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Spinal Tuberculosis (Pott's Disease)

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Spinal Tuberculosis (Pott's Disease)

Comprehensive guide to spinal tuberculosis including diagnosis, imaging, medical and surgical management, and outcomes for orthopaedic fellowship exam

complete
Updated: 2025-12-24
High Yield Overview

SPINAL TUBERCULOSIS (POTT'S DISEASE)

Diagnosis | Imaging | Medical Management | Surgical Indications

50%Of skeletal TB is spinal
T10-L2Most common levels
6-12 moStandard ATT duration
10-15%Require surgery

ANATOMICAL PATTERNS

Paradiscal
PatternMost common (50-75%)
TreatmentAdjacent vertebral body + disc involvement
Central
PatternIsolated vertebral body
TreatmentConcertina collapse, ivory vertebra
Anterior Subligamentous
PatternUnder ALL
TreatmentMulti-level scalloping, skip lesions
Posterior/Neural Arch
PatternRare (2-10%)
TreatmentPedicle, lamina, spinous process

Critical Must-Knows

  • Thoracolumbar junction (T10-L2) is most common site
  • Disc preservation early distinguishes from pyogenic infection
  • Cold abscess does not contain pus - caseous material
  • MRI is gold standard - sensitivity 96%, specificity 93%
  • Medical treatment first - surgery for specific indications

Examiner's Pearls

  • "
    Paradiscal type is most common - adjacent vertebrae + disc involvement
  • "
    Skip lesions in 10-15% - always image whole spine
  • "
    Psoas abscess is pathognomonic when combined with spine findings
  • "
    Neurological deficit from granulation tissue, abscess, or kyphosis

Clinical Imaging

Imaging Gallery

Conventional radiographs of the thoracic spine and the chest on initial presentation. (A) Compression fracture of the third thoracic vertebra (arrows). (B) Solitary pulmonary nodule of 2.5 cm in diame
Click to expand
Conventional radiographs of the thoracic spine and the chest on initial presentation. (A) Compression fracture of the third thoracic vertebra (arrows)Credit: Ringshausen FC et al. via Ann. Clin. Microbiol. Antimicrob. via Open-i (NIH) (Open Access (CC BY))

Critical Spinal TB Exam Points

Disc Preservation

Early TB preserves the disc while pyogenic infection destroys it early. This is a key differentiating feature. However, late-stage TB can involve the disc. Always compare with clinical tempo - TB is insidious, pyogenic is acute.

Cold Abscess

Cold abscess is characteristic of TB - it lacks acute inflammatory features and contains caseous neite, not pus. It can track along fascial planes (psoas abscess). The absence of local warmth and systemic toxicity distinguishes it from pyogenic abscess.

Imaging Sensitivity

MRI is essential - 96% sensitivity, 93% specificity. Changes visible within 3-5 days. X-rays only positive when 50% trabecular bone destroyed (4-6 months delay). Always image whole spine for skip lesions (10-15%).

Medical First

Medical treatment is primary - 85-90% respond to antitubercular therapy (ATT) alone. Surgery reserved for: progressive neurology, instability, failure of medical treatment, severe kyphosis. Even with neurology, medical treatment often effective.

Spinal TB vs Pyogenic Spondylitis

FeatureTuberculosisPyogenic
OnsetInsidious (weeks-months)Acute (days-weeks)
Disc involvementLate or sparedEarly destruction
Vertebral bodiesMultiple, skip lesionsUsually contiguous
Abscess wallThin, smoothThick, irregular
Posterior elementsSpared earlyOften involved
CalcificationPresent (pathognomonic)Rare
Mnemonic

COLD ABSCESS - TB Features

C
Caseous necrosis
Cheese-like material, not pus
O
Oligosymptomatic
Minimal local inflammatory signs
L
Long duration
Insidious onset over months
D
Disc spared early
Unlike pyogenic infection
A
Abscess tracking
Along fascial planes (psoas)
B
Bone destruction gradual
Less explosive than pyogenic
S
Skip lesions possible
Non-contiguous involvement
C
Calcification present
Pathognomonic feature
E
ESR elevated
Often very high (more than 50)
S
Slow response
Takes weeks for improvement
S
Subligamentous spread
Under anterior longitudinal ligament

Memory Hook:COLD ABSCESSES lack heat, redness, and acute toxicity - unlike pyogenic

