Musculoskeletal

Tuberculosis

Dr Daniel Baddoo

31/05/2015
Outline
 Introduction
 Historical aspect
 Microbiology
 Pathophysiology
 Clinical Presentation
 Investigation
 Management
 Complications
 Summary
Introduction
 1/3 of global population is infected with M.tuberculosis
 1% of the world population is newly infected each year
 TB remains the most frequent cause of death and disability
worldwide – 3million deaths/year
 National prevalence (Ghana) --- 264/100,000 population (2013)

Generally ↑ rate of TB due to

 ↑ no of people with immune suppression (HIV)
 Development of drug resistance strains
 Ageing population
 Increasing no of health care providers exposed to the dxs

 HIV remains the leading risk factor for reactivation of latent

Tuberculous infection
Historical aspect
 TB is an ancient dxs

 Spinal TB has existed >5,000years

 1st known description of tuberculous spondilytis was

written b/n 1500 & 700BC

 18th century, Pott noted the association b/n

Tuberculous involvement of the spine and paraplegia

 In the era before the availability of anti TBdrugs,

mortality rate ~60% among those considered to be
successfully treated
Musculoskeletal TB
Relative incidence

 Spine 50%(thoracic 50% ; cervical 25% ;lumbar 25%)

 Pelvis 12%
 Hip/femur 10%
 Ribs 7%
 Shoulder 2%
 Elbow + wrist 2%
 Multiple sites 3%

 Extrapulmonary TB more common in children than adults

 1/3 of children with tuberculosis have extrapulmonary TB

Microbiology
3 related micro-organisms

 Mycobacterium tuberculosis (most common)

 Mycobacterium africanum (rarely found outside N/W africa)

 Mycobacterium bovis (incidence ↓by pasteurisation)

In 1882, German microbiologist Robert Koch isolated a rod-
shaped bacterium now called Mycobacterium tuberculosis, or
simply, the Tubercle bacillus.
Mycobacterium tuberculosis
 Thin rods with rounded ends
 Non motile
 Non encapsulated
 Acid/alcohol fast
 Small pink rods histologically
 Grows only on enriched
medium
 Slow growth rate –
dependent on O2
 Pathophysiology
M tuberculosis reaches bone from

 blood stream (haematogenous)

 extension from contiguous infection ;
 spread from draining lymphatics ;
 direct traumatic introduction

Local immune processes confines small foci of disseminated infxns –

extrapulmonary foci remains latent
Failure of local immune defences = progression to clinically active dxs

 Infection can involve any bone & synovial membrane

 ? association b/n trauma & development of TB – (damage to inactive

lesion- reactivation & proliferation)
 The disease is characterized by a granulomatous
inflammatory process occurring through cell-
mediated immunity.

 This results in the formation of characteristic

granulomas, composed of aggregation of epithelioid
cells with or without Langhan’s giant cells, and
areas of caseation
Musculoskeletal tuberculosis

 Spinal tuberculosis

 Osteoarticular tuberculosis
Spinal tuberculosis
 It accounts for more than 50% of musculoskeletal tuberculosis
(Hodgson et al., 1967).

 It is most common during the first three decades, though the

disease may occur at any age between 1 to 80 years (Tuli, 1997).

 Most commonly, it affects the thoracic and thoraco-lumbar

spine (Tuli, 1997; Sankaran, 1993; Sridhar, 1995).

 TB of cervical spine is most common in children.

 The clinical manifestations of Pott's spine are protean.

Spinal TB – pathophysiology - i
 Spinal tuberculosis is usually a secondary
infection from a primary site in the lung or
genitourinary system.

 Spread to the spine is thought to be

hematogenous in most instances. Basic
lesion – osteomyelitis + arthritis involving
one or more vetebra.

 Typically, the infection begins in the

anterior aspect of the vertebral body
adjacent to the disk.
Spinal TB – pathophysiology- ii
 The infection then spreads to the adjacent vertebral bodies
under the longitudinal ligaments. Noncontiguous (skip)
lesions are also occasionally seen

 The most frequent site of spinal tuberculosis is the

thoracolumbar junction the incidence decreases above and
below this level.

 In adults, disc disease is secondary to the spread of infection

from the vertebral body.In children, because the disc is
vascularised, it can be a primary site

 Progressive bone destruction leads to vertebral collapse and

kyphosis
Spinal TB –
pathophysiology- iii
 The spinal canal can be narrowed by abscesses, granulation
tissue, or direct dural invasion, leading to spinal cord compression
and neurologic deficits.

