Paediatric musculoskeletal infections

1. PAEDIATRIC
MUSCULOSKELETAL
INFECTIONS
DR RITESH JAISWAL
M.B.B.S D.Ortho DNB (Ortho) M.N.A.M.S M.Ch (Ortho)
Fellowship in Joint Replacement ( Mumbai )
Fellow AO Trauma ( Switzerland )

2. OSTEOMYELITIS
Inflammation of bone caused by an infecting organism
Nelaton ( 1834 ) coined term osteomyelitis
It may remain localized or it may spread through
the bone to involve marrow, cortex, periosteum
and surrounding soft tissue

3. CLASSIFICATION
A ) Based on duration and type of symptoms
- Acute ( < 2 weeks )
- Subacute
- Chronic ( > 12 weeks )
B) Based on spread of infection
- Direct introduction through the skin
(a pinprick, an injection, a stab wound, a laceration, an open fracture
or an operation, particularly when biomaterials are implanted)
- Direct spread from a contiguous focus of infection
- Indirect spread via the bloodstream from a distant site such as
the nose or mouth, the respiratory tract, the bowel or the
genitourinary tract.

5. C) Based on host factors

6. ACUTE HAEMATOGENOUS
OSTEOMYELITIS ( AHO )
Introduction
Aetiology
Pathogenesis
Clinical features
Clinical investigations
Management

7. INTRODUCTION
- AHO is the most common type of bone infection in
infants and children.
- Haematogenous in origin
- Starts in metaphysis of active growing long bones
- More common in males in all age groups affected.
- Bacteriological seeding of bone generally is
associated with other factors such as localized
trauma, chronic illness, malnutrition, or an
inadequate immune system.

8. AETIOLOGY
Causative organisms
- Staphylococcus aureus - (> 70% of cases)
- Group A beta-haemolytic streptococcus (Streptococcus
pyogenes) which is found in chronic skin infections
- Newborn babies - Group B streptococcus.
- 1 and 4 years of age - the Gram-ve H. influenzae
- Other occasional Gram-negative organisms
(e.g. Escherichia coli, Pseudomonas aeruginosa, Proteus
mirabilis and the anaerobic Bacteroides fragilis) .

10. PATHOGENESIS
- Infection usually starts in the vascular metaphysis of a long bone
- Most often in proximal tibia or distal or proximal ends of the femur.
Predilection for metaphysis for bacterial colonization
1 ) 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
2 ) Relative vascular stasis and consequent
3 ) Lowered oxygen tension
4 ) Vessels in Hypertrophic zone of the physis easily allow bacteria to pass
through and adhere to type 1 collagen in that area.
5) Defective phagocytosis
6 ) Dead & Dying tissue of cartilage provide good nutritive material for
organism

16. NEONATES / INFANTS
- Due to anastomoses between metaphyseal
and epiphyseal blood vessels, infection can
also reach the epiphysis.
- Osteomyelitis in the metaphysis can result in
thrombosis of these vessels, leading to severe
osteonecrosis of the epiphysis.
- With development of the ossific nucleus, the
epiphyseal and metaphyseal blood supply
become independent, with the physis
providing a barrier to spread

17. - Metaphyseal cortex is thin and pus may penetrate
it, resulting in a subperiosteal abscess.
- This in turn deprives the cortex of periosteal
blood supply.
- If effective management is not instituted, the
segment of cortex becomes necrotic and forms a
sequestrum.
- The periosteum, however, retains osteogenic
properties and new bone is laid down, the
involucrum.
- The sequestrum and involucrum are the
hallmarks of chronic osteomyelitis.

19. CLINICAL PRESENTATION
History
- Bone pain/ limb pain of one to several days' duration
- recent local infection
- trauma
- obtain immunization history regarding H. influenza
- ask about prior antibiotic use, as it may mask symptoms
Symptoms
- limp or refusal to bear weight
- generally not toxic appearing
- fever , malaise
Physical exam
- Antalgic gait
- edematous, warm, swollen, tender limb
- evaluate for point tenderness in pelvis, spine, or limbs
- range of motion - restricted motion due to pain
- Lymph node enlargement
* Bone pain is an indication to investigate and treat aggressively for presumed
osteomyelitis.