Mnemonic

SPINE TB - Imaging Findings

S
Skip lesions
Non-contiguous vertebral involvement
P
Preservation of disc (early)
Key differentiator from pyogenic
I
Intraosseous abscess
Within vertebral body
N
Narrow disc (late)
Secondary to collapse
E
Epidural extension
Causing cord compression
T
Thin-walled abscess
Smooth margins
B
Bilateral psoas abscess
Characteristic tracking

Memory Hook:MRI is imaging modality of choice - sensitivity 96%

Mnemonic

SURGERY - Indications for Surgery

S
Severe kyphosis
More than 40-50 degrees
U
Unstable spine
Progressive deformity
R
Resistant TB
MDR-TB considerations
G
Granulation tissue
Compressing cord/roots
E
Extensive abscess
Large cold abscess
R
Regressing neurology
Progressive deficit despite ATT
Y
Yield diagnosis
Biopsy for confirmation

Memory Hook:Most patients (85-90%) respond to medical treatment alone

Overview and Epidemiology

Spinal tuberculosis (Pott's disease) is the most common form of skeletal tuberculosis, first described by Percivall Pott in 1779. It represents a significant cause of morbidity, particularly in endemic regions, and remains important in the Australian context due to immigration patterns.

Epidemiology:

  • Spinal TB accounts for 50% of all skeletal TB cases
  • Second most common form of extrapulmonary TB
  • Thoracolumbar junction (T10-L2) is most commonly affected
  • Approximately 10-15% have skip lesions (non-contiguous involvement)
  • Male to female ratio approximately 1.5:1
  • Can occur at any age but peaks in second and third decades

Global Burden:

RegionEstimated IncidenceRisk Factors
High endemicMore than 100/100,000Crowding, poverty, HIV
Intermediate10-100/100,000Immigration, immunosuppression
Low endemicLess than 10/100,000Imported cases, reactivation

Australian Context:

Australia has low TB incidence overall, but overseas-born individuals (particularly from high-burden countries) account for the majority of cases. Spinal TB may present in immigrants, refugees, or travelers, often as reactivation of latent infection years after initial exposure.

Immigration Pattern

In Australia, maintain high suspicion for spinal TB in patients from endemic regions (South Asia, Southeast Asia, Sub-Saharan Africa, Pacific Islands) presenting with chronic back pain and constitutional symptoms, even years after migration.

Pathophysiology and Anatomy

Route of Infection

Primary Infection:

  • Haematogenous spread from pulmonary focus (most common)
  • Arterial dissemination to vertebral bodies
  • Paradiscal arteries supply adjacent vertebrae (paradiscal type)
  • Batson's venous plexus may facilitate spread

Secondary Spread:

  • Subligamentous extension under ALL
  • Epidural spread causing cord compression
  • Paravertebral spread forming cold abscess
  • Psoas tracking along muscle sheath

Anatomical Patterns of Involvement

1. Paradiscal Type (50-75%):

  • Most common pattern
  • Involves adjacent vertebral bodies and intervening disc
  • Arterial spread via paradiscal arteries
  • Late disc destruction (unlike pyogenic)
  • May extend to multiple levels

2. Central Type:

  • Isolated vertebral body involvement
  • Concertina collapse
  • May produce ivory vertebra
  • Spares disc initially

3. Anterior Subligamentous Type:

  • Spreads under anterior longitudinal ligament
  • Multi-level involvement with anterior scalloping
  • Can produce skip lesions
  • Extensive yet may spare vertebral integrity initially

4. Posterior Type (2-10%):

  • Involves neural arch (pedicle, lamina, spinous process)
  • More common in lower lumbar spine
  • May cause early neurological deficit

Pathological Changes

Bone Changes:

  • Granulomatous inflammation
  • Caseous necrosis
  • Bone destruction and sequestration
  • Minimal new bone formation (unlike pyogenic)

Soft Tissue:

  • Cold abscess formation (paravertebral, epidural, psoas)
  • Granulation tissue proliferation
  • Fibrosis with healing

Neurological Compression:

  • Early: Epidural granulation tissue, abscess
  • Late: Bony compression from kyphotic deformity

Classification Systems

Kumar Classification (Neurological Status)

StageDescriptionNeurological Findings
INo deficitNormal
IISensorySensory loss only
IIIMotor - ambulatoryMotor weakness, can walk
IVMotor - non-ambulatoryCannot walk
VComplete paraplegiaNo function below lesion

Tuli Classification (Paraplegia Type)

Type A: Active Disease with Paraplegia

  • A1: Minimal bone loss, severe deficit
  • A2: Moderate bone loss, severe deficit
  • A3: Extensive bone loss with deficit

Type B: Healed Disease with Paraplegia

  • B1: Cord compression from healed kyphosis
  • B2: Reactivation in previously healed lesion

This classification guides surgical approach and prognosis for neurological recovery.

