tuberculosis of the skeletal system

TUBERCULOSIS OF
THE SKELETAL
SYSTEM
Dr.Diwakar Pratap
GMC, Haldwani

Content
 General Considerations
 Extra-Spinal regional Tuberculosis
 Tuberculosis of the spine
 Tuberculosis of the Hip joint
 Tuberculosis of the Knee joint
 Tuberculosis of the Shoulder joint
 Miscellaneous bone tuberculosis

General Considerations
 1) Epidemiology and Prevalence
 2) Pathology and Pathogenesis
 3) Diagnosis and Investigations
 4) Anti Tubercular Drugs
 5) Principals of management of Osteoarticular Tuberculosis.

Tuberculosis: Epidemiology and Prevalence
 It is a chronic granulomatous disease caused by bacteria of “Mycobacterium
Tuberculosis” complex.
 “ YAKSHMA” - described in Rig Veda and Atharva veda (3500 BC)
 “ Phthisis” – described by Greeks and Roman’s civilizations.
 Tuberculosis lesions have been recorded in Egyptian mummies.
 Lichtor and Lichtor (1957) reported the evidence of Tb in Bones, Joints and Spine.
 Percival Pott in 1779 described Tb of the Spinal Column.
 Laennec discovered the basic microscopic lesion ‘tubercle’ . Also inventor of
stethoscope.
 Robert Koch in 1882 isolated “ Mycobacterium Tuberculosis”

 Refugees
 IV drug abusers
 HIV Patients
 Alcoholics
 Elderly
 People with Poor Nutrition
 Therapeutically Immunosupressed Patients
 Organ transplant receipients
 Patients on Cancer chemotherapy.
The Risk of Infection

30 million people are suffering from Tuberculosis (2010 data).
3 million people die every year due to Tuberculosis.
Nearly 6 million cases of Tuberculosis in India (2010 data).
1-3% cases are of Skeletal tuberculosis of all Tuberculosis.

Regional Distribution of osteoarticular Tuberculosis
 Spine - 44%
 Hip - 8.1%
 Knee - 8.9%
 Sacroiliac Joint - 6.9%
 Elbow - 5.1%
 Metatarsal and Phalanges – 4.4

Pathology and Pathogenesis
 Osteoarticular Tb lesion is a result of hematogenous dissemination from primarily
infected visceral focus.
 The Primary focus may be active or quiescent. Can be either in the lungs/ lymph
nodes of the mediastinum/ Kidney or other viscera.
 The infection reaches skeletal system through Batson’s plexus of veins.
 Tubercular bacilli reach the joint space via the blood stream through sub-synovial
vessels, or indirectly from the lesions in the epiphyseal bone.

Cold Abscess
 A cold abscess is formed by a collection of products of liquefaction and the reactive
exudates.
 Composed of Serum, leucocytes, caseous materials, bone debris, and the tubercle
bacilli.
 The cold abscess feels warm, though the temperature is not raised as high as in
acute pyogenic infections.

Type of the disease
Caseous Exudative type
 More destruction, more exudation and
abscess formation.
 Onset is less insidious, constitutional
symptoms and local signs of inflammation
are marked.
 Sinus and abscess formation are common.
Granular Type
 Less destruction, abscess formation is rare.
 Insidious onset.

Diagnosis of skeletal Tuberculosis
 X-rays: Localized osteoporosis, articular margins and bony cortices become hazy
“ washed out” appearance.
 Blood Investigations: Lymphocytosis, low hemoglobin and raised ESR.
 Biopsy
 PCR : Also useful in differential diagnosis with Brucellosis, Typhoid infection and
Syphilitic infection.
 Radio-isotope scan
 Modern Imaging Techniques:
CT Scans, MRI, USG.

Anti Tubercular Drugs
Drugs Daily adult dose Main drug toxicity
Isoniazid
(5-10mg/kg/BW)
300-400mg in single/2 divided
dose
Peripheral neuropathy
convulsions, hepatitis
Rifampicin
(10mg/kg/BW)
450-600mg in single/2 divided
dose
Pinkish staining of urine,liver
damage, bowel upset.
Pyrazinamide
(25mg/kg/BW)
750mg in single/2 divided dose Hepatotoxicity, gouty arthritis
Ethambutol
(15-20mg/kg/BW)
800mg in single / 2 divided dose Retrobulbar neuritis with loss of
vision, color blindness
Streptomycin inj.
(20mg/kg/BW)
1gm injection
(In children and elderly twice a
week)
Vestibular damage,
deafness,rashes,nephrotoxicity.

