CARIES SPINE AND
SPINAL STENOSIS
DR. NADIR MEHMOOD
ASSOCIATE PROFESSOR SURGERY
IIMC-T, RLY HOSP
CLINICAL ASPECTS OF TUBERCULOSIS
• Pathogenesis of
tuberculosis
–Infection versus disease
•Host factors
•Pathogen factors
PATHOGENESIS
• Host factors include
– Social e.g.
• Poverty
• alcoholism
– Age e.g.
• Newborn
• Teenage girl
• Old age
– Immunity e.g.
• HIV
• Gamma interferon
PATHOGENESIS
• Organism factors e.g.
–Virulence factors
–[Drug resistance]
PATHOGENESIS
• Tuberculous disease is a consequence
of:
– Primary infection e.g. In a baby
– Reactivation
• ‘natural’
• Associated with immunosupression
– Re infection
PULMONARY TB TYPICALLY AFFECTS
THE UPPER ZONES OF THE LUNG
CLINICAL FEATURES
• Clinical illness
–Pulmonary
–Extrapulmonary
CLINICAL ILLNESS
TB may affect any tissue of the body
including:
– Skin and soft tissue
– Lymph nodes
– Bones and joints
– Intra abdominal structures including
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peritoneum
Kidneys
Adrenal glands
Lymph nodes
– Central nervous system
• Tuberculoma
• meningitis
Clinical clues for TB
• Clinical symptoms – usually ‘chronic’ rather than
acute
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Fever
Sweats
Weight loss
Focal symptoms
• Epidemiology
– History of TB, HIV
– Country of origin, recent travel/work
– Contact with TB
• Investigations- CP ESR,URINE R/E, CXR, X-RAYS,
C/S, SKIN TESTS,ELISA, CRP, PCR, CT, MRI
TB – guidelines for the clinician
• Great mimicker
• Low index of suspicion
• Pulmonary TB usually easy to
consider
• Non pulmonary often requires
‘lateral thinking’
What will happen if diagnosis or
treatment for TB spinal osteomyelitis
is delayed?
MENINGES OF THE SPINAL CORD
What will happen if treatment delayed? – gibbus formation
(acute angulation of spine with or without neurological
damage)
The physical appearance – Potts disease
of spine - gibbus
• Progress
– Increasing back pain and neurological
symptoms – mild leg weakness
• Treatment
– Continue therapy
– consider surgical decompression
• Further progress
• Weakness of legs
• Neurosurgery and internal splinting
• Other considerations - clinical
• Has the patient got HIV?
• Is vitamin D level normal?
• Other considerations epidemiological
• From where has the pt got infection?
• To whom might the pt have given it?
TREATMENT OF TB
• BTS guidelines – 1999
Thorax 2000: 55; 210-218
• NICE guidelines – 2006
– Sensitive TB – 4 drugs for 2 months
2 drugs for 4 months
– Resistant TB - 6 drugs for 24 months (second
line drugs are not so effective)
[Eng, Wales & NI 2004, 6.8% Isoniazid resistant, 1%
MDR TB (R to Isoniazid and rifampicin)]
Problems of TB therapy
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Toxicity e.g. liver
Multiple therapy
Prolonged treatment
Drug interactions
Compliance
– Treatment will not work if not taken
– DOTS (Directly Observed Therapy) if:
• Likely poor compliance
• MDRTB
Public health - avoiding transmission
• TB is statutorily notifiable disease
• Multidisciplinary approach – medical, TB
nurses, CCDC etc.
• Identify and manage possible sources of infection and
contacts
• Considerations
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treat as OP where possible
multi occupancy housing, social deprivation
negative pressure rooms in hospitals (limited facility)
beware transmission in OP setting e.g. waiting area
WHY FAILURE?
• Patient non compliance
–Deliberate
–Failure to understand e.g. language,
culture
–Social e.g. alcohol
• Patient movement e.g. ‘lost to
follow up’
• Lack of medical/nursing support
• others
Summary
• TB is a challenging disease for the
clinician
• Must have microbiology before starting
treatment – more rapid lab tests?
• Need to encourage compliance
• Need for multidisciplinary approach to
diagnosis and management and control
• Need shorter, better, cheap anti TB
regimes
SAMPLE MSQs
• The starting pathogenesis in TB is;
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Secondary TB
Miliary TB
Ghon focus
CNS involvment
GIT involvment
• The advanced stage in Potts disease is
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Paresis
Lost urinary control
Gibbus formation
Paraplegia
Death
• Poor compliance to treatment, TB of any site becomes
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Resistant to treat
MDRTB
XDRTB
MILIARY TB
TB ABSCESS