Moon Classification (Bone Destruction)

Stage 1: Minimal bone destruction with no instability Stage 2: Moderate bone destruction, potential instability Stage 3: Severe bone destruction, definite instability

MRC (Medical Research Council) Classification

Group I: No neurological involvement Group II: Minor neurological involvement Group III: Moderate neurological involvement Group IV: Complete paraplegia

Healing Criteria (Imaging)

On MRI, healing is indicated by:

  • Resolution of marrow edema
  • Fatty marrow signal return
  • Abscess resolution
  • Bony ankylosis
  • Reduced contrast enhancement

These classifications help standardize assessment and guide treatment decisions.

Rajasekaran Classification (Kyphosis Progression)

Factors predicting kyphosis progression:

  1. Initial loss of vertebral body height

    • More than 50% = high risk
  2. Site of lesion

    • Thoracic = higher kyphosis risk
    • Lumbar = lower kyphosis risk
  3. Age at presentation

    • Children at higher risk
    • Growing spine deforms more
  4. Number of vertebrae involved

    • Multi-level = worse prognosis

Final Kyphosis Prediction Formula:

Final kyphosis = Y + (a × b)

Where:

  • Y = initial kyphosis
  • a = 5.5 (thoracic) or 2.5 (lumbar)
  • b = number of vertebrae involved

This helps predict final deformity and guides surgical timing decisions.

Clinical Assessment

History

Presenting Symptoms:

SymptomFrequencyCharacteristics
Back pain90-95%Insidious, localized, constant
Constitutional50-70%Weight loss, night sweats, fever
Neurological20-30%Weakness, sensory changes
Deformity30-40%Visible kyphosis (gibbus)
Abscess20-30%Swelling (groin, flank)

Key History Elements:

  • Duration of symptoms (typically weeks to months)
  • Constitutional symptoms (weight loss, night sweats, low-grade fever)
  • Neurological symptoms (weakness, numbness, bowel/bladder)
  • Contact history (TB exposure)
  • Country of origin and travel
  • Immunocompromise (HIV, diabetes, immunosuppressants)
  • Previous TB treatment

Physical Examination

Spinal Assessment:

  • Gibbus deformity (angular kyphosis)
  • Localized tenderness
  • Paraspinal muscle spasm
  • Restricted range of motion
  • Cold abscess (paravertebral, groin, flank)

Neurological Examination:

  • Motor power (myotomes)
  • Sensory level
  • Reflexes
  • Long tract signs (spasticity, clonus, Babinski)
  • Bladder/bowel function
  • Gait assessment

Systemic Examination:

  • Lymphadenopathy
  • Pulmonary findings (primary TB)
  • Peripheral cold abscess
  • Signs of other organ involvement

Cold Abscess Features

A cold abscess lacks the cardinal signs of inflammation (calor, rubor, dolor, tumor). It presents as a non-tender, fluctuant swelling that may track to distant sites (groin in psoas abscess). The absence of acute inflammatory features is characteristic.

Red Flags

  • Rapidly progressive neurological deficit
  • Complete paraplegia
  • Bladder/bowel dysfunction
  • Respiratory compromise (cervical lesions)
  • Signs of MDR-TB or treatment failure

Investigations

Laboratory Investigations

Essential Tests:

TestExpected FindingNotes
ESRElevated (often more than 50)Useful for monitoring
CRPElevatedLess specific than ESR
Mantoux/IGRAUsually positiveDoes not confirm active disease
Sputum AFBMay be positiveIf pulmonary involvement
HIV serologyRule out coinfectionImportant for management

Imaging Protocol

Plain Radiographs:

  • First-line imaging
  • Positive only when 50% trabecular bone destroyed
  • May take 4-6 months to show changes
  • Shows: vertebral destruction, collapse, kyphosis

MRI (Gold Standard):