20. DIAGNOSIS
* Early diagnosis of acute hematogenous osteomyelitis is
important as the course of the disease and its ultimate
prognosis depend on the rapidity and adequacy of
treatment.
* Acute hematogenous osteomyelitis should not be ruled
out simply on the basis of a lack of sepsis, because this
disease may be more or less virulent depending on the
organism involved and the host resistance
* Early in the course of the disease, the swelling is
localized to the metaphysis of the involved long bone
hence local signs may be absent unless the infection
has spread subcutaneous .

21. INVESTIGATIONS
LAB :
1 ) CRP- raised in 98%
- may be normal in neonates and patients with comorbidities
(e.g. immunocompromise, anaemia, sickle cell disease)
2) ESR –
- >20 mm h–1 in 80% of cases, but is non specific.
3 ) WBC count
- elevated in only 35–40%
4 ) Blood cultures - only positive in 30–50%

22. RADIOGRAPHS-
- Early films may be normal or show loss of soft tissue planes
and soft tissue edema
- New periosteal bone formation (5-7 days)
- Osteolysis (10-14 days)
- Late films (1-2 weeks) show metaphyseal rarefaction
(reduction in metaphyseal bone density) or possible abscess

23. Bone scan
- Can confirm diagnosis in 24-48hrs
- Highly sensitive but less specific
- Useful in multifocal infections or
the site is hard to localize.
-Cold scan may indicate either
- disease process is not well
advanced
- hypoperfusion, as in
osteonecrosis.

24. MRI
- most sensitive test for osteomyelitis (97–100%)
and has a specificity of 73–92%.
- It defines
(1) soft-tissue extension
(2) intraosseous collection
(3) joint involvement and
(4) planning for the surgical approach

25. ASPIRATION
- Identifies the infecting organism in 75–80% of cases
- Fluid may be aspirated from a subperiosteal abscess
- Large-bore spinal needle used to perforate the thin
metaphyseal cortex & aspirate a purulent intramedullary
collection.
- Bone aspiration may be useful in areas where MRSA is
common
- Initial treatment can be with vancomycin, and this can
be changed when other organisms are found to be
responsible.

26. DIFFERENTIAL DIAGNOSIS
- Septic arthritis
- Non-septic arthritis, including juvenile idiopathic arthritis
- Transient synovitis
- Neoplasia - Ewing’s sarcoma, osteosarcoma, leukaemia,
metastatic neuroblastoma
- Langerhan’s cell histiocytosis
- Sickle cell disease
- Fracture (especially in the neuromuscular patient)
- Avascular necrosis: Perthes disease, haemophilia, infarct
- Gaucher disease
- Haemarthrosis e.g. haemophilia

27. MANAGEMENT
The aims of treatment are:
1 to prevent overwhelming sepsis
2 to cure the local disease as rapidly as possible
3 to prevent complications
- growth plate damage
- pathological fracture
- osteonecrosis
- deep vein thrombosis
- chronic osteomyelitis
* Prompt diagnosis and appropriate intravenous antibiotics
can lead to complete resolution with no further sequelae.

28. While managing AHO 3 factors to be considered:
(1) the patient
(2) the organism
(3) the bone

29. PATIENT :
- Common in lower socioeconomic classes
- Delayed presentation is common.
- Well established infection before starting treatment
- Late presentation common in
- Immunocompromised (e.g. on steroids)
- Misdiagnosed as a fracture
- Neonate (As pseudoparalysis is only clinical sign )
- Associated comorbidities having less predictable clinical outcome :
- Diabetes mellitus
- Haemoglobinopathies
- Chronic renal disease
- Rheumatoid arthritis

30. ORGANISM
- S. aureus is the commonest infecting
organism.
- Organisms specific in certain age groups and
patient
- Important to know for antibiotic selection.
- H. influenzae and K. kingae need to be
considered in nonresponders
- In some areas community-acquired MRSA is a
significant cause.

31. Organism Antibiotic
Neonate Streptococcus Cefotaxime
oxacillin and
gentamicin
Staphylococcus
aureus
Coliforms
Gram negative
bacilli
Infant/child Staphylococcus Oxacillin and
aureus ampicillin
Sickle cell Salmonella Cefotaxime or
disease
chloramphenicol

32. BONE
- COMMON SITES - metaphysis of proximal tibia and distal femur
- Rarely extend in diaphysis if treated early
- AHO of pelvis, clavicle and calcaneus/talus less common hence
delayed diagnosis
- Largely cancellous bone make eradication difficult and
treatment prolonged.
- Early Antibiotics on the assumption of AHO.
- Deterioration or lack of response requires consideration of
repeat imaging, debridement or a change in antibiotics.
- A repeat MRI is useful to identify further collections
(intraosseus or subperiosteal) or spread of infection.
- Infected deep vein thromboses may be visualized in vessels
abutting AHO, which may result in septic embolization and
require anticoagulation.

