Tuberculosis

Bones and
Joints
Amanda Leong Weng Yan
Emerine Soh Jing Wei
Chen Chin Yen (Nicole)
Tuberculosis
(in general)
Tuberculosis
Causal Organisms Mycobacterium tuberculosis

Mode of Transmission Airborne

Predisposing factors Diabetes, drug abuse, prolonged corticosteroid

medications, AIDS

Classifications - Pulmonary
- Extrapulmonary

Pathology Granulomatous reaction which is associated with

tissue necrosis and caseation
Pathogenesis
❖ Enters the body via lung (respiratory droplet) or gut (infected milk product)

1. Primary Complex (Ghon Complex)

- Combinations of initial lesion in lung, pharynx or gut is a small one with lymphatic spread to
regional lymph nodes (middle or lower zone of the lung)
- Usually the bacilli are fixed in the nodes: no clinical illness (but occasionally the response is
excessive, with enlargement of glands in the neck or abdomen)
- 2 important sequelae:
(1) within nodes which are healed or even calcified, bacilli may survive for many years
(2) the body has been sensitized to the toxin (a positive Mantoux or Heaf test being an index of
sensitization) and, should reinfection occur
2. Secondary Spread
- If resistance to the original infection is low = widespread dissemination (bloodstream)
- Leading to giving miliary tuberculosis, meningitis or multiple tuberculous lesions.
- Some of the extrapulmonary foci develop into destructive lesions to which the term
‘tertiary’ may be applied.

3. Tertiary Lesion
- Bones / joints are affected in about 5% of patients with tuberculosis
- Vertebral bodies & large synovial joints (predispose)
- In established cases it is difficult to tell whether the infection started in the joint and then
spread to the adjacent bone or vice versa. (synovial membrane and subchondral bone have a
common blood supply)
- Once bacilli gained foothold, they elicit
chronic inflammatory reaction
- Characteristic microscopic lesion:
tuberculous granuloma ( tubercle )
- Within affected area, small patches of caseous
necrosis appear ---- center may break down to
form abscess
- Bone lesions tend to spread rapidly (
epiphyseal cartilage has no barrier to invasion,
soon the infections reach the joint )
- If synovium is involved, it become thick & oedematous ----- give rise to marked
effusion
- At the edges of joint along the synovial reflection, there may be active bone erosion

- Increased vascularity cause local osteoporosis

- If unchecked, caseation & infection extend into surrounding soft tissues ------ cold
abscess produced
- May burst through skin, forming a sinus / tuberculous ulcer

● If articular cartilage is severely damaged, healing is by fibrosis & incomplete ankylosis

with progressive joint deformity
● Within the fibrocaseous mass, mycobacteria may remain imprisoned, retaining the
potential to flare up into active disease many years later
Clinical Features
❖ History of previous infection or recent ❖ Muscle wasting
contact with tuberculosis ❖ Synovial thickening
❖ Pain ❖ Enlarged and tender regional
❖ Swelling lymph node
❖ Fever, night sweats, lassitude and loss ❖ Limited movement
of weight ❖ Joint stiffness and deformity
❖ Night cries’:
the joint, splinted by muscle spasm during the
waking hours, relaxes with sleep and the
inflamed or damaged tissues are stretched or
compressed, causing sudden episodes of
intense pain.
Diagnosis: Lab Investigations
Specimen Diagnostic Tests
- AFB culture & sensitivity
Pulmonary - Ziehl-Neelsen stain
- Sputum - Auramine fluorescent stain
- Nucleic acid amplification
Extrapulmonary - Lowenstein-Jensen culture
- Fluid examination (CSF, ascitic, - Pleural fluid: adenosine deaminase
pleural pericardial, joint)
- Tissue biopsy: bone marrow/liver Baseline blood tests
- FBC
- CRP
- BUSE
- LFT
Diagnosis: Imaging
❖ Soft-tissue swelling and periarticular osteoporosis
❖ The bone ends take on a ‘washed-out’ appearance
and the articular space is narrowed.
❖ In children the epiphyses may be enlarged (result
of long-continued hyperaemia)
❖ Erosion of the subarticular bone ( both sides of the
joint, indicating an inflammatory process starting
in the synovium)
❖ Spine: bone erosion + collapse around a diminished
intervertebral disc space; the soft-tissue shadows
may define a paravertebral abscess
Diagnosis
Features that should trigger more active investigation are:
• a long history of pain or swelling
• involvement of only one joint
• marked synovial thickening
• severe muscle wasting
• enlarged and matted regional lymph nodes
• periarticular osteoporosis on X-ray
• a positive Mantoux test
Differential Diagnosis
1. Transient synovitis
2. Monoarticular rheumatoid arthritis
3. Subacute arthritis
4. Hemorrhagic arthritis
5. Pyogenic arthritis
Management
REST
➢ Those who are diagnosed and treated early are kept in bed only until pain and
systemic symptoms subside, and thereafter are allowed restricted activity until
the joint changes resolve (usually 6 months to a year).
➢ Those with progressive joint destruction may need a longer period of rest and
splintage to prevent ankylosis in a bad position; however, as soon as symptoms
permit, movements are again encouraged.
Management
CHEMOTHERAPY
➢ ‘Intensive phase treatment’
- Isoniazid 300–400 mg + rifampicin 450–600 mg + fluoroquinolones 400–600 mg
- Daily for 5–6 months
➢ ‘Continuation phase treatment’
- Isoniazid and pyrazinamide 1500 mg per day for 4½ months and isoniazid and rifampicin
for another 4½ months.
- 9 months
➢ ‘Prophylactic phase’
- Isoniazid and ethambutol 1200 mg per day
- 3–4 months.
Management
OPERATION
➢ Cold abscess
- Immediate aspiration or draining
➢ If the joint is painful and the articular surface is destroyed
- Arthrodesis or replacement arthroplasty may be considered.