  • Sensitivity 96%, Specificity 93%
  • Changes visible within 3-5 days
  • Essential for soft tissue assessment
  • Detects epidural extension and cord compression
  • Identifies skip lesions

MRI Findings:

  • T1: Hypointense marrow signal
  • T2/STIR: Hyperintense marrow edema
  • Contrast: Rim enhancement of abscess
  • Epidural extension
  • Skip lesions
  • Psoas/paravertebral abscess

CT Scan:

  • Superior bone detail
  • Calcification within soft tissue (pathognomonic)
  • Bony destruction pattern
  • CT-guided biopsy assistance

Tissue Diagnosis

Biopsy Indications:

  • Atypical presentation
  • Negative Mantoux/IGRA
  • MDR-TB suspected
  • Exclude malignancy
  • Failed empirical treatment

Methods:

  • CT-guided percutaneous biopsy
  • Open surgical biopsy
  • Abscess aspiration

Histopathology:

  • Caseous necrosis
  • Epithelioid granulomas
  • Langhans giant cells
  • AFB staining
  • PCR (GeneXpert)

Management

📊 Management Algorithm
tuberculosis spine potts management algorithm
Click to expand
Management algorithm for tuberculosis spine pottsCredit: OrthoVellum

Antitubercular Therapy (ATT)

Standard Regimen (WHO):

PhaseDurationDrugs
Intensive2 monthsHRZE (4 drugs)
Continuation4-10 monthsHR (2 drugs)

Drug Dosages:

  • H (Isoniazid): 5 mg/kg (max 300 mg)
  • R (Rifampicin): 10 mg/kg (max 600 mg)
  • Z (Pyrazinamide): 25 mg/kg (max 2 g)
  • E (Ethambutol): 15 mg/kg (max 1.2 g)

Duration Controversy:

  • Standard: 6-9 months
  • Extended: 12-18 months (complex cases)
  • WHO recommends 6 months for uncomplicated
  • Many centers use 9-12 months for spinal TB

Monitoring:

  • Baseline: LFTs, uric acid, visual acuity
  • Monthly: LFTs during intensive phase
  • Clinical response assessment
  • Radiological healing (MRI at 6 months)
  • ESR trending

Drug-Resistant TB:

  • MDR-TB requires specialist management
  • Second-line drugs (fluoroquinolones, injectables)
  • Extended duration (18-24 months)
  • Specialist input essential

Hepatotoxicity Risk

Monitor LFTs closely during ATT. Risk factors for hepatotoxicity include age more than 35, pre-existing liver disease, alcohol use, and concurrent hepatotoxic medications. Stop ATT if ALT rises more than 5x ULN or symptoms develop.

Medical therapy alone achieves good outcomes in 85-90% of cases when neurological deficit is not severe.

Indications for Surgery

Absolute Indications:

  1. Progressive neurological deficit despite ATT
  2. Severe or worsening kyphosis (more than 40-50 degrees)
  3. Spinal instability
  4. Large abscess requiring drainage
  5. Tissue diagnosis (when needed)
  6. MDR-TB with poor response

Relative Indications:

  • Moderate neurological deficit with poor recovery
  • Significant kyphosis (more than 30 degrees)
  • Large psoas abscess
  • Bony instability
  • Severe pain despite medical treatment

Timing:

  • Urgent: Rapidly progressive neurology
  • Semi-elective: Stable neurology, mechanical issues
  • Elective: Deformity correction after healing

Goals of Surgery

GoalApproach
DecompressionAnterior or posterior
DebridementRemove caseous material
StabilizationInstrumented fusion
Deformity correctionKyphosis correction
Tissue for diagnosisHistology and culture

Surgery combined with ATT improves neurological recovery and prevents deformity progression in selected cases.

Surgical Approaches

Anterior Approach:

  • Traditional approach for thoracic/lumbar
  • Direct access to disease focus
  • Effective debridement
  • Anterior reconstruction
  • Hong Kong technique (radical debridement + strut graft)

Posterior Approach:

  • Pedicle screw instrumentation
  • Posterior decompression (costotransversectomy)
  • Combined with anterior debridement
  • Less morbid approach
  • Better for multilevel disease

Combined Anterior-Posterior:

  • Indicated for severe instability
  • Circumferential debridement
  • Optimal correction
  • Higher morbidity

Minimally Invasive:

  • Video-assisted thoracoscopic surgery
  • Percutaneous instrumentation
  • Reduced morbidity
  • Selected cases

Instrumentation Considerations

Titanium preferred:

  • MRI compatible
  • Minimal artifact
  • Good biocompatibility
  • Can instrument in active infection

Fusion Approach:

  • Autograft (iliac crest, rib)
  • Titanium mesh cage
  • Strut graft (fibula)
  • Bone graft substitutes

Postoperative Care

  • Continue ATT for full course
  • Monitor wound healing
  • Neurological surveillance
  • Bracing (variable practice)
  • Rehabilitation

Surgical outcomes are generally good when combined with appropriate medical therapy.