 The kyphotic deformity is caused by collapse in the anterior spine.

 Lesions in the thoracic spine are more likely to lead to kyphosis

than those in the lumbar spine.

 A cold abscess can occur if the infection extends to adjacent

ligaments and soft tissues. Psoas / Retropharngeal abscess

 Abscesses in the lumbar region may descend down the sheath of

the psoas to the femoral trigone region and eventually erode into
the skin.
Kyphosis ; Gibbus
History

 Detailed history essential and high index of

suspicion
 Pain common; chronicity; mild/may be severe to
cause inability to walk-infective process or
mechanical failure
 Constitutional symptoms- fever, night sweat,
anorexia, wt loss, general malaise
 Exhibition of features of the primary disease
 Physical examination
 General – malnourished, weight loss, pale
stigmata of chronic disease

 Chronic draining sinuses, psoas abscess

 Thoracic kyphosis, acute gibbus, coronal

plane deformity

 Focal tenderness- muscle spasm due to pain

 Neurological compromise- paraplegia 10%

 Focal pulmonary signs

Psoas abscess from Potts dxs
 Percivall Pott first described
disease in 1779

“that kind of palsy of lower

limbs which is frequently
found to accompany a
curvature of the spine”
Paraplegia

 While the bony disease is still active (early)

 Arising after the bony disease has healed (late)

Causes of neurologic compromise
(active phase of dxs)
 Inflammatory oedema

 Extradural compression from posterior extension of

an abscess (pus, caseous material, granulation
tissue, sequestrum)

 Direct invasion of the dura

 Spinal cord infarction- irreversible paraplegia; thrombosis of critical

spinal arteries

 Spinal tumour syndrome- tubercular granulomas in extradural,

intradural or intramedullary location
Causes of neurologic compromise
(healed phase of dxs)

 Spinal stenosis

 Direct compression from an

internal gibbus deformity

 Constriction by peridural
fibrosis
Management Principles

 Establish a diagnosis
 Establish a baseline status against which treatment
responses can be monitored
 Identify abscess formation that may require surgical
drainage
 Identify impending or actual neurological
compromise
 Establish the extent of bony destruction and identify
impending or actual mechanical failure of the spine
Investigations
 Haematological – FBC, ESR, inflammatory markers
 Mantoux
 Serology – ELISA
 GeneXpert (TB / MDR-TB)
 MGIT (liquid culture medium)
 (Retroviral test)

Radiological
 Plain X-rays
 CT Scan
 MRI
 Bone scan

Microbiology is definitive method

Z-N stain – identifies 104 AFBs/ml
Culture – more sensitive identifies 103AFBs/ml
Biopsy
In countries where
 TB is prevalent, limited medical facilities ; suggestive hx +
clinical signs + radiological signs = Rx (no need for biopsy)

Indications for biopsy

 Failed response to adequate chemotherapy
 Suspected resistance strains
 Substantial neurologic impairment

Anti TB drugs initaited at time of biopsy --- ↓likelihood of

dissemination of the dxs during the procedure
 Ixgn - Radiological
 Approx. 50% of trabecular bone destroyed before it
can be seen on x’rays. Dass et al(2002)

 MRI –detects 4-6 months earlier, 96% sensitive; 95%

specific-soft tissue extension, abscess, neural
structure visualised

 CT scan-evaluates extent of bone destruction,

calcification within abscess, guides reconstruction
and biopsies

 Bone scan- 95% sensitive; 75% specific

 Radiography
 Radiographic changes - present relatively late.

 Lytic destruction of anterior portion of vertebral

body
 Increased anterior wedging
 Collapse of vertebral body
 Reactive sclerosis on a progressive lytic process
 Enlarged psoas shadow with or without
calcification
 Osteoporotic vertebral end plates
 Intervertebral discs may be shrunk or destroyed
 Bone lesions may occur at more than one level.
Treatment

 Non-operative
 Chemotherapy

 Operative
 Single stage/two stage
 Anterior approach
 Posterior approach
 Combined approaches

 Debridement + bonegraft
 Instrumentation using titanium cage filled with allograft
DOTS

Spinal TB
 HRZE - 2months
 HR - 7 months

 The bacillus is killed by drugs (chemotherapy) NOT the

scarpel/knife !!!
 The role of surgery is to manage the complications of the
disease – (adjunct to appropriate antibiotic chemotherapy)
 Isoniazid(H) – most potent bactericidal drug
hepatotoxic ; peripheral neuropathy