**** The longer the period of quiescence, the less the risk of reactivation of the
disease
****There is always some risk and it is essential to give chemotherapy for 3 months
before and after the operation
TB Shoulder (1-2%)
❖ Starts as osteitis
❖ Two sequelaes:
1. Abscess and sinus formation (exudative)
2. Caries sicca (non exudative)
❖ Clinical features
- Deltoid wasting
- Diffuse warmth and tenderness
- Constant ache
- Limited ROM
- Enlarged axillary lymph node
 TB Elbow (10%)
❖ Starts with synovitis or osteomyelitis
❖ Clinical features:
- Constant aching
- Limited ROM
- Marked wasting
- Joint is held flexed, swollen, warm and
tender
- Enlarged supratrochlear and axillary
lymph node
 **Involvement of the flexor tendon compartment may give rise
TB Wrist to a large fluctuant swelling that crosses the wrist into the palm
(compound palmar ganglion)

❖ Clinical Features: ❖ X ray:

- Constant aching - Localized osteoporosis
- Irregularity of the radiocarpal and
- Limited ROM
intercarpal joints
- Hand weakness - Bone erosion
- Forearm wasting
- Swollen and tender wrist
TB Hand: Tuberculous Tenosynovitis
❖ Diagnosis: synovial biopsy
❖ Treatment: Synostectomy + Prolonged chemotherapy
‘Fishmonger’s infection’ (chronic infection of the hand)
❖ Causal organism: Mycobacterium marinum
❖ MOT: Prick injuries from fish spines or hard fins in
people working with fish or around fishing boats.
❖ Clinical features:
- Superficial granuloma
- Synovitis of tendon or joint (deep infection)
❖ Management
- Superficial lesions often heal or excise
- Deep lesions: surgical synovectomy.
- Prolonged antibiotic treatment is needed to avoid
recurrence
- Broad-spectrum tetracycline such as minocycline, or
else chemotherapy with ethambutol and rifampicin
Skeletal
/Spinal
TB
Spinal TB is a.k.a. Pott’s Disease
Epidemiology
Skeletal tuberculosis - most frequent type of extrapulmonary tuberculosis

- Spinal TB (a.k.a. Pott’s disease) - 50%

- Thoracic spine (preferred location)
- often involves more than 2 levels
- most frequent form of
skeletal tuberculosis
- Cervical spine (rare)
- upper cervical spine involvement
- most dangerous
- Other bones - 50%

