3. It is a condition in which pathogenic
organisms multiply and spread with in the
body tissues.
As a result the host compete the organisms
resulting in inflammatory response.
SIGNS OF INFLAMATION:
Pain, redness, swelling, heat and loss of
function.
4. Direct introduction through skin.
Direct spread from a contiguous focus of
infection.
Indirect spread via the blood stream from a
distant site.
5. General supportive measures and analgesia.
Rest of the affected part.
C/S and proper antibiotics administration.
Operative is—Removal of dead tissues.
Stabilization of bone if fractured.
Continuity of bone if fractured.
Soft tissue and skin covering.
7. It is mainly disease of children.
Spread of infection is usually
haematogenous.
In adults haematogenous infection is only
20%.
CAUSATIVE ORGANISMS:
Staphylococcus aureus – 70%.
H Influenza in children 1-4years.
E coli in infants.
8. Inflammation and suppuration.
Bone necrosis and new bone formation
Resolution and healing OR chronicity.
Mainly involves metaphysis due to acute
arterial loops below epiphysis which causes
sluggishness of blood flow leading to
bacterial stasis and decreased phagocytic
reticuloendothelial function.
9.
10.
11. Pain and fever.
Refusal to use the limb and it is held still.
Pulse rate increased, temperature elevated.
Swelling, redness, edema, warmth and local
tenderness.
12. X-RAY
1st week no bony lesion only soft tissue
edema.
2nd week extra cortical out line due to
periosteal reaction(new bone)
3rd week patchy rarefaction of metaphysis.
4th week bone destruction
5th week osteoporosis and
sclerosis(sequestrum).
13.
14. USG- Subperiosteal collection.
MRI- Bone marrow inflammation.
Bone Scan- Increased uptake.
15. TLC- Increased.
DLC- Polymorphonuclear leucocytosis.
CRP-Increased with in 12-24 hours.
ESR- Increased with in 24-48 hours.
Aspirate- for cells, organisms, gram stain and
culture and sensitivity.
17. Four important aspects of treatment are
Supportive treatment for pain and
dehydration.
Splintage (rest) of the affected limb.
Appropriate antimicrobial therapy.
Surgical drainage.
19. Organism may be less virulent.
Patient may be more resistant.
May be sequel of acute osteomyelitis.
Distal femur and distal and proximal tibia are
common site of involvement.
20. Well defined cavity in cancellous bone
surrounded by thick sclerotic bone.
Cavity is lined by granulation tissue
containing acute and chronic inflammatory
cells.
Cavity contains seropurulent fluid.
21. Pain and slight swelling.
Limping and muscle wasting.
Local tenderness.
LABORATORY INVESTIGATION:
TLC, DLC are normal.
ESR is elevated.
Biopsy is confirmative.
22. Radiolucent cavity 1-2cm in diameter
surrounded by a halo of sclerosis.
Metaphyseal region no periosteal reaction.
Diaphyseal region periosteal reaction.
Bone scan shows markedly increased up take.
25. Antibiotic (flucloxacine and fucidic acid) i.v
for one week followed by oral for other six
weeks.
Curettage if x-ray shows no healing after
antibiotic course, this is followed by an other
course of antibiotics.
26. It may be sequel of acute osteomyelitis, open
fractures, operation.
Causative organism are mixed
(Staphylococcus, Streptococcus, E. coli,
Proteus and Pseudomonas)
27. Sequestrum (dead bone)
Involcrum (new bone formation)
Sclerosis (dense bone)
Sinus formations
Pathological fracture
28. Sinus with seropurulent discharge
In flare up there is pain, pyrexia, redness and
tenderness
Slight swelling
Local tenderness
29. X-RAY– Sequestra (dead bone)
Involucrum– (new bone) periosteal reactions
Sclerosis around the lesion
Osteoporosis of the whole bone
Bone scan– increased up take
CT, MRI– extent of bone destruction, hidden
abscesses and Sequestra.
TLD, DLC, ESR may be raised.
C/S, PCR
30.
31.
32. It depends upon the local involvement and
host condition.
LESION TYPE HOST CATEGORY
Stage 1 Medullary Type A Normal
Stage 2 Superficial Type B Compromised
Stage 3 Localized (systemic or
Stage 4 Diffuse local)
Type C Compromised
(systemic and local)
33. ANTIBIOTICS– four to six weeks
According to c/s, but should be least toxic and
penetrable to the sclerotic bone.