Complications

Disease-Related Complications

ComplicationIncidenceManagement
Kyphosis30-50%Surgical correction if severe
Paraplegia20-30%Decompression ± steroids
Cold abscess20-30%Drainage if large
Sinus formation5-10%Debridement, prolonged ATT
Spinal instabilityVariableInstrumented fusion

Neurological Complications

Pott's Paraplegia:

  • Early onset (active disease): Better prognosis
  • Late onset (healed disease): Worse prognosis
  • Causes: Abscess, granulation tissue, bony compression

Prognosis Factors:

  • Duration of deficit (shorter = better)
  • Completeness (incomplete = better)
  • Age (younger = better)
  • Vertebral destruction extent

Treatment-Related Complications

Medical:

  • Hepatotoxicity (2-10%)
  • Drug reactions
  • Drug interactions
  • MDR development

Surgical:

  • Infection
  • Neurological injury
  • Hardware failure
  • Pseudarthrosis
  • Recurrence

Long-Term Sequelae

  • Residual kyphosis
  • Chronic pain
  • Residual neurological deficit
  • Adjacent segment disease
  • Growth disturbance (paediatric)

Kyphosis Prevention

Early recognition and appropriate treatment can prevent severe kyphosis. Children are at higher risk of progressive deformity. Consider early surgery in children with significant vertebral destruction to prevent late kyphotic deformity.

Outcomes and Prognosis

Neurological Recovery

Prognosis by Presentation:

PresentationRecovery RateTimeframe
Early/mild deficit70-80%3-6 months
Moderate deficit50-70%6-12 months
Complete paraplegia20-30%Variable

Favourable Factors:

  • Short duration of deficit
  • Incomplete paraplegia
  • Younger age
  • Compression by soft tissue (not bone)
  • Early treatment initiation

Treatment Outcomes

Medical Treatment Alone:

  • Success rate: 85-90%
  • Healing time: 6-12 months
  • Residual kyphosis: 30-50%

Combined Medical + Surgical:

  • Neurological improvement: 70-90%
  • Fusion rate: 90-95%
  • Deformity correction maintained

Long-Term Prognosis

Factors Affecting Outcome:

  • Extent of initial disease
  • Timing of treatment
  • Adequacy of ATT
  • Surgical technique
  • Patient compliance

Return to Activity:

  • Light activities: 3-6 months
  • Full activities: 6-12 months
  • Depends on neurological status

Outcome Summary

With appropriate treatment, most patients with spinal TB achieve good outcomes. Medical treatment alone is sufficient in 85-90%. Neurological recovery is expected in 70-80% of those with incomplete deficits. Surgery improves outcomes in selected cases with specific indications.

Evidence and Guidelines

Duration of ATT for Spinal TB

Level I-II
Key Findings:
  • 6 months ATT as effective as longer regimens in uncomplicated cases
  • No difference in relapse rates between 6 and 12 months
  • Extended treatment may be warranted in complex cases
  • Compliance is more important than duration
Clinical Implication: Shorter regimens with good compliance are effective and improve adherence
Source: WHO Guidelines 2020; Cochrane Review 2013 [1,2]

Surgery vs Medical Treatment Alone

Level II-III
Key Findings:
  • Medical treatment alone effective in 85-90% of uncomplicated cases
  • Surgery improves neurological recovery in selected patients
  • Earlier surgery may benefit those with significant neurological deficit
  • Combination approach best for complex cases
Clinical Implication: Surgery complements but does not replace medical therapy
Source: MRC Studies; Cochrane Review 2013 [3,4]

MRI for Diagnosis and Monitoring

Level II
Key Findings:
  • MRI sensitivity 96%, specificity 93%
  • Changes visible within 3-5 days
  • Superior to CT for soft tissue and epidural assessment
  • Whole spine imaging detects skip lesions (10-15%)
Clinical Implication: Always image entire spine to detect non-contiguous disease
Source: Multiple studies [5,6]