Staging of the tuberculosis of the joints
Stages Clinical Radiology Treatment
Synovitis ROM >75% Soft tissue swelling,
Osteoporosis
Chemotherapy
Early Arthritis ROM 50-75% Above + moderate
diminution of joint space
+ marginal erosion
Chemotherapy +
Movements
Advanced arthritis Movements restricted
>75%
Above + marked
diminution of J.Space
+destruction of J.
surface
Chemotherapy +surgery
(Generally arthrodesis in
lower limb)
Advanced arthritis +
sub/dislocation
Ankylosis Joint is disorganized with
sub/dislocation
Chemotherapy +surgery
(Corrective Osteotomy/
Arthrodesis)

Tuberculosis of the Hip Joint
 The initial focus of Tuberculous lesion may start in the acetabular roof, epiphysis,
metaphyseal region or in greater trochanter region.
 As the upper end of the femur is intra-articular the joint gets involved rapidly.
 Clinical features : Pain, Limping, deformity, and fullness around the hip.

Stages Clinical findings Radiologic features
Synovitis Apparent lengthening, Flexion,
Abduction, ER
Soft tissue swelling, Osteopenia in
sub chondral region
Early Arthritis Apparent shortening, Flexion,
Adduction , IR
Osteopenia, marginal bony
erosions on both surface
(Acetabular and femoral head)
Advanced Arthritis Flexion, Adduction, IR, True
shortening
Above + Reduction in joint space
Advanced arthritis with sub/
dislocation
Flexion, Adduction, IR, with gross
shortening
Gross destruction
“ Mortar and pestle appearance”

Management of Tb Hip
 Anti Tubercular therapy (ATT).
 Traction to be applied ( To relieve Muscle spasm, prevents/corrects deformity, prevents
subluxation/dislocation).
 Hip mobilization exercises to be done with gradual increase in duration and
frequency.
 Non weight bearing for 12 weeks followed by partial weight bearing for next 12
weeks.

Surgical Management
 In Synovial stage : Arthrotomy and synovectomy
 In Early arthritis : Synovectomy + removal of loose bodies, pannus covering articular
cartilage.
 In advanced arthritis : Debridement along with arthrodesis/ Girdlestone’s Excisional
arthroplasty of the joint.

Regional distribution of Spine TB
 Cervical – 12%
 Cervicodorsal – 5%
 Dorsal – 42%
 Dorsolumbar – 12%
 Lumbar – 26%
 Lumbosacral – 3%

Types of vertebral lesions
 5 types:
 Paradiscal- Arterial spread
 Central – Venous spread
 Anterior- Subperiosteal spread
 Appendicular
 Articular

 5 types:
1. Paradiscal- Arterial spread
2. Central – Venous spread
3. Anterior- Subperiosteal
spread
4. Appendicular
5. Articular

• 5 types:
spread
4. Appendicular
5. Articular

5 types:
spread
4. Appendicular
5. Articular

Clinical features of spinal TB
 Back Pain/Night cries
 Stiffness
 Deformity (Gibbus/Knuckle/Kyphosis)
 Restricted movements of spine
 Malaise
 Loss of weight/appetite
 Night sweats
 Evening rise of temperature
 Neurological deficit

Pathogenesis of TB Spine
Secondary infection.
Primary site in the lung, viscera or
lymph glands.
Hematogenous Spread / Batson
plexus of veins.
Delayed hypersensitivity immune
reaction. Inflammatory reaction with
Langhan’s giant cells, epithelioid cells,
and lymphocytes.
The granulation tissue
proliferates, producing
thrombosis of vessels.

 Granulomatous inflammation leads to erosion of
vertebrae.
 Associated disc degenaration due to end arteritis,
finally complete destruction.
 Weakening of trabeculae compression
collapse. – Deformity.