33. Factors to consider for switching from parenteral
to oral antibiotics
● The patient: immunocompromised vs healthy
● The organism: Staphylococcus aureus vs
Escherichia coli, Pseudomonas, methicillin-
resistant Staphylococcus aureus
● The bone: proximal tibia vs pelvis, clavicle,
calcaneus
● The clinical response: rapid clinical improvement
vs repeat surgical debridement

34. ROLE OF C-REACTIVE PROTEIN
- Values during treatment can be useful to monitor
control of infection.
- With concordant clinical findings, a declining CRP
indicates when a change from intravenous to oral
antibiotics is appropriate.
- For uncomplicated AHO, the CRP is likely to have
normalized by day 9.
- Antibiotic treatment should be continued orally
for a total of at least 3–4 weeks, although
intravenous antibiotics may be discontinued after
clinical normalization

35. DURATION OF TREATMENT
- Clinical course to be monitored closely
- Surgical interventions & antibiotics use should
be appropriate
- I/V antibiotics ( 6 – 12 weeks ) until all clinical
features are resolved in resistant/intractable
cases and compromised hosts

36. SURGICAL INTERVENTION
- Surgical debridement is mandatory if abscess is
localized by MRI
- Approach is guided by the imaging.
- Small abscesses in difficult locations can be drained
percutaneously with the help of ultrasound
guidance or CT scanning
e.g. pelvic osteomyelitis.
- The bone does not usually need to be ‘drilled’ as
part of the debridement, as usually the
intraosseous collection has decompressed into a
subperiosteal collection.

37. - Leave large drains in the wounds following
debridement and close the skin edges loosely
with sutures.
- The patient returns to the operating room 24–48
hours later, for a repeat washout/debridement.
- Definitive closure is performed only when the
infection is controlled.
- If a large amount of pus is still present at the
‘second look’, the wound is left open and a
suction dressing applied.

39. FOLLOW UP
- At 3, 6 and 12 weeks
- for clinical examination
- Plain radiography and blood investigations
(WBC count, ESR and CRP).
- Patients on home flucloxacillin have weekly
liver function tests and neutrophil counts, as
there is a high rate of flucloxacillin associated
neutropenia.

40. CHRONIC OSTEOMYELITIS
2 types :
A ) PRIMARY CHRONIC OSTEOMYELITIS
- when the inflammation is low grade
- BRODIES ABSCESS
- SCLEROSING OSTEOMYELITIS
- TUBERCULOUS OSTEOMYELITIS
- CHRONIC RECURRENT MULTIFOCAL OSTEOMYELITIS
B ) SECONDARY CHRONIC OSTEOMYELITIS
- When acute pyogenic infection is persistent

41. BRODIES ABSCESS
- Described by Sir Benjamin Brodie in 1832
- Insidiously developing chronic pyogenic osteomyelitis
- Commonly result of infection by organisms of low virulence
- common in the upper tibial metaphysis.
- Since it is a localized form of suppuration it may also be termed a
chronic bone abscess.
- Although often referred to as a subacute form of osteomyelitis the
lesion may persist for many years.

42. CLINICAL PRESENTATION
- H/O trivial trauma may +
- Intermittent mild to moderate pain may present for
weeks to months
- Temperature usually normal
- mild swelling +/-
- Limp, muscle wasting, tenderness +/-
- Its relative mildness is presumably due to the organism
being less virulent or the patient more resistant (or both).

43. RADIOGRAPH
- a circumscribed, round or oval
radiolucent ‘cavity’ 1–2 cm in
diameter.
- common in the tibial or femoral
metaphysis, rarely in calcaneum
- Sometimes the ‘cavity’ is
surrounded by a halo of sclerosis
(the classic Brodie’s abscess)
- occasionally it is less well defined,
extending into the diaphysis
- Metaphyseal lesions cause little or
no periosteal reaction
- Diaphyseal lesions may be
associated with periosteal new
bone formation and marked
cortical thickening.
- If the cortex is eroded, the lesion
may be mistaken for a malignant
tumour.