Neurological Recovery Predictors

Level III
Key Findings:
  • Duration of paralysis inversely correlates with recovery
  • Incomplete lesions recover better than complete
  • Early decompression improves outcomes in selected cases
  • Age affects recovery potential
Clinical Implication: Time is neural function - early diagnosis and treatment are key
Source: Tuli 1969; Multiple retrospective studies [7,8]

Exam Viva Scenarios

Practice these scenarios to excel in your viva examination

VIVA SCENARIOStandard

Classic Pott's Disease Presentation

EXAMINER

"A 35-year-old man from India presents with 4 months of progressive back pain, night sweats, and weight loss. He has low-grade fever and difficulty walking due to leg weakness. MRI shows T11-12 vertebral destruction with anterior soft tissue collection."

EXCEPTIONAL ANSWER
**Opening Statement:** "This presentation is highly suspicious for spinal tuberculosis (Pott's disease) given the insidious onset, constitutional symptoms, country of origin, and MRI findings of vertebral destruction with paravertebral abscess." **Assessment:** 1. **Clinical examination:** - Full neurological assessment (likely incomplete paraplegia) - Document motor level and power - Cold abscess in groin/flank? - Signs of other TB (lymph nodes, lungs) 2. **Investigations:** - Basic bloods: FBC, ESR, CRP, LFTs, renal function - Mantoux test/IGRA - HIV serology - Chest X-ray (pulmonary TB) - Sputum AFB if productive cough - CT chest for pulmonary involvement 3. **Imaging review:** - MRI whole spine (skip lesions in 10-15%) - Assess epidural extension - Document number of levels involved - CT for bone detail **Management:** **1. Medical Treatment (Primary):** - Start ATT: HRZE for 2 months, then HR for 4-10 months - Baseline LFTs before starting - Consider bed rest and bracing initially **2. Surgical Considerations:** - Indications in this case: moderate neurological deficit, abscess - If neurology stable/improving on ATT: continue medical - If progressive despite 2-4 weeks ATT: consider surgery **3. Surgery if indicated:** - Anterior debridement and fusion, or - Posterior instrumentation with anterior debridement **4. Monitoring:** - Weekly neurological exams initially - Monthly LFTs - ESR trending - Repeat MRI at 3-6 months
KEY POINTS TO SCORE
Recognize clinical triad: pain, constitutional symptoms, neurology
MRI whole spine to detect skip lesions
Medical treatment first in most cases
Know surgical indications precisely
Monitor for treatment response and complications
COMMON TRAPS
✗Rushing to surgery before adequate medical trial
✗Not imaging whole spine (missing skip lesions)
✗Forgetting HIV testing in TB presentation
✗Not monitoring for hepatotoxicity on ATT
LIKELY FOLLOW-UPS
"When would you consider surgery urgent?"
"How do you differentiate from pyogenic spondylitis?"
"What duration of ATT would you recommend?"
"How would MDR-TB change your management?"
VIVA SCENARIOStandard

Spinal TB vs Pyogenic Infection

EXAMINER

"A 50-year-old man presents with back pain and low-grade fever. MRI shows L3-4 vertebral body involvement with disc changes and paravertebral collection. Both TB and pyogenic infection are being considered."