Prevalence worldwide - approx. 2 million people

→ Developed countries - resurgence → Developing regions - significant increase

Pathology
1. Pulmonary TB
2. Hematogenous spread - (through the Batson’s plexus or by
lymphatic drainage)
3. Localisation of infection - in a vertebral body adjacent to the
intervertebral disc
4. Bone destruction and caseation → vertebral bodies collapse
→ sharp angulation (gibbus or kyphosis)
- Cervical spine - collapses into kyphosis
5. Local spread - to disc space and the adjacent vertebrae
(anterior subchondral region)
- Cervical spine - formation of retropharyngeal abscess (Scrofula - neck TB) - points
behind the sternocleidomastoid muscle (at the side of the neck)
- Lumbar spine - paravertebral abscess may track along muscle planes to involve the
sacroiliac or hip joint (TB Hip), or along the psoas muscle to the thigh.
Pathology
1.
2.
3.
4.
5.

6. Cord damage (a major risk)

- due to pressure by the abscess, granulation tissue, sequestra or displaced bone, or
ischaemia from spinal artery thrombosis.
- may cause neurological signs varying from mild weakness to tetraplegia, in late cases.

*Because spinal TB is slowly developing, the spinal cord tolerates the gradually
increasing extradural compression without immediate neurological deficits.

7. Possible outcomes
- Healing → spontaneous bony fusion of the involved levels
- Persistent infection → spinal cord attenuation and late-onset paraplegia.
- Reactivation of healed disease
 Clinical Features (children > adults)

Neck (Cervical spine) Spine (Thoracic or lumbar spine)

Chief Neck pain and stiffness Long history of ill health and backache
complaints &
history Neglected cases - retropharyngeal abscess causes Children <10 years - concurrent pulmonary TB

- dyspnoea and dysphagia

- swelling at the side of the neck

Physical Neck - extremely tender Back - local tenderness

Examination
All movements are restricted Spinal movements are restricted.

Late cases Cold abscess pointing in the groin (occasionally)

- obvious kyphosis
- fluctuant abscess in the neck Late cases
- retropharyngeal swelling - gibbus deformity
- pectus carinatum (‘pigeon chest’) deformity

Neurological Limbs - examined for neurological defects. Legs - paresthesia and weakness
Examination
Spastic paraparesis - common in adults
Cervical
Kyphosis

Scrofula
Pectus carinatum
Atypical Features
Even in areas where tuberculosis is no longer as common as it was in the past, it is important to be
alert to the possibility of this diagnosis. The task is made harder when the patient presents with
atypical features:

- Lack of deformity, e.g. a patient with a primary epidural abscess

- Involvement of only the posterior vertebral elements
- Infection confined to a single vertebral body
- Involvement of multiple vertebral bodies and posterior elements (especially in HIV-positive
patients) resulting in a kyphoscoliosis
Patterns of
Vertebral
Involvement
Patterns of Vertebral Involvement
Paradiscal Central
- The contiguous areas of two adjacent - The body of a single vertebra is affected.
vertebrae along with the intervening disc - Presents as destruction, ballooning of
are affected. vertebral bodies, and concentric
- Narrowing of the joint space and collapse.
indistinct paradiscal margin of vertebral - This leads to early collapse of the
bodies. weakened vertebra. The nearby disc
- The disc space narrows due to either may be normal.
atrophy or prolapse into the vertebral
body of the disc tissue.
- With further progression, anterior
wedging or collapse occurs, resulting in
varying degree of kyphosis.
Patterns of Vertebral Involvement
Anterior Posterior (Appendiceal)
- Infection is localised to the anterior part - There is involvement of the posterior
of the vertebral body. arches (spinous process, lamina, pedicle,

- Spreads up and down under the anterior and transverse process as well as lateral

longitudinal ligament masses of the atlas)

- The collection of tuberculous - Pedicular or laminar destruction

granulation tissue and necrotic material - Erosion of the adjacent ribs in the
leads formation of paravertebral thoracic region or posterior cortex of
abscess the vertebral body with relative sparing
of the intervertebral discs

- A large paraspinal mass.

