Tuberculosis Bone Disease

Tuberculosis Bone Disease

By: Ang Jian GangDenise ChoongNg Chin Lin

Tuberculosis(TB)

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, spine, and brain.

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 TB(10.8% of US extrapulmonary TB cases)

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

Primary infectionBacillemiaHaematogenous seedingof organism to disc spaceSoft nucleus centre & fibrousannula wall weaken, decay& collapseCauses disc space to close,squeezing down on nerve rootcausing painSpreads to vertebral bodies above, belowBones waekened, crumbledunder the weight of human body

Deformed spinal columnCompresses spinal cordProducing functional impairmentDeformed vetebrae heal& fuse. Further compressNerve 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

May burst to form sinus

Pathogenesis

Caseous exudative type

More in children

More destruction

More exudation

Abscess formation

Granular typeMore in adultsLess destructiveInsidious onset/ courseAbscess formation rare

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 cordCaseous tisse, debris, sequestra, internal gibbus, stenosis of canal, deformityHealed diseasePoor prognosis

Kumar's classification of TB paraplegia

stageClinical features

1NegligibleUnaware of neurological deficit, plantar extensor/ ankle clonus

2MildWalk with support

3ModerateNonambulatory, paralysis in extention, sensory loss50%/ 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.

Treatment of tuberculosis Guidelines, Fourth edition, WHO 2010http://whqlibdoc.who.int/publications/2010/9789241547833_eng.pdf

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

M c D e v i t t e t a l : E x t r a p u l m o n a r y T u b e r c u l o s i s : p p . 3 6 4 0 , 4 8Hospital Physician September 2008

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

M c D e v i t t e t a l : E x t r a p u l m o n a r y T u b e r c u l o s i s : p p . 3 6 4 0 , 4 8Hospital Physician September 2008http://www.turner-white.com/memberfile.php?PubCode=hp_sep08_tuberculosis.pdfTreatment of tuberculosis Guidelines, Fourth edition, WHO 2010

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

Extrapulmonary Tuberculosis: An OverviewAm Fam Physician.2005Nov1;72(9):1761-1768.http://www.aafp.org/afp/2005/1101/p1761.html

MRI spine

osteomyelitis involving T10 and T11 vertebral bodies and disc space(A; arrow)and an adjacent multiloculated paravertebral abscess(B; arrow).

CT abdomen

left iliopsoas abscess(arrow)that likely originated from tuberculous osteomyelitis involving the T12, L1, and L2 vertebrae.

Kyphosis occurs as a result of the conditions preference to affect the anterior portion of the vertebral body while typically sparing the posterior section

Extrapulmonary Tuberculosis: An OverviewAm Fam Physician.2005Nov1;72(9):1761-1768.http://www.aafp.org/afp/2005/1101/p1761.html

Kyphosis

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Treatment

Medical

Surgical

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,(9-12months) 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/memberfile.php?PubCode=hp_sep08_tuberculosis.pdf

Treatment of tuberculosis Guidelines, Fourth edition, WHO 2010. Available from: http://whqlibdoc.who.int/publications/2010/9789241547833_eng.pdf

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Tuberculosis Bone Disease

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