44. LAB :
- WBC count and blood culture are normal.
- ESR may be raised
BONE SCAN
- shows markedly increased activity
BIOPSY
- To confirm when clinical and radiographic findings are non-specific
- If fluid is present sent for bacteriological culture -
+ in half of cases and organism is almost invariably
Staphylococcus aureus.

45. MRI
- Penumbra sign a hyperintense rim around the
main cavity on T1 -weighted MRI, helps to
distinguish infection from other lesions.

46. DIFFERENTIAL DIAGNOSIS
- osteoid osteoma
- Eosinophilic granuloma
- Non-ossifying fibroma
- Enchondroma
- Unicameral bone cyst
- Leukaemia
- Ewing’s sarcoma

47. TREATMENT
- IF DIAGNOSIS IS NOT DOUBTFUL
- conservative
- Immobilization
- Antibiotics (flucloxacillin and fusidic acid)
intravenously for 4 or 5 days
orally for another 6 weeks
- healing, may take up to 12 months.
- IF DIAGNOSIS IS DOUBTFUL
- Open biopsy with curettage
- Curettage is also indicated if the X-ray shows that there is no
healing after conservative treatment,followed by a further course
of antibiotics.

48. SCLEROSING OSTEOMYELITIS
- In 1893 Garré described a rare form of non-
suppurative osteomyelitis
- characterized by marked sclerosis and cortical
thickening.
- There is no abscess, only a diffuse enlargement of the
bone at the affected site – usually the diaphysis of one
of the tubular bones or the mandible.
- The patient is typically an adolescent or young adult
with a long history of aching and slight swelling over
the bone.
- Occasionally there are recurrent attacks of more acute
pain accompanied by malaise and slight fever.

49. Pathology -
- Chronis osteomyelitis has destructive
(necroinflammatory) and reparative (new bone
formation) processes simultaneously
- In sclerosing OM , osteosclerosis markedly
predominant
- This type is difficult to diagnose with confidence
because cultures are often negative.
Differential diagnosis
- osteoid osteoma and other bone lesions
associated with marked sclerosis.

50. RADIOGRAPHS
- Increased bone density and cortical thickening
- Marrow cavity may be obliterated
- No abscess cavity.
Diagnosis can be difficult.
- The biopsy will disclose a low-grade inflammatory lesion with
reactive bone formation.
- Microorganisms are seldom cultured but the condition is usually
ascribed to a staphylococcal infection.
Treatment
- the abnormal area is excised and the exposed surface thoroughly
curetted.
- Bone grafts, bone transport or free bone transfer may be needed.

51. Chronic recurrent multifocal
osteomyelitis
A condition characterized by idiopathic
inflammatory disease of the skeleton that meets
the following criteria
- multiple sites of apparent osteomyelitis
- No pathological findings
- No response to antibiotics
- Primarily occurs in children/adolescents
- Peak age of onset is 10 years old
- Girls >> boys
Common site
- the tubular long bones and clavicle are most frequently affected

52. Associated conditions
- Pustulosis palmoplantaris syndrome
- a rare chronic relapsing condition causing red
patches and pustules on the soles of the feet
and palms of the hands
- Rheumatologic condition with no infectious
agents
- SAPHO Syndrome –
CRMO associated with: synovitis, acne,
pustulosis, hypersotosis, osteitis

53. Clinical Presentation
- fever
- malaise
- localized pain
- swelling
- focal tenderness

54. INVESTIGATIONS
Radiograph:
Eccentric metaphyseal lesions with sclerosis and
new bone formation
Bone scan :
Can help determine other sites of disease
MRI :
determine presence or absence of soft tissue
involvement

55. Lab
- WBC typically normal
- ESR and CRP may be elevated
Biopsy & Culture
- Negative
- Establish diagnosis of exclusion

56. TREATMENT
- Nonoperative
- NSAIDS
- Pamidronate
* Pamidronate can provide symptomatic
improvement and stimulate remodelling

57. PROGNOSIS
- traditionally thought as having a relatively
benign sequelae
- several case reports of growth disturbance
have been reported

58. SEPTIC ARTHRITIS
Inflammation of synovial joints due to bacterial
infection of the joint.
It typically affects large joints
- hip (35%)
- knee (35%)
- ankle (10%),
- other joints may be affected
Usually single joint is affected
common in the younger child

59. ETIOLOGY
1. Haematogenous spread (commonest mechanism)
Infective focus elsewhere in the body via bloodstream
2. Local spread from adjacent bone or soft-tissue infection
i.e. osteomyelitis
3. Direct seeding into a joint following surgery or penetrating
trauma.
* In early infancy, before the formation of the growth plate, the
transphyseal blood vessels may act as a route for the transfer of
bacteria into the joint e.g. the hip.
* In the hip, elbow and shoulder joints, septic arthritis may develop after
metaphyseal osteomyelitis, as the metaphyses of these joint are intra-
articular.