Fusidic acid, Clindamycine and Cephalosporin
are good examples.
SURGICAL:
Debridement, dealing with dead space, bone
stabilization if pathological fracture and soft
tissue coverage.
34. Direct invasion through penetrating object.
Direct spread from adjacent bone abscess.
Blood spread, from distant site.
Causative organism is usually Staphylococcus
aureus.
35. Inflammatory reaction giving rise to
seropurulent discharge and increase in
synovial fluid.
Destruction of articular cartilage by bacterial
and proteolytic enzymes and inflammatory
cells.
36. There may be—
1- Complete resolution and return to normal.
2- Partial loss of articular cartilage and
fibrosis of the joint.
3- Complete loss of articular cartilage and
bony ankylosing of the joint.
4- Bone destruction and permanent
deformity.
37.
38. INFANTS– septicemia, irritable, refuses to
feed, rapid pulse and fever.
CHILDREN– pain, reluctant to move the limb,
redness and swelling over the joint, fever and
rapid pulse.
ADULTS– painful, swollen and inflamed joint,
movements are restricted,
39.
40. USG– Early cases and especially hip joint.
X-RAYS– In early cases only soft tissue
swelling and subluxation of the joint, later
there may be dislocation, destruction or
ankylosing.
MRI and Bone Scan are helpful in diagnosing
obscure sites such as SI joint.
47. SUPORTIVE CARE– Analgesia, I.V Fluid,
Splintage.
ANTIOBITICS– For infants and children
flucloxacilln and third generation
cephalosporin.
Adults– Flucloxacilln and fusidic acid.
One week I.V and three weeks oral.
48. ASPIRATION– Repeated.
DRAINAGE–Where there is pus it should be
drained.
AFTER CARE– Physiotherapy when joint is
pain free.
49. INFANTS and CHILDREN– Subluxation and
dislocation of hip joint. Instability of knee
joint. Growth retardation and deformities due
to growth plate damage.
ADULTS– Restricted movements or complete
ankylosis of joint.
50. PATHOLOGY:
Causative organism– Mycobacterium
tuberculosis.
1. Primary complex.
2. Secondary spread.
3.Tertiary lesion.
Skeletal metastasis is by tertiary lesion.
Main sites of involvement are vertebral
bodies and large synovial joints.
51.
52.
53. H/O Previous infection or recent contact.
Pain and swelling of the joint.
Fever, night sweat, lassitude and weight loss.
Muscle wasting, synovial thickening, and
regional lymphadenopathy.
Joint stiffness and deformity.
SPINE– Local abscess (psoas), localized
kyphosis and/or weakness and instability of
lower limbs.
54. Soft tissue swelling.
Peri-articular osteoporosis.
Narrowing of the joint space.
Cystic lesion in adjacent bone.
No periosteal reaction.
SPINE– Bony erosion and collapse around
diminished intervertebral space.
Soft tissue shadow for paravertebral abscess.
55. ESR elevated and relative lymphocytosis.
Mantoux or Heaf test positive.
Synovial fluid– cloudy, proteins are increased,
sugar is decreased,WBC elevated,AFB
positive in 20%.
Synovial biopsy.
56. Long history of pain and swelling.
One joint.
Synovial thickening.
Muscle wasting.
Enlarged regional lymph nodes.
Peri articular osteoporosis on x-ray.
Synovial biopsy.
58. It starts as synovitis or some times
osteomyelitis in adjacent bone.
Once arthritis develops there is rapid
destruction and pathological dislocation.
CLINICL FEATURES:
1- Onset is insidious with aching in the groin
and thigh.There is slight limp.
59. 2- Initially the joint is flexed, adducted and
extremes of movements are restricted and
painful.
3- Later there is flexion, adduction, medial
rotation, muscle wasting, restriction of all
movements, pain and spasm.
60. 1- Initially there is general rarefaction and
joint space is normal.
2- Later there is destruction of femoral head
and/or acetabulum.
3-There may be sublaxation or even
dislocation.
61.
62.
63.
64.
65.
66. CONSERVATIVE: Only in early cases.
1- Chemotherapy.
2- Rest, skin traction or abduction brace for
children.
SURGICAL: In later cases.
