguinate if
infection present.
• Make antero-medial incision 5-7.5cms over affected part of
tibia.
• Periosteum elevated, any compressed pus will escape.
• Drill several holes 4mm through cortex into medullary canal, if
pus escapes drill to outline
• cortical window and cortex removed with osteotome.

36. Technique for drainage of acute OM
TIBIA
• Evacuate any intra medullary pus and necrotic tissue.
• Irrigate cavity with 3L saline with pulsatile lavage system with
antibiotics.
• Skin closed loosely over drains, do not close
wound if it produces excessive tension on skin

37. Technique for drainage of acute OM
TIBIA

38. After treatment
• Long leg posterior slab is applied with foot in neutral position,
ankle at 90 degrees, knee at 20 degree flexion.
• Antibiotics continued based on culture sensitivities
• 2 week coarse of IV antibiotics given if culture is grown
positive.

39. Complications of acute OM
• Early:
1) Septic arthritis.
2) Thrombophlebitis
3) deep vein thrombosis
4) Multiple pyogenic abscess.
5) Adverse reactions of antibiotics

40. Complications of acute OM
• Late
1) Chronic osteomyelitis
2) Pathological fracture
3) Local growth disturbances over growth-due to prolonged
hyperemia
4) Premature closure of epiphysis
5) Deformity

41. Neonatal OM
• Occurs in 2 distinct varieties
1)Seen in 2-8 weeks of age
• S.aureus: MC
• Manifests by lack of movement, visible swelling of extremity.
• Fever and irritability not present, inflammatory response not
mounted, so diagnosis difficult.
• High index of suspicion, aspiration done and antibiotics to be
started.
2) Second form encountered in NICU units
• - Typically seen in LBW infants, neonates requiring
endotracheal intubation & IV lines.

42. Features in neonatal OM
• In children < 2 years, transphyseal blood vessels cross the
physis, allow the spread of infection into the epiphysis.
• Cortex is porous, pus collects in sub-periosteal space.
• Susceptible to shortening and angular deformity.
• Even joint is also involved, hip joint being common.

43. Features in neonatal OM
-Pelvis of 1yr old girl who had osteomyelitis of proximal
femur and septic arthritis of hip.
-These infections resulted in destruction of physis and
epiphysis

44. Sub-Acute Osteomyelitis

45. Subacute Osteomyelitis
• Subacute osteomyelitis is a consequence of an altered host-
pathogen relationship characterized by
 decreased bacterial virulence,
 Increased host resistance,
 or a combination of these factors
• Microbes get entrapped in fibrous tissue proliferation.

46. Subacute Osteomyelitis
• Incidental finding on radiographs-
localized radiolucency surrounded
by sclerotic margin(Brodie’s abscess).

47. Sub acute OM
Features-
• Insidious onset, indolent course
• Mild pain , temp
• Blood culture –Negative
• Aspiration , biopsy – Positive in 60% cases

48. Sub-acute OM
• Plain radiographs show
poorly permeative lytic
changes in the left proximal
femur.

49. Sub acute osteomyelitis
CT scan shows permeative cortical erosions with
periosteal reaction.
MRI shows diffuse femoral marrow signal changes with a
fluid collection adjacent to bone suggestive of abscess
rather than liquefied tumor necrosis.
Biopsy and culture confirm the diagnosis of subacute OM

50. Gledhill Classification for subacute OM
This classification system is based
on
 Anatomic location,
 Response of the surrounding
tissue to infection
 Similarity to benign or malignant
tumors
1.Central metaphyseal (1a,1b)
2.Eccentric metaphyseal
3.Diaphyseal cortical
4.Diaphyseal with periosteal new
bone
5.Epiphyseal
6. Vertebral lesion

51. Brodie Abscess
• Localised subacute osteomyelitis.
• Long bones lower limb.
• In Adults Metaphyseal-epiphyseal area
• Intermittent pain, local tenderness.
• X ray- lytic lesion ,sclerotic rim.
• S. aureus in 50% , negative culture in 20%.

52. Differential diagnosis of Sub-Acute OM
When lesion is metaphyseal
• Ewing sarcoma
• Osteoid osteoma
• Osteogenic sarcoma
• Langerhens cell histiocytosis
When lesion is epiphyseal
• Chondroblastoma
• Fungal osteomyelitis
• Tuberculous osteomyelitis
• Aneurysmal bone cyst
• Giant cell tumor

53. Treatment
Immobilization
 surgical drainage -
a) Open biopsy
c) Curettage of the lesion
d) Bone grafting
intravenous antibiotics followed by 6 weeks of oral
antibiotics once the levels of inflammatory markers have
decreased.

54. Special Situations
Garre’s sclerosing OM
• Long standing chronic OM.
• Common in children.
• Mandible > Tibia.
• Excessive periosteal reaction by an extremely
sensitive periosteum in response to low grade
anaerobes.
• Swelling+ but pain-/sinus-/sequestrum-/pus-.
• Treatment- antibiotics plus NSAIDS.

55. Special Situations
Vertebral Osteomyelitis
• commonly stems from a disc-space infection seeded through
hematogenous dissemination or surgery.
• Usually a/w severe pain and limited ability to function.
• MRI is an important imaging modality to detect.

56. Vertebral Osteomyelitis
• Usually cured without
surgery, even though there
may be extensive bone
involvement.
• A six-week course of
antibiotic therapy is
commonly recommended

57. Chronic recurrent multifocal osteomyelitis
(CRMO)
• Inflammatory bone condition.
• Mainly affect the metaphysis
of long bone, in addition to the
spine.
• Initially osteolytic, later hyper-osteotic
and sclerotic lesson.
• Associated with other
inflammatory condition
like Psoriasis and IBD.

58. Chronic recurrent multifocal osteomyelitis
(CRMO)
• Arthritis of adjacent and distal joint is frequent.
• NSAIDS are effective.
• In children with spinal lesions, Infliximab +/- bisphosphonate
& bisphosphonate alone showed favourable outcomes
• In children with persistently active symptoms and abnormal
MRI findings, additional treatments including DMARDs, TNF
inhibitors, and/or bisphosphonates are necessary to induce
remission and reduce skeletal damage .
• Antibiotics are ineffective.