61. Group Causative organism
Neonate Staphylococcus aureus*, Group B Streptococcus,
Escherichia coli, H. influenza
Early childhood (to 3 years) Staphylococcus aureus*, Kingella kingae**,
Streptococcus pneumonia, Neisseria meningitidis
Childhood (3–12 years) Staphylococcus*, Group A β-haemolytic Streptococcus
Adolescent (12–18 years) Staphylococcus aureus*, Group A βhaemolytic
Streptococcus, Neisseria gonorrhoea
Other risk factors:
Sickle cell Salmonella species, Staphylococcus aureus,
Foot puncture Streptococcus pneumonia Pseudomonas aeruginosa,
Staphylococcus aureus
There is an increasing incidence of MRSA across all age ranges

62. CLINICAL FEATURES
Fever
Malaise
Anorexia
Limp or inability to bear weight
O/E
Joint effusion
erythema
warmth and tenderness
Restricted range of movement
In hip joint involvement –
Attitude is - hip in external rotation, abduction and a degree of flexion.
Pseudoparalysis (a lack of active movement of the affected joint)
Is only positive sign seen in infants

63. Kocher’s Criteria
Kocher et al identified four independent
predictors of septic arthritis
- Fever (>38.5°C)
- Inability to bear weight
- Erythrocyte sedimentation rate >40 mm/h
- White blood cells >12 000 /mm3

64. DIAGNOSIS
Clinical examination
Lab investigations
- CBP, ESR
- C-reactive protein (CRP)
- Blood cultures
- white blood cell count may be raised in only 30–60% of cases.
- level of CRP is elevated early on in the disease process and
normalizes within a week of effective treatment
- CRP is effective in monitoring response to treatment.
- ESR may take 24–48 hours to elevate and 3 weeks to normalize

65. Radiography
- Joint space widening
- Soft-tissue swelling
- Bone changes ( take > 2 weeks to appear )
- To exclude other conditions

66. USG
- First-line imaging modality for septic arthritis.
- To determine the presence of a joint effusion
- Findings of synovial thickening and capsular
thickening can help to differentiate septic arthritis
from transient synovitis

67. MRI
If clinical picture & USG is not convincing
To rule out as it osteomyelitis or tumour.

68. JOINT ASPIRATION
INDICATIONS
- Joint sepsis with effusion
- Prior administering antibiotics
To be done under sterile precautions in the OT
Under image intensifier and arthrogram
- Gram stain to confirm the presence of organisms.
- WBC >50 000 /ml with >75% polymorphonuclear cells is
suggestive of sepsis.
- + Gram stain only in 30% of cases joint sepsis

69. DIFFERENTIAL DIAGNOSIS
- Transient synovitis (aseptic inflammation of the synovium)
- Osteomyelitis
- Juvenile rheumatoid arthritis

70. TREATMENT
- Septic arthritis is an orthopaedic emergency.
- Permanent chondral destruction and avascular necrosis
can be avoided with early treatment
Bacteria and leucocytes release proteolytic enzymes
↓
Rapid proteolytic Breakdown
↓
Inflammatory effusion
↓
Joint destruction

71. - Early surgical drainage
- Administration of intravenous antibiotics
- Open surgical lavage remains the gold standard
- Mini invasive / Arthroscopically is preferred
* A delay in acquiring an ultrasound should not delay surgical
drainage.

72. - Broad-spectrum cephalosporin initially
- Later as per microorganism & sensitivity
- Administered for a period of 3–6 weeks
- Oral antibiotics can be started once
- Patient is afebrile for 48 hours
- CRP/ESR levels return to close to baseline

73. Sequelae of septic arthritis
- chondral damage
- avascular necrosis
- growth arrest
- angular deformity
- leg length discrepancy
- Tom Smith arthritis.

74. THANKS
FOR YOUR
ATTENTION