EXCEPTIONAL ANSWER
**Opening Statement:** "Differentiating TB from pyogenic spondylitis is crucial as management differs significantly. I would use clinical, laboratory, imaging, and if needed, tissue features to distinguish between them." **Clinical Differentiation:** | Feature | Tuberculosis | Pyogenic | |---------|--------------|----------| | Onset | Insidious (weeks-months) | Acute (days-weeks) | | Fever | Low-grade, intermittent | High, spiking | | Local signs | Minimal (cold) | Marked inflammation | | History | Endemic exposure, past TB | Recent infection source | **Laboratory:** - Pyogenic: Elevated WCC, high CRP - TB: Normal WCC, elevated ESR (often very high) - Blood cultures: Often positive in pyogenic - IGRA/Mantoux: Positive in TB **Imaging Differentiation:** | MRI Feature | Tuberculosis | Pyogenic | |-------------|--------------|----------| | Disc involvement | Late, may be spared | Early, destroyed | | Vertebral levels | Often multi-level, skip | Usually contiguous | | Abscess wall | Thin, smooth | Thick, irregular | | Posterior elements | Spared early | Often involved | | Calcification | Pathognomonic | Absent | | Subligamentous spread | Common (under ALL) | Less common | **Tissue Diagnosis:** - CT-guided biopsy if uncertain - Histology: Caseating granulomas (TB) vs acute inflammation (pyogenic) - AFB stain and culture - GeneXpert PCR for TB - Bacterial culture **Clinical Pearl:** "In this case with insidious presentation and low-grade fever, I would favour TB. However, the disc involvement pattern on MRI will be key. If disc is relatively preserved with subligamentous spread, TB is more likely. If disc is destroyed early with thick-walled abscess, pyogenic is more likely."
KEY POINTS TO SCORE
Clinical tempo: insidious (TB) vs acute (pyogenic)
Disc preservation in early TB, destruction in pyogenic
Abscess wall: thin/smooth (TB) vs thick/irregular (pyogenic)
Skip lesions and subligamentous spread favour TB
Tissue diagnosis if uncertain
COMMON TRAPS
✗Assuming all spinal infections are the same
✗Not getting tissue diagnosis when uncertain
✗Missing skip lesions (not imaging whole spine)
✗Forgetting that late TB can destroy disc too
LIKELY FOLLOW-UPS
"What if cultures are negative?"
"How does HIV affect the presentation?"
"Can you treat empirically for TB?"
"What if the patient fails to respond to treatment?"
VIVA SCENARIOChallenging

Pott's Paraplegia Management

EXAMINER

"A 28-year-old woman presents with complete paraplegia of 2 weeks duration. MRI shows T7-8 vertebral destruction with large epidural collection causing severe cord compression. She has confirmed pulmonary TB on sputum."

EXCEPTIONAL ANSWER
**Opening Statement:** "This is Pott's paraplegia - complete paraplegia secondary to spinal tuberculosis with cord compression from epidural abscess/granulation tissue. Given the complete deficit, I would consider urgent surgical decompression combined with antitubercular therapy." **Immediate Assessment:** 1. **Neurological documentation:** - ASIA Impairment Scale (likely A or B) - Exact sensory level - Any sacral sparing? (prognostic) - Bladder/bowel function 2. **Medical stabilization:** - DVT prophylaxis - Bladder care (catheter) - Skin pressure care - Nutrition assessment **Management Decision:** **For Complete Paraplegia (2 weeks duration):** - Prognosis for recovery guarded (20-30%) - Urgent surgical decompression still indicated - Combined with ATT - Earlier intervention = better chance **Surgical Plan:** - Approach: Posterior with costotransversectomy or anterior thoracotomy - Goals: Decompression, debridement, stabilization - Instrumentation: Pedicle screws, anterior strut graft - Tissue for histology/culture **Medical Treatment:** - Start ATT immediately (don't wait for surgery) - HRZE intensive phase - Continue through surgical period **Postoperative:** - ICU monitoring initially - Continue ATT for 9-12 months (complex case) - Rehabilitation program - Spinal cord injury management **Prognosis Discussion:** "With complete paraplegia of 2 weeks, recovery prospects are limited. However, decompression may convert complete to incomplete deficit, improving long-term function. Even without motor recovery, surgery stabilizes spine and prevents further deformity." **Why Surgery:** 1. Complete paralysis with documented compression 2. Large epidural collection 3. Potential to convert complete to incomplete 4. Prevent kyphosis progression 5. Tissue diagnosis confirmation
KEY POINTS TO SCORE
Complete paraplegia with compression = surgical indication
Prognosis correlates with duration and completeness
Surgery + ATT (don't delay ATT for surgery)
Goals: decompression, stabilization, tissue diagnosis
Rehabilitation and SCI management essential
COMMON TRAPS
✗Delaying ATT until after surgery
✗Expecting full recovery with complete long-duration deficit
✗Forgetting spinal cord injury management principles
✗Not counseling about realistic prognosis
LIKELY FOLLOW-UPS
"Would you manage incomplete paraplegia differently?"
"What approach would you use for this level?"
"How long would you continue ATT?"
"What factors predict neurological recovery?"

MCQ Practice Points

Most Common Location

Q: What is the most common location for spinal tuberculosis?

A: The thoracolumbar junction (T10-L2) is the most common site for spinal TB. The thoracic spine is involved in approximately 50% of cases, lumbar in 35%, and cervical in 15%. The paradiscal region is the most common pattern of involvement.