•Formation of cold abscess
•Collect under ant-long-ligament
•Vertebral collapse
•Expression of collection of tuberculous debris
Slides along VB and invade the
vertebral canal through
intervertebral foramen.
Pathology of Abscess Formation
Diverted forward along
different anatomical sites

Neurological deficit
 10-30% cases – Neurological deficit.
 Age: 1st 3 decades.
 Disease below L1 vertebrae rarely
causes Paraplegia.
 Highest Incidence of paraplegia seen
in TB of lower thoracic vertebrae

Classification of TB Paraplegia
Early onset paraplegia
 Appears within 2 years of onset.
 Underlying pathology
Inflammatory edema
TB Granulation tissue
Abscess
Caseous tissue
 Ischaemic lesion of cord (Rare)
 Good prognosis
Late onset paraplegia
 Appears more than 2 years of
disease in vertebral column
 Underlying pathology –due to
mechanical pressure on cord
TB Debris
TB Sequestra from body and disc
Internal gibbus
 Canal stenosis / Severe deformity
 Poor prognosis

Staging of Neurological Deficit
Stage Severity Clinical Features
I Negligible Patient unaware of neurodeficit, physician detects plantar
extensors or ankle clonus
II Mild Patient aware of deficit but walks with support
III Moderate Non ambulatory due to spastic paralysis (in extension),
sensory deficit less than 50 %
IV Severe III + Flexor spasm / Paralysis in flexion / Flaccid/ Sensory
deficit more than 50 % / Sphincter Involved

Pathology of TB Paraplegia
 Extradural mass:
• The Commonest mechanism affecting spinal cord function
• Material compressing may be
 Fluid pus
 Granulation tissue
 Caseous material
Bony Disorders:
• Sequestra from disc or body
• Internal Gibbus
• Pathological Dislocation

Clinical features of Pott’s Paraplegia
o Paraplegia itself – Rare
o Spontaneous muscle twitching in lower limbs
o Clumsiness while walking
o Extensor plantar response
o Exagerrated reflexes – Sustained clonus of patella and ankle
o Motor affected first – then Sensory
o Sense of position and vibration – last to disappear

Investigations
o CBC:
Hb% ↓
Lymphocytosis
o ESR:
Raised in active stage of disease
Normal ESR over period of 3 months suggests patient is in stage of repair.
o Biopsy

Radiological Investigations
 Xray:
o Reduced disc space
o Blurred paradiscal margins
o Destruction of bodies
o Loss of trabecular pattern
o Increased prevertebral soft tissue shadow
o Subluxation /dislocation
o Decreased lordosis/Kyphosis
• Skipped lesions: More than one TB Lesion in vertebral
column with one or more healthy vertebrae in between the 2
lesion.

BONE SCAN (Technitium (Tc) – 99 m )
 Increased uptake (60% patients) with active
tuberculosis
 > 5mm lesion size can be detected.
 Avascular segments and abscesses show
a cold spot due to decreased uptake.
 Highly sensitive but nonspecific.
 Aid to localize the site of active disease and to
detect multilevel involvement

Biopsy :For definitive diagnosis
CT or ultrasound guided or open biopsy during a
surgical procedure.
Z-N staining: a quick and inexpensive
method.
Culture :
 results are available only after a few
weeks
 positive only in 60% of cases; most
specific.
Histology: demonstration of tubercle, 80%
cases.

Differential Diagnosis
 SPINAL INFECTIONS
o pyogenic
o brucellosis
o fungi / syphilis
 NEOPLASTIC
o Extradural – Lymphoma / Metastasis etc.
o Intradural extramedullary – Meningioma /neurofibroma
 DEGENERATIVE / OSTEOPOROTIC
 TRAUMA
 CONGENITAL DEFECTS
 SPINAL OSTEOCHONDROSIS

MIDDLE PATH REGIME
 Rest on hard bed
 Chemotherapy
 X-ray & ESR once in 3 months kyphosis measurement
 MRI/CT at 6 months interval for 2 years
 Gradual mobilization is encouraged in absence of neural deficits with spinal braces & back
extension exercises at 3 – 9 weeks.
 Abscesses – aspirate when near surface & instil 1gm Sterptomycin inj.

INDICATIONS- SURGICALTREATMENT
 Doubtful diagnosis
 Failure to respond to conservative Rx
after 3-6 weeks therapy.
 Symptomatic abscess.
 Neurological indications.
 Mechanical instability.
 Deformity.
 Recurrence of disease.