Imaging
Chest X-ray - to exclude pulmonary TB

Spine X-ray (of ENTIRE spine - possibility of noncontiguous

involvement)

- (picture may mimic fungal & parasitic infestations)

- Earliest signs - local osteoporosis of 2 adjacent vertebrae,
loss of crispness of the end plates
- Narrowing of disc space
- Kyphosis - erosion & collapse of adjacent vertebral bodies
- Paraspinal soft-tissue shadows - edema, swelling or
paravertebral abscess
Imaging
MRI or CT scans

- cold abscesses
- Paravertebral soft tissue
shadow
- Widened mediastinum
- Retropharyngeal abscess
- Psoas shadow
- neurological compression
- posterior vertebral element
involvement
- paravertebral abscesses
- epidural abscess
- cord compression
X-ray & CT Scan of Cervical Spine
MRI of
Thoracic &
Lumbar
spine
Special Investigations
- Mantoux and Tine (skin tests with attenuated mycobacterium) - sensitive but non-specific
(they will react in vaccinated patients)
- ESR - non-specific
- WBC
- count - usually normal
- differential - lymphocytosis and platelets
raised
- HIV status
- Biopsy - to confirm the diagnosis & exclude
drug-resistant strains
- Microscopy
- Culture - takes up to 6 weeks
- Histology
- PCR - 1-2 days - sensitive and specific
Differential Diagnosis
Differential Diagnosis

- Pyogenic infections - disc-space collapse

- Fungal infections
- Parasitic infestations e.g. hydatid disease
- Malignant disease (tumor) - involvement of a single vertebral body

True Spinal TB

- involvement of vertebrae either side of a preserved disc

- However, TB is a great mimic and the presentation and appearances can be similar to all of
the above.
Treatment - Cervical Involvement
Initial treatment→ Anti-TB therapy

Depending on the stage of disease: Surgery is for

- Neurologically intact patients without signs of - drainage of large retropharyngeal abscess

instability - decompression of threatened spinal cord
→ external immobilization of the neck in cervical - fusion of unstable spine
brace or plaster case for 6 weeks up to 6 months
- Neurological compromise or with instability
→ skull tongs traction
- Bone destruction with severe kyphosis deformity
→ debridement of necrotic bone and anterior
cervical vertebral fusion with bone grafts as an
alternative to prolonged immobilization
Anti-TB Therapy
WHO recommends 9 months of treatment for tuberculosis of bones or joints

1. Intensive phase (2-6 months)

- Isoniazid 300–400 mg
- Rifampicin 450–600 mg
- Fluoroquinolones 400–600 mg daily
2. Continuation phase (4-9 months)
- Isoniazid and Pyrazinamide 1500 mg per day for 4½ months
- Isoniazid and Rifampicin for another 4½ months
3. Prophylactic phase
- Isoniazid and Ethambutol 1200 mg per day for a further 3–4 months
Directly Observed Therapy (DOTS) regimen - to avoid poor compliance
Treatment - Thoracic Involvement
Objectives

- eradicate or at least arrest the disease

- prevent or correct deformity
- prevent or treat associated neurological deficit

Principle

- Minimal deformity and normal or mild neurological impairment

→ Medical therapy (anti-TB therapy)
- Marked kyphosis or progressive neurological deficit
→ Surgery: surgical debridement and corrective instrumented fusion → Anterior resection
of diseased tissue and anterior spinal fusion with a strut graft → early and complete
eradication of the infection and prevention of spinal deformity (Figure 18.26).
Treatment - Thoracic Involvement
Ambulant chemotherapy alone Continuous bed rest and Operative treatment
chemotherapy
- for early or limited disease - when there is an
with no abscess formation - for more advanced abscess that can
or neurological deficit. disease readily be drained
- 6–12 months, or - when there are no - for advanced disease
- until X-ray shows available skills and with marked bone
resolution of the facilities for radical destruction and
bone changes anterior spinal surgery threatened or actual
- patient is - where technical severe kyphosis
constitutionally well problems are too - neurological deficit
- ESR has returned to daunting (e.g. in (paraparesis) that has
normal lumbosacral not responded to drug
- Disadvantage - tuberculosis) – provided therapy.
noncompliance there is no abscess that
needs to be drained.
Treatment - Thoracic Involvement
Operative Treatment

- Excise all infected and necrotic material

- Reconstruct with
- autogenous rib/fibula/iliac crest
- allograft humerus shafts
- titanium cages
- Anterior- or posterior-based approach using a
vertebral column resection technique
- Posterior instrumentation may be required for
increased stability (e.g. in children)
Complications - Pott’s
Paraplegia (most feared complication of spinal tuberculosis)