Disc Preservation

Q: Which feature distinguishes spinal TB from pyogenic spondylitis?

A: Early disc preservation distinguishes TB from pyogenic infection. In pyogenic spondylitis, the disc is destroyed early as bacteria can survive in disc tissue. In TB, the avascular disc is relatively resistant to mycobacterial infection, though late TB can involve the disc.

Imaging Sensitivity

Q: What is the sensitivity of MRI for detecting spinal tuberculosis?

A: MRI has 96% sensitivity and 93% specificity for spinal TB. Changes are visible within 3-5 days of infection onset. Plain radiographs only become positive when 50% of trabecular bone is destroyed, which may take 4-6 months.

Skip Lesions

Q: What percentage of spinal TB patients have skip lesions?

A: 10-15% of patients have skip lesions (non-contiguous vertebral involvement). This is why whole spine imaging with MRI is recommended in all suspected cases of spinal TB to detect all levels of involvement.

Treatment Response

Q: What percentage of patients with uncomplicated spinal TB respond to medical treatment alone?

A: 85-90% of patients with uncomplicated spinal TB respond to antitubercular therapy alone without surgery. Surgery is reserved for specific indications including progressive neurology, instability, and failure of medical treatment.

Australian Context

Epidemiology in Australia

Australia has low overall TB incidence (approximately 5.5 per 100,000 population), but overseas-born individuals account for more than 85% of TB cases. Countries of origin with high TB burden include India, Philippines, Vietnam, China, and Sub-Saharan African nations.

Spinal TB typically presents as reactivation of latent infection, sometimes decades after initial exposure. Clinicians should maintain high suspicion in patients from endemic regions presenting with chronic back pain and constitutional symptoms.

Diagnostic Approach

Australian guidelines recommend tissue diagnosis when possible, particularly given the low prevalence and need to confirm diagnosis before prolonged treatment. GeneXpert PCR is widely available and provides rapid results with drug susceptibility information.

Treatment Considerations

ATT in Australia follows WHO guidelines with modifications for local resistance patterns. Standard regimens of 6-9 months are typically prescribed, with extension to 12 months for complex cases. Rifampicin interactions with other medications require careful management.

Multidisciplinary Care

Management of spinal TB in Australia typically involves infectious disease physicians, orthopaedic or neurosurgeons with spinal expertise, radiologists, and public health teams. Notification to public health authorities is mandatory for all TB cases, and contact tracing is essential.

Follow-up and Monitoring

Patients require long-term follow-up to ensure treatment completion, monitor for complications, and detect relapse. DOT (Directly Observed Therapy) programs are available for patients at risk of non-compliance. Rehabilitation services assist with functional recovery following neurological involvement.

SPINAL TUBERCULOSIS (POTT'S DISEASE)

High-Yield Exam Summary

Key Facts

  • •50% of skeletal TB is spinal
  • •T10-L2 most common location
  • •Paradiscal type most common (50-75%)
  • •Skip lesions in 10-15% - image whole spine

TB vs Pyogenic

  • •TB: Insidious onset, low-grade fever, disc spared early
  • •Pyogenic: Acute onset, high fever, early disc destruction
  • •TB: Thin smooth abscess wall, calcification
  • •Pyogenic: Thick irregular wall, no calcification

Imaging

  • •MRI gold standard: 96% sensitivity, 93% specificity
  • •Changes visible on MRI in 3-5 days
  • •X-ray: positive only when 50% bone destroyed (4-6 months)
  • •Always image whole spine for skip lesions

Management

  • •Medical first: 85-90% respond to ATT alone
  • •ATT: HRZE 2 months, then HR 4-10 months
  • •Surgery: progressive neurology, instability, large abscess
  • •Combined approach for complex cases

Surgical Indications (SURGERY)

  • •Severe kyphosis (more than 40-50 degrees)
  • •Unstable spine
  • •Resistant (MDR) TB
  • •Granulation tissue compressing cord
  • •Extensive abscess
  • •Regressing neurology despite ATT
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FRACS Guidelines

Australia & New Zealand
  • NHMRC Guidelines
  • MBS Spine Items
Related Topics

ACDF - Anterior Cervical Discectomy and Fusion

Adjacent Segment Disease

Adult Spinal Deformity

Ankylosing Spondylitis