1- Chemotherapy
2- Incision drainage, joint debridement.
3- Arthrodesis above 14 years of age.
4-Total hip replacement in older.
67. Early disease, properly treated almost normal
hip.
Treated after articular destruction, there may
be fibrous ankylosing.
In untreated cases the leg becomes thin,
shortened, adduction and flexion deformity.
Dislocation of the hip.
68. PATHOLOGY:
SpinalTB is about 50% of all skeletalTB.
Mostly involve thoracic spine.
Blood borne infection settles in the vertebra
near intervertebral disc. Infection spread to
the adjacent vertebra. So there is destruction
of two adjacent vertebrae resulting in angular
kyphosis (gibbus).
69. Para vertebral abscess may form and may
track down.
There is risk of cord damage due to pressure
by abscess, granulation tissue, sequestra or
displaced bone.
With healing the vertebrae recalcify and may
be bony fusion between them.
70.
71.
72.
73.
74. Long history of ill health and backache.
In late cases gibbus deformity is the feature.
May be features of concurrent pulmonaryTB.
May be cold abscess pointing in the groin.
Paraesthesia and weakness of the legs.
Local tenderness in the back and restriction
of spinal movements.
In cervical spineTB dyspnoea, dysphagia and
stiff painful neck.
75. In children below 10 years with thoracicTB
develop pectus carinatum (pigeon chest).
Neurological examination may show motor
(spastic) and/or sensory changes in lower
limbs.
Atypical features may be epidural abscess,
involvement of single vertebra, multiple
vertebrae and posterior vertebral elements.
76. Paraplegia is most feared complication.
1- EARLY ONSET: With in 2 years of disease.
CAUSES: Pressure due to oedema, abscess,
caseous material, granulation tissue or
sequestra.
2- LATE ONSET:
CAUSES: Cord compression due to increasing
deformity and vascular insufficiency of cord.
77. Lower limb weakness with upper motor
neuron lesion, sensory dysfunction, urinary
incontinence.
TREATMENT:
I- Chemotherapy.
2- Surgical decompression.
PROGNOSIS:
After surgical decompression it is good for
early onset and poor for late onset.
78. X-RAY: Entire spine should be x-rayed.
Early changes are local osteoporosis of two
adjacent vertebrae, narrowing of the
intervertebral disc space and fuzziness of the
end plates.
Late changes are bone destruction and
collapse of adjacent vertebral bodies into
each other.
79. Para spinal soft tissue shadows are due to
swelling or paravertebral abscess.
Chest x-ray is essential.
MRI and CT: For hidden lesions such as
epidural abscess and cord compression.
80.
81.
82.
83. Mantoux test is positive.
ESR is increased.
Needle biopsy for histological and
microbiological diagnosis. It may CT guided.
Open biopsy which is diagnostic and
therapeutic.
D/D: Other (pyogenic, fungal, parasitic)
infection.
Malignant such as metastatic bone disease.
84. OBJECTIVES OFTREATMENT:
1-To eradicate or at least arrest the disease.
2-To prevent or correct the deformity.
3-To prevent or treat the major complication
i.e. paraplegia.
Treatment may be conservative only i.e.
chemotherapy or operative i.e. combination
of chemotherapy and surgery.
85. 1- Ambulant chemotherapy: For early or
limited disease, with no abscess or
neurological deficit. It should be continued
for 6-12 months or until x-ray shows the
resolution of the bony changes.
2- Continuous bed rest and chemotherapy:
For advanced disease when necessary skills
and facilities are not available.
86. 3- SURGICALTREATMENT:
Indications:
1- Abscess which can be drained.
2- Marked bone destruction that can cause
severe kyphosis.
3- Neurological deficit.
87. CHEMOTHERAPY: 1- Rifampicin– 600 mg
daily for 6-12 months.
2- Isoniazid– 300mg daily for 6-12 months.
3- Pyrazinamide– 2 gm. daily for 2 months.
For resistant cases Isoniazid may be replaced
with Ethionamide – 1 gm daily or
Streptomycin – 1 gm i/m daily.
88. SURGICAL:
1- Drainage of abscess.
2- Anterior approach, removal of all infected
material and bone graft, may be added with
anterior instrumentation.
3- If multiple levels are involved then anterior
or posterior fusion and instrumentation is
required.
