Transcript T.B. OSTEOMYELITIS

Chronic Osteomyelitis
Factors responsible for chronicity
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Local factors: Cavity, Sequestrum, Sinus,
Foreign body, Degree of bone necrosis
General: Nutritional status of the involved
tissues, vascular disease, DM, low immunity
Organism: Virulence
Treatment: Appropriateness and compliance
Risk factors: Penetrating trauma, prosthesis,
Animal bite
Chronic Osteomyelitis
Types
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A complication of acute Osteomyelitis
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Post traumatic
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Post operative
Chronic Osteomyelitis
Clinical picture
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Continuous or intermittent suppuration and
sinus formation with acute exacerbations.
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Pain, fever, redness, and tenderness
during acute exacerbations.
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Discharging sinus with +ve/-ve culture.
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Pathological fracture.
Chronic Osteomyelitis
Investigation
 Lab tests/ culture
 Plain X-ray:
Bone rarefaction surrounded by the dense
sclerosis, sequestration and cavity formation
 Sinogram
 Bone scan & gallium scan
To detect chronic multifocal osteomyelitis
 CT Scan & MRI
 Biopsy
Chronic Osteomyelitis
Complications
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Recurrence & Recurrence & Recurrence
Pathological fractures
Growth disturbance
Amyloid disease
Epidermoid carcinoma of the fistula
CHRONIC OSTEOMYELITIS
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Sequel of acute/open fracture/opt.
C/F: pain, discharging sinus, scars
Xray- bone resorption, sequestra,
CT/MRI: extent of bone loss, oedema,
hidden abscess
Lab-raised ESR pus-cs
TREATMENT
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Antibiotics.
Local treatment.
Operations.
After care.
TUBERCULOSIS
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A surgeon could
gain experience in
the management of
TB. Of bone and
joint only if he
choose to work in
econmically less
developed countries.
(edit, Br.Med.J>1968)
T.B. OSTEOMYELITIS
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1/3 population infected.
Over 80,000 people in Nepal have TB.
22,000 develop Pul. TB every year.
Total 50,000.
10,000 die of TB.
LEADING CAUSE OF DEATH.
1 – 3% skeletal TB
TB
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Cause by Mycobacterium tuberculosis,
occasionally by M.bovis/africanum.
Also known as tubercle bacilli as they
produce lesion – tubercles.
Acid fast bacilli.
Transmission – airborne droplets.
Risk- extent of exposure to droplets and
susceptibility to infection.
TB Primary infection
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Exposure to tubercle bacilli – Lungs –
multiplication of bacilli in terminal
alveoli (Ghon focus) – lymphatic drain it
to hilar lymph nodes – (PRIMARY
COMPLEX) – BLOOD – SPREAD.
TB
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C/F:Cough >3wks.,sputum production,
weight loss, monoarticular.
Respiratory – haemoptysis, chest pain,
breathlesness.
Constitutional:fever/night sweat ,
tiredness , loss of appetite.
Physical sign: non specific,muscle
wasting, loss of ROM
TB
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3 days sputum.
Ziehl-Neelsen stain.
X-ray: cavitation, infilteration,
lymphadenopathy.
Full blood count:Relative lymphocytosis,^
ESR,Anemia.
Serology.
Lymphnode biopsy.
CT/ MRI
BONE TUBERCULOSIS
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Spread from primary complex to any
bone/joints.
Can effect any bone but the weight
bearing bones are more likely to be
affected.
Spine –commonest, hip, knee , foot.
STAGES OF ARTICULAR TB
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1 – SYNOVITIS.
2 – EARLY ARTHRITIS.
3 – ADVANCED ARTHRITIS.
4 – ADV.ART. PATHOLOGICAL
DISLOCATION /
SUBLUXATION.
5 – AFTER MATH TERMINAL OF GROSS ARTHRITIS.
STAGES
C/F
XRAY
PROGNOSIS
1 synovitis ROM>75%
SOFT TISSUE SWELLING,
OSTEOPOROSIS
NEAR NORMAL
2 early
arthritis
ROM50-75%
JT.SPACE DIMINITION AND
MARGINAL EROSION
RESTORATION
UPTO 75%
3 Adv.
arthritis
ROM >75%
ALL
DIRECTION
DESTRUCTION OF JT.
SURFACE
ANKYLOSIS
4Adv. Arth
path/disln
DO
DISORGANISE JT.
DIS/SUB.LOCATION
ANKYLOSIS
5
Aftermath
GROSS
DEFORMITY
DEFORMED JT. , OA
ANKYLOSIS
TB - TYPES
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Caseous exudativemore destruction,
exudation & abscess
formation.
Symptoms more
marked.
Onset is less
insidious.
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Granular type – less
destructive. Abscess
formation rare. Dry
lesion.
adults
TUBERCULOSIS
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Spine is the most
common site of skeletal
TB
TUBERCULOSIS
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Pathology
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Blood borne - settles
in vertebral body
anteriorly
usually more bone
destruction, more
sequestra, larger
abscess, gaseous
pus than pyogenic
OM
intervertebral discs
preserved until late
disease
TB SPINE -Classification
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12345-
pre-destructive
early destructive.
mild angular kyphos.
moderate angular kyphos.
severe kyphos (humpback)
STAGES –1 & 2
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Predestructive –
straightening of
curvatures , spasm
of perivertebral
muscles, MRImarrow oedema.
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Early destructive –
Diminished disk
space and paradiscal
erosion.MRI-marrow
oedema and break
of osseous
margin.CT-marginal
erosion /cavitaion
STAGE 3,4&5 –Body
destruction with Kyphos
Mild
2-3 vertebra
moderate
severe
>3 body
>3 body
Kyphosis –
10-30*
30-60*
>60*
TB SPINE –D/D
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AGE- anomalies.
Infection.
Tumour.
Traumma.
Osteoporosis ,Osteochondrosis.
Spondylolisthesis.
TB SPINE
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C/F:Back pain of variable duration, fever and
weight loss.
O/E: local tenderness, spasm, mild kyphosislate Gibbus, cold abscess and paraparesis.
DIAGNOSIS: XRAY-erosion of the anterior
edges of the superior and inferior boarders of
adjacent vertebral bodies with narrowing of
disc space.
USG :paravertebral abscess.
Biopsy/ CT scan
TB HIP
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C/F: pain/limping, irritable hip –child. Gradual
loss of range of movement, flexion deformity,
wasting of thigh muscles.
Xray: both hip to compare.Early changes –
rarefaction of the bone and widening of the
joint space, later destruction of the joint.
Synovial bioposy.
TB KNEE / ANKLE.
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C/F: pain and synovial swelling, muscle
wasting., contracture, draining sinuses.
X-ray.
Synovial biopsy.
PRINCIPLES OF
MANAGEMENT OF TB
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General.
Rest, mobilization & brace.
Abscess, effusion & sinuses.
Antitubercular drugs.
surgery
TB PROBLEMS
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Diagnosis.
Treatment .
Anti tuberculous drugs.
Tuberculous lesion
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Resolve completely.
Complete healing with varying degree of
deformity / loss of function.
Lesion may be complete walled off and the
caseous tissue may calcified.
Persist as a low grade ch.fibromatous
granulating & caseating lesion.
Infection may spread.
Damage growth centre with shortening.
CONCLUSION
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Slow progressive course of clinical symptoms
and radiological signs of tuberculosis creates
difficulty in early diagnosis.
Anti tuberculous treatment is effective but the
functional outcome depends on early
diagnosis before the development of
radiological evidence of joint destruction.
Always keep TB in D?Diagnosis
Thank you for not sleeping
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