Early-onset paresis (usually within 2 years) Late-onset paresis

- due to pressure by inflammatory oedema, an - due to direct cord

abscess, caseous material, granulation tissue compression from
or sequestra. increasing deformity,
- Clinical features: lower-limb weakness, or vascular
upper motor neuron signs, sensory insufficiency of the
dysfunction and incontinence. cord.
- CT and MRI: cord compression - Prognosis: poor
- Prognosis: good neurological recovery recovery following
following surgery. decompression
HIV & Spinal Tuberculosis
- HIV is the main reason for resurgence of TB in the developing world
- TB used to be AIDS-defining
- not always the case now due to the high incidence of both diseases in some regions
- Some HIV patients have relatively good CD4 counts
- Patients with significantly impaired immunity are prone to developing opportunistic
infections and atypical mycobacterial infections.
- There may be increasing atypical TB presentation in HIV patients.
HIV & Spinal Tuberculosis
Management

- Medical and surgical management is essentially the same

- Advanced disease - consider patient’s ability to survive a surgical insult
- Often have large paraspinal abscesses with little kyphosis, and a simple procedure (i.e.
costotransversectomy) is all that is required.
- Initiation of anti-retrovirals should be considered but may result in increased TB disease
due to a recovering immune system (immune reconstitution inflammatory syndrome, IRIS)
- IRIS - life-threatening and needs to be managed by an infectious diseases specialist.
TB Hip
Intro
◆ Tuberculosis of hip is second commonest to Pott’s disease
◆ Common in first 3 decades of life
◆ Males > Females
◆ Usually monoarticular(single joint)
Pathogenesis
1. TB of hip is secondary to primary focus
in the lungs, lymph nodes or any
viscera(main parts)
2. It is spread from the primary focus
through hematogenous route and reach
either to synovium or bone
3. Site of initial focus
a. Acetabular roof
b. Epiphysis
c. Metaphyseal region/Femoral Neck
(Babcock’s triangle)
d. Greater trochanter
e. Synovial membrane
f. Trochanteric bursa(lateral aspect)
● Inhalation and Primary Infection:
● TB starts with inhaling bacteria (M. tuberculosis).
● Primary infection occurs in the lungs.
● Spread to Hip Joint:
● Bacteria travel through the bloodstream to various organs.
● Rich blood supply makes the hip joint vulnerable.
● Formation of Granulomas:
● Immune response forms granulomas to contain the infection.
● Granulomas develop within the hip joint.
● Caseous Necrosis:
● Caseous necrosis (cheese-like cell death) occurs in granulomas.
● Contributes to cartilage and bone destruction.
● Articular Involvement:
● Infection reaches synovium and articular surfaces.
● Causes synovitis, effusion, and erosion of cartilage and bone.
● joint Destruction and Deformity:
● Untreated TB leads to progressive joint destruction.
● Results in deformities, instability, and functional impairment.
● Spread to Adjacent Structures:
● Infection can extend to pelvis or surrounding tissues.
● Forms cold abscesses, sinus tracts, and affects neighboring bones.
● Systemic Symptoms:
● Symptoms include fever, night sweats, weight loss, and fatigue.
● Reflect the overall impact of tuberculosis on the body.
 Synovium Small tubercles coalesce
↓ & undergo caseation
Synovial membrane ↓
become congested & Cold abscess
swollen ↓
(synovitis) Perforate Capsule
↓ ↓
Granulation tissue Tracks down area of least
extends over bone resistance
↓ ↓
Necrosis of Femoral triangle, inguinal
subchondral bone, region, gluteal region,
sequentra greater trochanter,
↓ ischiorectal fossa,
Kissing lesion on either medial/lateral/posterior
side of the joint aspect of thigh
Stages
1. Stage of synovitis (FABER-AL)
2. Stage of arthritis (FADIR-AS)
3. Stage of erosion (FADIR-TS)
Stage of Synovitis
(FABER-AL)
◆ Affected limb presents with flexion,
abduction & external rotation (FABER)
deformity due to effusion in the joint
◆ Apparent lengthening due to synovial
hypertrophy & synovitis
◆ Restriction of terminal range of movements
Stage of Arthritis
(FADIR-AS)
◆ Progressive destruction of the joint
◆ Active stage: spasm of adductor & flexor
muscles leads to flexion, adduction &
internal rotation (FADIR) deformity of
affected limb
◆ Muscle wasting
◆ Apparent shortening
◆ Restricted hip movements in all planes
Stage of Erosion
(FADIR-TS)
◆ Cartilages are destroyed
◆ Femoral head & acetabulum are eroded
◆ Pathological subluxation/dislocation of hip
◆ FADIR deformity
◆ True shortening
Clinical Features
Symptoms: Signs:
◆ Fever (evening rise of ◆ Limping gait (early stage: painful,
temperature) advanced: painless)
◆ Cough ◆ Late stage signs:
◆ Pain (insidious onset, at groin ◆ Deformity: flexion, adduction &
area, may radiate to medial abduction
thigh & knee, night cries) ◆ Muscle wasting in gluteal region &
◆ Swelling around hip region thigh
◆ Constitutional symptoms (loss ◆ Scars & sinuses (cold abscess) -
of weight, loss of appetite, perianal, gluteal, trochanteric,
night sweats) inguinal, femoral areas
◆ Pathological
subluxation/dislocation
◆ Limb length inequality
Physical Examination
General Examination
◆ Build & Nourishment (Poorly nourished & cachexic)
◆ Anemic
◆ Lymphadenopathy

