Tuberculosis Bone Disease

By: Ang Jian Gang

Denise Choong
Ng Chin Lin

TB Tuberculosis(TB)
is a disease caused by a
bacterium called
Mycobacterium
tuberculosis.(Gram +ve
AFB)

The bacteria usually attack

the lungs, but TB bacteria
can attack any part of the
body such as the kidney,

Epidemiology

TB continues to be an important
disease both globally and in
Malaysia. In 2010, there were an
estimated 8.8 million new cases of
TB globally with 1.1 million deaths
among HIV-negative cases of TB
and an additional 0.35 million
deaths among people who were
HIV-positive.
Skeletal TB accounts for 10% to
35% of cases of extrapulmonary

Epidemiology

Important high risk groups:

Close TB contacts

Immunocompromised patients:

DM

HIV

Malignancy

COPD

Malnutrition

Use of Immunosuppresant drugs in RA

Substance abuser

People living in overcrowded conditions

Skeletal TB

Refers to TB involvement of the

bones or joints
Bone & joint TB develop generally
2-3 years after the primary focus
Forms of skeletal TB:

Spondylitis (Pott's disease)(most

common)

Arthritis

Osteomyelitis

Spine TB(Spondylitis)

Anatomy

Thoracic vertebrae-12

2nd to 8th are typical and the

remaining 5 are atypical
Identified by presence of costal
facets on the sides of vertebral
bodies

Anatomy

Blood supply

1 anterior spinal artery

2 posterior spinal arteries

Radicular arteries reinforce these

2 segmental arteries on each side

supply each vertebra
Prevertebral venous plexus
(Brescet-Batson) communicates
freely with veins of brain, abdomen,
pelvis & lower limbs

Pathogenesis

Haematogenous
Primary
seeding
Bacillemia
infection
of organism to disc
Causes disc space to
Soft nucleus
centre &
space
close,
fibrous
squeezing down on
annula wall weaken,
nerve root
decay
causing pain
Bones waekened,
& collapse
crumbled
Spreads to
under the weight of
vertebral
human body
bodies above,
below
Deformed spinal
Deformed vetebrae
column
heal
Compresses spinal cord
& fuse. Further
Producing functional
compress
impairment
Nerve roots

Pathogenesis

Cold abscess
Formed by collection of products of
liquefaction and reactive exudation
Composed of mainly serum,
leucocytes, caseous material, bone
debris, TB bacilli
Tracks away along neighbouring
vessels and nerves to reach surface

Pathogenesis
Caseous
exudative type

Granular type

More in children

Less destructive

More destruction

More exudation

Insidious onset/
course

Abscess
formation

Abscess formation
rare

More in adults

Regional distribution

Cervical(12%)

Cervico-thoraco(5%)

Thoracic(42%)

Thoraco-lumbar(12%)

Lumbar(26%)

Lumbar-sacral(3%)

Anatomical lesion

1. Paradiscal- destruction of
adjacent end plates and dimunition
of disc space
2. Appendeceal(posterior)involvement of pedicles, laminae,
spinous process
3. Central- cystic or lytic concertina
collapse

4. Anterior- longitudinal ligament

5. synovitis in post facet

Clinical features

Constitutional
symptoms(40%)
Malaise
Loss of weight/
appetite
Night sweats

Specific features

Pain/ night cries

Stiffness

Deformity/Gibbus

Restricted ROM

Enlarged lymph nodes

Abscess

Neuro-deficit(20%)

TB spine with neuro-deficit

Motor functions affected before/

greater than sensory
Sense of position and vibration last
to disappear
Mainly seen in adults due to

Inelasticity of prevertebral fascia

Loss of flexibility of spine

Degenerative changes like OA

Griffith sedon classification

TB paraplegia

Early onset
paraplegia(within 2
years) inflammatory
oedema, granulation
tissue, caseous tissue
and rarely ishaemic
lesion of cord

