Bone Infections

1.  DR MALIKGHULAMYASIN
 FCPS ORTHO.
 ASSISTANT PROFESSOR

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.

6.  OSTEOMYELITIS
 Acute
 Sub acute
 Chronic
 SEPTIC ARTHRITIS
 Acute
 Sub acute
 Chronic

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.

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).

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.

16.  Cellulitis.
 Acute supurative arthritis.
 Streptococcal necrotizing Myositis.
 Acute rheumatism.
 Sickle-cell crisis.
 Gauchers disease.

17.  Four important aspects of treatment are
 Supportive treatment for pain and
dehydration.
 Splintage (rest) of the affected limb.
 Appropriate antimicrobial therapy.
 Surgical drainage.

18.  Epiphyseal damage and altered bone growth
 SepticArthritis.
 Metastatic Infection.
 Pathological Fractures.
 Chronic Osteomyelitis.
 Septicemia.

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.

24.  Cystic tuberculosis.
 Eosinophilic granuloma.
 Osteoid Osteoma.
 Ewing's Sarcoma.
 Chondroblastoma.

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

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.

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,

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.

44.  TLC, ESR elevated, Blood culture is positive.
 Synovial fluid aspirate, decreased glucose
increased proteins andWBC, Gram stain and
C/S.

45.  1. Acute osteomyelitis.
 2. Other type of infections (psoas abscess).
 3.Trauma (traumatic synovitis,
haemarthrosis).
 4. Irritable joint.
 5.Haemophilic bleed.

46.  6. Rheumatic fever.
 7. Juvenile rheumatoid arthritis.
 8. Sickle-cell disease.
 9. Gauchers disease.
 10. Gout and pseudo gout.

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.

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.

57.  1.Transient synovitis.
 2. Monarticular rheumatoid arthritis.
 3. Sub acute arthritis.
 4. Haemorrhagic arthritis.
 5. Pyogenic arthritis.
 TREATMENT:
 1- Chemotherapy and rest.
 Surgery– I/D, arthrodesis, arthroplasty.

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.

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.

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.

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.