Surgeries for Pott’s Spine
 Anterio-lateral decompression (MC)-Spine is
opened from its lateral side & access is made to the front and
side of the cord. The cord is laid free from granulation tissue,
caseous material, bony spur or sequestrum
 Costo-transversectomy-Removal of 2 inches of rib
& transverse process and pus comes out.
 Radical debridement and
arthrodesis(Hongkong operation).
 Laminectomy-Indicated in spinal tumor syndrome and
paraplegia resulted from post spinal disease.

 Knee Joint is the largest joint in the body
having the largest intra articular space.
 It is the 3rd most common site for
osteoarticular tuberculosis.
 Accounts for nearly 10% of all skeletal
tuberculous lesion.

Pathology
 The initial focus occurring by hematogenous
dissemination may start in the synovium, or in the
subchondral bone (Distal femur, proximal Tibia, Patella).
 The synovium lesion may for many months remain
purely as tubercular synovitis.
 The synovial membrane gets congested, edematous and
studded with tubercles.
 The synovial lining which is normally a single cell layer
in thickness becomes hypertrophied and thickened with
granulation tissue.

 The joint fluid in the initial stages is increased
(Serous, Opaque, turbid, yellowish and may contain
fibrinous flakes).
 In advanced stage of the disease tuberculous process
becomes osteoarticular.
 The Tuberculous granulation tissue like the pannus
erodes the articular margins, destroys the bone and
involves the cruciate ligament, periarticular tissues,
capsule and ligaments.

 The Pannus may erode the margins of the articular
cartilage, grow between the articular cartilage and
the subchondral bone, thus detaching the cartilage
from the bone.
 Nutrition of the articular cartilage is thus
interfered.
 It looses its smooth glistening appearance, there
may be fibrillation of its surface, it becomes
roughened, pitted and erosion of the cartilage
exposes the subchondral bone.

 As the disease advances large areas at pressure
points show osseous destruction and the whole
joint is obliterated with granulation/fibrous tissue,
capsular apparatus and ligaments are disrupted and
joint gets a triple deformity.
 Triple deformity
I. Flexion deformity
II. Posterior subluxation
III. Lateral rotation

Clinical Features
• The onset and course is insidious
• The knee shows
– Swelling
• warm
• patellar tap is present due to synovial effusion
• the thickened synovium
– filling up all parapatellar fossa appreciated earliest in medial parapatellar fossa.
• When the arthritis has set
– movements are grossly restricted,
– painful
– accompanied by muscle atrophy.
• regional lymphadenopathy.

• Quadricep muscle shows gross wasting
• In the neglected case
– triple deformity
• Once the flexion deformity established
– tensor fasciae latae further increases the deformity.
• In long case
– Posterior capsule of the knee joint gets contracted

• Monoarticular affections
– rheumatic arthritis (in children)
– chronic traumatic synovitis due to chronic internal derangement ofknee (e.g.
• meniscal tears
• loose bodies
• osteochondritis dissecans
• chondromalaciapatellae
• Rheumatoid arthritis (in adults)
• subacute pyogenic arthritis/synovitis

• Hemarthrosis
• villonodular synovitis
• synovial chondromatosis

Treatment
• Non operative treatment with antitubercular
drugs is employed in
– tubercular synovitis
• Traction is applied to
– prevent (or correct) flexion and subluxation
deformity
– keep the joint surfaces distracted.
• In addition to the systemic drugs, the joint
may be aspirated

• With the quiescence of acute local signs, gently active and
assisted knee bending should be.
• Usually after 12 weeks of treatment the patient may be
permitted ambulation with suitable orthosis and crutches.
• After 6 to 12 months of treatment, in cases with
favorable response, the crutches or orthosis may be
discarded.
• Unprotected weight bearing is usually permitted 9 to 12
months after the start of treatment.

 Arthrodesis of the grossly destroyed knee in children should be deferred till the completion of
growth potential of the distal femur and proximal tibia.