Active disease

Good prognosis

Late onset(more than 2

years of onset)
recrudescence of
disease or
mechanical
compression of cord
Caseous tisse, debris,
sequestra, internal
gibbus, stenosis of
canal, deformity
Healed disease
Poor prognosis

Kumar's classification of TB
paraplegia
stage

Clinical features

Negligible

Unaware of neurological deficit, plantar extensor/ ankle

clonus

Mild

Walk with support

Moderate

Nonambulatory, paralysis in extention, sensory loss<50%

Severe

Paralysis in flexion/sensory loss>50%/ sphinters involved

Gibbus deformity, structural

kyphosis, distorts spinal canal
anatomy

Pulmonary tuberculosis (PTB)

refers to a case of TB involving the
lung parenchyma
A patient with both pulmonary and
extra pulmonary TB should be
classified as a case of PTB.

Diagnosis

History

Physical examination

Investigations

1/3 who present with extrapulmonary

tuberculosis will have a known
history of pulmonary tuberculosis

Clinical presentation

Progressive localized back pain

Muscle spasms/rigidity

Neurologic manifestations

-Paresthesia

-Sensory loss

-Weakness

-Paraplegia (Potts paraplegia)

Cold abscess(swelling without erythema/increased heat)

Constitutional symptoms

-Fever

-Night sweats

-Weight loss

Retrospective review

Back pain 100%

Constitutional symptoms consistent
with tuberculosis 48%
Neurological symptoms 29%
Children: epiphyseal region of bones
is highly vascularized
Bone involvement with TB is much
more common in children than adults

Gibbus-palpable spinous process

produced by the anterior wedging
and angulation of adjacent vertebral
bodies that occur as the disc space
deteriorates

Investigations

Bloods: FBC, ESR

Acid-fast staining

Mycobacterial culture

Histology-caseating granuloma

CT spine- degree of bone destruction, interventional

biopsy(PCR) and drainage
MRI spine-extent of infection(involvement of soft tissue and
abscess) and assessing for evidence of cord compression
T2-weighted uniform thin rim enhancement is a
pathogenomic finding suggesting either caseation necrosis
or a cold abscess in tuberculosis

Infection begins in the anteroinferior

aspect of the vertebral body with
destruction of the intervertebral disc
and adjacent vertebrae
The resulting anterior wedging and
angulation of adjacent vertebral
bodies with disc space obliteration
Paraspinal and psoas abscesses can
develop, with extensions to the
surface or adjacent tissues

MRI spine

CT abdomen

Kyphosis occurs as a result of the

conditions preference to affect the
anterior portion of the vertebral body
while typically sparing the posterior
section

Kyphosis

Treatment
Medical

Surgical

5/29/15

Indications for medical treatment

Organism identified

Antibiotic sensitivity

Single disc space involvement

without significant vertebral
Non progressive Minimal or no
neurologic deficit

Indications for surgical treament

Neurological deficit

medical co-morbidities such as

sepsis or coagulopathy.
Failed medical therapy and
progression of disease despite best
medical therapy

Chronic pain after medical

management
Prominent deformity -kyphotic
deformity (especially in kyphotic
angles of 50 to 60 degrees or more)
Significant instability

Medical treatment include

Antibiotics- Isoniazid,rifampin,(912months) pyrazinamide, and
ethambutol (2months)+pyridoxine
With monitor of LFT

Brace (such as Thoracic lumbosacral

orthosis) and follow-up imaging at 8
weeks
Analgesia
High protein diet , bedsore care

Disease response to therapy can be

assessed by

Clinically symptoms improve

ESR

CRP

Imaging

There is different apporach depend

on which level of vetebrae are
involved

References

Mc Devitt et al:Extrapulmonary
Tuberculosis:pg.3640,48;Journal
Hospital Physician September
2008. Available from:
http://www.turner-white.com/member
file.php?PubCode=hp_sep08_tubercul
osis.pdf
Treatment of tuberculosis Guidelines,
Fourth edition, WHO 2010. Available
from: http://