 Streptomycin(S)- bactericidal
orthotoxicity

 Ethambutol (E)– bacteristatic

Retrobulbar neuritis

 Rifampicin(R)
 Parazinamide(Z) –most potent sterilising drug
Jaundice /GI side effects
Role of surgery
 diagnosis --- biopsy

 management of the complications of

the disease – debridement ,
osteotomy,
arthroplasty,
arthrodesis .
Operative management
Indications

 Neurologic deficit (acute neurologic deterioration, paraparesis,

paraplegia)

 Spinal deformity with instability or pain

 No response to medical therapy (continuing progression of

kyphosis or instability)

 Large paraspinal abscess

 Nondiagnostic percutaneous needle biopsy sample

 Surgical procedures
 Drainage of abscesses

 Debridement + bonegraft

 Instrumentation using titanium cage filled with allograft

 Perioperative antiTB Rx
Hong Kong procedure
Spinal tuberculosis
differential diagnosis

 pyogenic infections
 Metastasis
 Lymphoma
 Myeloma
 Sarcoidosis

 No pathognomonic imaging signs allow tuberculosis to be readily

distinguished from other conditions.

 A history of chronicity and slow progression is suggestive of

tuberculosis.
 Most patients with Pott’s disease (62-90% of patients in reported
series) have no evidence of extraspinal tuberculosis, further
complicating a timely diagnosis.
 Team approach

Consultations
 Orthopaedic surgeons

 Neurosurgeons

 Physicians

 Clinical psychologist

 Rehabilitation teams
Osteoarticular Tuberculosis
 Usually presents as gradually worsening arthritis
 Systemic and pulmonary symptoms frequently
absent
 Rarely involves more than one joint – helps to
differentiate it from other types of polyinflammatory
dxs
 Generally affects large weight bearing joints
 Slow to develop compared to pyogenic infections
 Clinical symptoms may not appear till 18months
after onset of dxs
Pathophysiology
 Tuberculous granulation tissue formation in synovium ---
destruction of synovial attachments

 Cartilage no longer nourished from synovium ----progressive

destruction

 Granulomatous lesion erodes & replaces normal bone - -

cartilage is indirectly attacked by the subchondral erosion and
superficial pannus formation

 Cutaneous sinuses may occur in advanced cases --- 2o bacterial

infxn

 Healing is associated with joint fusion (ankylosis)

Clinical features
 Classical symptoms –
fever ,wt loss, night sweats
usually absent
 Night cries (children)
 Pain
 Restriction of movements
 Joint swelling
 Muscle wasting
 Deformity
 Cold abscesses
 Draining sinuses
Investigation
 Haematological – FBC, ESR, inflammatory markers
 Mantoux
 Serology – ELISA
 Retroviral test
 Radiological
 Plain X-rays
 CT Scan
 MRI
 Bone scan

Microbiology is definitive method

Synovial fluid analysis
Z-N stain – identifies 104 AFBs/ml
Culture – more sensitive identifies 103AFBs/ml
Radiological features
 Osteopaenia
 Narrowing of joint
space
 Cystic degeneration in
bone adjacent to joint
 Subchondral erosions
 Enlargement of
epiphysis in children
 Soft tissue swelling
Tuberculous arthritis of the hip jt

 concentric decrease in the joint space,

 irregular articular margins of femoral head as well as
acetabulum,
 areas of destruction of the femoral head
 marked osteopenia
Treatment

 Non-operative
 Chemotherapy

 Operative
 Osteotomy
 Arthroplasty
 Arthrodesis
TKR – ff TB arthritis – knee jt
THR – following TB hip jt
THR – following TB hip jt
Tuberculous arthritis – ankle jt
Tuberculous Osteomyelitis
 < 5% of cases of osteo-articular TB

 Duration of symptoms --- days to months

 Co-existing visceral disease is uncommon

 Sinuses are common (bluish discoloration at the periphery,

undermined edges, sero-sanguinous discharge, mattered draining LN
and fixation to bone)

 Xray – lesion may be metaphyseal or diaphyseal

 May penetrate physis and extend into
adjacent joint
 Sequestrae may be found

 Common presentation is a solitary

lytic lesion with sclerotic rim

DD –
 Broodie’s abscess

 Chronic osteomyelitis

 Granulomatous lesion
Poncets disease
 Reactive polyarthritis developing in the presence of active TB
elsewhere

 Knees, ankle, elbow more commonly affected than small

joints of hands and feet

 In 50% of cases, 1o focus not identified

 30% of cases show radiological evidence of pulmonary TB

 20% - evidence of infection in GU tract

 Summary
Thank You!