Local Examination
Look:
◆ Antalgic gait (early), Stiff hip gait, Trendelenburg gait
◆ Muscle wasting at gluteal region & thigh
◆ Cold abscess (perianal, gluteal, trochanteric, inguinal femoral areas)
◆ Limb length inequality
Local Examination
- Always check spine for
mobility & deformity
Feel: - Must also check ipsilateral
◆ Local rise of temperature knee & contralateral hip
◆ Swelling
◆ Tenderness at femoral triangle
◆ Muscle spasm
◆ Trochanteric thrust tenderness
◆ Globular mass in gluteal region (dislocated hip)
◆ Lymphadenopathy (External iliac & deep inguinal
LN) - enlarge & matted

Move:
◆ Restricted range of movement (depends on stage)
 Measurement
Stage 1 Stage 2 Stage 3
(Stage of Synovitis) (Stage of Arthritis) (Stage of Erosion)

● Apparent length ↑ ● Apparent length ↓ on ● Apparent length ↓ on

on affected limb affected limb affected limb
● Real length are ● Real length equal on ● Real length ↓ on
equal on both limbs both limbs affected limb
● Apparent ● Apparent ● True shortening
lengthening shortening
Investigations
◆ Baseline investigations: FBC w/ white cell differential
count(lymphocytosis), Hb (anemia), ESR & CRP
(increased in acute)
◆ Mantoux test (positive)
◆ Imaging:
◆ X-ray of pelvis including both hip (AP & lateral view)
◆ USG: effusion can be detected in early arthritis/synovitis, USG
guided aspiration can also be done
◆ CT scan: detect changes in acetabulum & femur
◆ MRI: useful to detect pathology early
◆ Synovial fluid analysis
◆ Synovial biopsy (arthroscopy/open) & sent for histopathology, AFB
staining, PCR, C&S
X-ray
1. Stage of synovitis
● Sometimes no findings
● Haziness of articular margin
● Rarefaction (decrease density )of bones
2. Stage of arthritis
● Phemister triad Phemister triad:
● Bony lesion in femoral head, acetabulum or both ● Periarticular
● Reduction in joint space osteoporosis
3. Stage of erosion ● Peripheral osseous
● No joint space erosion(loss bone
disease)
● Destruction of femoral head & acetabulum (articular ● Gradual diminution
surface) (decrease size)of joint
● Travelling acetabulum, posterior hip dislocation, space
mortar & pestle, protrusio acetabuli
Shanmugasundaram
Classifications Stable hip forms:
● Normal
● Atrophic
● Perthes

Unstable hip forms:

● Travelling
acetabulum
● Dislocating
● Protrusio
acetabuli
● Mortar &
Pestle
Differential Diagnosis
In children:
◆ Perthes disease
◆ Juvenile rheumatoid arthritis
◆ Transient synovitis
◆ Hemorrhagic arthritis
◆ Pyogenic arthritis