Operative Treatment
• In the synovial stage
– arthrotomy and synovectomy should be carried out.
• In early arthritis,
– synovectomy,
– removal of loose bodies, debris, pannus, loose articular cartilage and
– careful curettage of osseous juxta-articular foci
• Postoperatively antitubercular drug therapy,
– traction,
– intermittent active and assisted exercises,
– suitable brace ambulation should be continued

• In adults with advanced arthritis or in cases which resulted in painful fibrous ankylosis during
the process of healing, the knee joint may be treated by arthrodesis.
• This option provides
 painless stable knee
 prevents recrudescence
 corrects deformity
 patients can do long hours of standing and walking.
 However it imposes a lot of restrictions in sitting,using public transport and many other social activities.

TUBERCULOSIS OF
SHOULDER JOINT

 The incidence of tuberculosis of shoulder
joint is rare and accounts for only 1–2.8% of
cases of skeletal Tb
 Tuberculous disease of the shoulder is rare
constituting nearly 1-2% of skeletal
tuberculosis.
 The disease originates in the head of the
humerus, glenoid of the scapula or rarely
from the synovium.

 It is extremely uncommon for the disease to
present at the stage of synovitis.
 Painful limitations of abduction and external
rotation occurs early and there is marked wasting
of the deltoid, supraspinatus and other muscles.
 As the disease progresses there is marked
destruction and atrophy of upper end of the
humerus and glenoid and the shoulder undergoes
fibrous ankylosis.

 The common variety is a dry atrophic form (Caries
sicca)
 Very rarely there may be swelling and cold abscess
or sinus formation presenting in the deltoid region
along with biceps tendon, in the axilla or in the
supraspinatous fossa.
 In the unattended cases the scapula-humeral
muscles contract. Pull the humeral head against the
glenoid and fix the shoulder in adduction.

Three types of Tb shoulder
Type I: “caries sicca”
Marked wasting of the shoulder. Painful restriction
of all movements.
Type II: “caries exudata”
Swelling of the joint, cold abscess. Sometimes a
sinus.
Type III: “caries mobile”
Restriction of active movements of the shoulder.
Nearly full passive abduction.

 Adhesive capsulitis / frozen shoulder/ periarthritis
 Rheumatoid arthritis of the shoulder joint.

Radiological findings
 Generalized rarefaction of bones is present
with varying degree of erosion of articular
margins or actual destruction of upper end of
humerus or the glenoid.
 In the absence of sinus formation little
periosteal reaction is seen.
 In advanced cases inferior subluxation of the
humeral head.

Management
 ATT
 Shoulder spica in 70-90 degrees of abduction,
30 degrees forward flexion and 30 degrees of
internal rotation to encourage ankylosis of
gleno-humeral joint in functioning position.
 Following 3 months of spica is replaced by
abduction brace.
 Scapulo-thoracic and elbow joint movements
are encouraged after spica removal.

Arthrodesis of Shoulder-Extra articular arthrodesis
 Before the availability of effective
antitubercular drugs bony fusion of the joint
was obtained by an extra articular operation
carried out by inserting an autologous tibial
strut graft (12-15cm) between the scapula and
humerus through a posterior approach.

Intra articular arthrodesis
With the availability of effective anti
tubercular drugs intra-articular arthrodesis
is preferred.
Synovectomy, joint debridement, removal
of loose sequestra , destroyed tissue,
freshening of the joint surfaces and
insertion of bone grafts at the site of
desired fusion.

Tuberculosis of the short tubular bones
 Tuberculosis of the metacarpal, metatarsal
and phalanges is uncommon after the age of 5
years.
 In children the disease may occur in more
than one short tubular bone at a time.
 Tuberculous infection of metacarpals,
metatarsals and phalanges is known as
tuberculous dactylitis.

 The hand is more frequently involved than the
feet.
 During childhood these short tubular bones have a
lavish blood supply through a large nutrient artery.
 The interior of the short tubular bone is converted
virtually into a tuberculous granuloma.
 This leads to a spindle shaped expansion of the
bone aka “ Spina Ventosa"

 With the occlusion of the nutrient artery of the
involved bone and the destruction of internal
lamellae, there is endosteal destruction and
concomitant subperiosteal new bone formation.
 Abscess and sinus formation is quite common.
 Differential diagnosis : 1) chronic pyogenic
Osteomyelitis
 Management : ATT, bracing
excisional arthroplasty, corrective osteotomy or
amputation.

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