In adults:
◆ Rheumatoid arthritis
◆ Septic arthritis
General Treatment
Stage 1 (Conservative): ◆ Traction:
◆ Antituberculous treatment ◆ Relieve muscle
◆ Traction, rest followed by mobilisation spasm
◆ Surgical intervention if not responsive ◆ Prevents & correct
Stage 2: deformity
◆ Antituberculous treatment ◆ Maintain joint
◆ Traction space
◆ Joint debridement
Stage 3:
◆ Antituberculous treatment
◆ Girdlestone arthroplasty
◆ Arthrodesis
◆ Hip replacement
Surgery
◆ Joint debridement
◆ Pus, necrotic tissue, inflamed synovium
and dead cartilage are removed
◆ The joint is washed thoroughly with
saline & close the wound

◆ Girdlestone’s excision arthroplasty (aka femoral head ostectomy)

◆ Head and neck of femur + greater trochanter + acetabulum are
excised with the dead necrotic & granulation tissue
◆ Provides a mobile, painless hip joint with control of infection
and correction of deformity
◆ Results in instability & permanent shortening of the limb
◆ Arthrodesis(artificial ankylosis)
◆ Indication : stiff hip with functional position
◆ Usually not done before the age of 14
◆ Convert stiff & painful hip to stiff & painless hip
◆ Cons: inability to squat, sitting cross-legged & kneeling
◆ Corrective osteotomy
◆ Indication: bony ankylosis of the hip with unacceptable functional
position
◆ Subtrochanteric corrective osteotomy of femur
◆ Total hip arthroplasty
◆ Indication: Older patients, stage 3 & usually after 1 year of healing
◆ No rule for hemiarthroplasty because acetabulum is almost always
involved
Tuberculosis
of Knee, Ankle
& Foot
 Tuberculosis of Knees
- 3rd common site of osteoarticular tuberculosis.
- Can happens at any age.
- More common in children
Pathophysiology
Initial focus
1. Hematogenous Tubercular synovitis.
dissemination in the
synovium Articular margins eroded by
2. Subchondral bone pannus, involves the cruciate
Synovial membrane
3. Juxta-articular osseous ligaments, periarticular
focus congested & edematous
tissues, capsule & ligaments.
followed by the thickening
Tuberculous abscess in
of the lining.
- Subchondral bone
- Epiphyseal bone
Joint fluid increased.
- Metaphyseal bone
Clinical features
Early features Late features

Swollen joint Composite deformity

- Thigh (quadriceps) muscle - Posterior & lateral subluxation/
wasted dislocation of tibia
- Patellar tap positive - Flexion + external rotation
Pain - Valgus
Warm knees
Low grade fever
Synovial thickening
Restricted & painful movement
Regional lymphadenopathy
Diagnosis
1. History of chronic joint pain
2. Synovial biopsy
3. X-ray
- Marked osteoporosis
- Enlargement of bony epiphyses (in children)
- Marginal erosions of joint
- Diminution of joint space

Differential diagnosis
1. Rheumatoid arthritis
2. Subacute pyogenic arthritis/ synovitis
3. Synovioma
Detailed X-ray findings
- Synovial stage
- Marked osteoporosis
- Increased soft tissue swelling
- Arthritis stage
- Loss of definition of articular surfaces
- Marginal erosions of joint
- Diminution of the joint space
- Destruction of bone
- Enlargement of bony epiphyses (in children)
- Advance stage
- Gross destruction of bone ends
- Osteolytic cavities
- Tubercular sequestra
- Triple deformity
Treatment
Non-operative
1. General anti-TB drugs
2. Joint aspiration
3. Traction
4. Permitted ambulation with walking aids after 12 weeks
- Unprotected weight bearing 9-12 months after

Operative treatment
1. Arthromtomy & synovectomy
2. Arthrodesis (child vs adults)
3. Arthroplasty
Tuberculosis of ankle & foot
Begins as synovitis/ osteomyelitis

Present as
● Pain, swollen ankle
● Markedly wasted calf
● Painful during walking
● Warm skin
● Restricted movements
● Sinus formation

Sinus formation
Diagnosis
Imaging Test
1. X-ray
- regional osteoporosis, sometimes a bone abscess and, with
late disease, narrowing and irregularity of the joint space
2. MRI Scan
- Define bone & soft tissue involvement
3. Biopsy
- Identify the causal organisms

Treatment
1. General anti-TB treatment
2. Removable splint
3. Calliper
4. Arthrodesis
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