Treatment of spinal tuberculosis - presented at the Postgraduate teaching course held at KEM Hospital, Mumbai in March 2016.
The talk highlights steps in diagnostic workup and treatment algorithm for management of spinal tuberculosis.
Please see notes attached to clinical slides. They contain details about clinical presentation and treatment approach chosen for the case presented
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Consultant Spine Surgeon Discusses Treatment of Spinal Tuberculosis
1. Dr. Kshitij Chaudhary, MS, DNB
Consultant Spine Surgeon
Sir HN Reliance Foundation Hospital
Mumbai
T R E A T M E N T O F S P I N A L
T U B E R C U L O S I S
6. • Thoracic and Lumbar TB (MILD DISEASE)
• Excluded
• Severe deficit, “could not walk across the room”
• Significant extra-spinal infection
• > 3 levels VB destruction
• Antibiotics for >1year
• Random Allocation
• Chemotherapy alone
• Debridement + No fusion
• Radical Surgery + Reconstruction (Hong Kong Op)
• FU 15 years
• Similar outcome - 87% favorable outcome
MRC trials
Favorable outcome
no evidence of CNS involvement,
No sinus
No clinically evident abscess
no radiological evidence (Xrays) of disease activity
no restriction of normal physical activity
SPINAL DEFORMITY NOT INCLUDED
7. Fusion @ 15y
5% of Chemotherapy alone had alarming ↑ in kyphosis 51 to 70 deg
No late onset myelopathy
Kyphosis @ 15y
8. Is 15y-follow-up enough?
Review of 60 patients conservatively Rx
25 patients - late onset paraplegia
65% - presenting more than 20 years later
9. Conservative Regime
Bed Rest for 6-9 months, (prolonged hospitalization if unable to
walk)
Antibiotics: SM, PAS, INH for 24 months
Supervision: 3-6mo X-rays (kyphosis), ESR
Resumption of activity: with brace
JBJS Br 1975
10. Surgery
Advanced neurological deficit with sphincter involvement
Flexor spasms
Do not show progressive neurological improvement in 3-4 weeks
Worsening of neurological deficit
JBJS Br 1975
11. 200 cases with neurological deficit
76 (38%) improved with antibiotics and bed rest (baseline
deficits??)
6 died
118 surgery
14 (12%) died → meningitis, urinary infections, renal failure, bedsores
81 (69%) recovered fully
13 (11%) walking with support
10 (8%) no improvement
JBJS Br 1975
12. 104 lesions (conservatively treated)
Follow up of at least 1 year
NOT ENOUGH Follow up
No real conclusions can be drawn
JBJS Br 1975
13. Middle Path regime
Rationale
Endemic countries / resource poor
Morbidity of surgery
Limited expertise available for surgery
Does not apply to
Severe deficits
Severe column destruction (anticipation of severe deformity)
15. Investigations
Take time to see the X-rays,
count levels, think
Describe the pathology first
A - Alignment (kyphosis, translation,
dislocations)
B - Bone destruction
C - Cartilage (Disc)
D - Density (osteopenia)
E - Environment (paraspinal abscess)
Radiographs
18. Other investigations
CBC
ESR, CRP
LFT and Renal function
± Total protein, albumin
± HIV
Xray Chest (15% Pulm TB)
Mantoux
Serological test (IgG, IgM)
TB gold
19. Core Biopsy
High risk for drug resistance
Previous ATT
Noncompliance / incorrect ATT
Atypical presentation
Multifocal disease
Children
Immunocompromised
Endemic City (Mumbai)
Image guided
39. Indications for Surgery
Severe neurological deficit
Neurological worsening on treatment
Mild deficit but not responding to antibiotics
Neurological deficits due to “hard” lesions
Spinal tumor syndrome
NEUROLOGICAL DEFICIT
42. Indications for Surgery
Extensive destruction of column
Progressive / severe kyphosis
Circumferential destruction (dislocation, translation)
Childhood tuberculosis (spine-at-risk signs)
DEFORMITY
43. Extensive destruction of column
Reserved for Complications
Severe destruction - Anticipation of significant deformity/instability
25y ♀ Normal Neurology, Back pain 12 mo
3y PO3y PO
>1 Thoracic or >1.5 Lumbar VB destroyed
44. SW 15y ♂
18o D9
56o
+4 mo +4 mo +4 mo
+4 mo
↑ Deformity
Normal Neurology
Progressive severe kyphosis
63. Questions?
What is the goal of treatment?
Site / Direction of Compression?
Number of levels?
Posterior column integrity?
Alignment? Deformity?
Osteoporosis?
Medical Co-morbidities? Pulmonary?
SURGICAL EXPERTISE / COMFORT?
Facilities / Infrastructure?
70. Surgery
Avoid a half-hearted attempt
Best possible decompression.
Best possible reconstruction.
Cage / Graft from good bone to good bone
± Instrumentation → early mobilization
Keep Safety of patient in mind.
71. T H A N K Y O U
Sir HN Reliance Foundation Hospital
Mumbai
Editor's Notes
These statements are almost clichéd, but nevertheless true.
It worthwhile emphasizing that Spinal TB is a medical disease
And surgery is reserved for complications
But Chemotherapy alone group had significantly higher kyphosis and non union.
5% had alarming increase in kyphosis to 70 deg
However, no case of late onset myelopathy due to deformity was reported in the MRC trials
The Hong Kong group however has suggested that the 15 year FU of MRC trails if probably insufficient as they are now seeing many patients who were conservatively treated during the study period, now presenting with late onset myelopathy. 65% of these patients have presented >20 years after antibiotic treatment
This is another Classic paper that everyone should read.
What was the conservative regimen applied in this study?
Bed rest 6-9 months (hospitalised if unable to walk)
Antibiotics for 2 years (no rifampicin at that time)
Indications for surgery from neurological point of view were:
Advanced neurological deficit with sphincter involvement
Flexor spams
Those that do not show progressive neurological improvement in 3-4 weeks of AKT.
Recurrence of neurological deficit.
of the 200 patients in this series with neurological deficit.
76(38%) improved with antibiotics.
However, the paper is not clear on how many of these patients had severe deficits (e.g. Non ambulators). I suspect many of those recovered had milder deficits to begin with.
6 died
Remaining 118 had surgery
Not very good outcomes by today’s standards
12% mortality (surgical and anesthesia has advanced quite a bit since then).
What is interesting is that only 69% with surgery fully recovered neurology. Was this because neurological decompression was delayed in may patient’s with the hope that antibiotics would work. We don’t know.
Not much can be concluded from this study about the eventual deformity in conservatively treated patients.
MRI spine in all patients.
Screen entire spine (incidence of non contiguous lesions is 16-71%
CT scan - Not as a routine.
For surgical planning.
Mantoux, serological test and TB gold test have no value and should not be done
Ask for CT guided core biopsy before starting ATT in all patients.
The incidence of MDR TB is increasing and it is important to know antibiotic sensitivity.
some patient groups are at a high risk for MDR and it is absolutely must to attempt a biopsy before starting AKT.
5 things you will ask for in a biopsy
PCR based test.
Greater sensitivity
Faster turnaround time (48hrs)
Detection of resistance (Rif) - aide in starting MDR treatment early
Can detect MTB in smear negative samples
But in spinal TB, if Gene Xpert is negative - does not rule out tuberculosis
Smear negative sensitivity is low 47%
Smear positive sensitivity is high 100%
Specificity is obviously is 100% (DNA PCR test)
Culture are must for drug sensitivity testing.
MGIT results available in few weeks.
Sensitivity is ~50 to 60% (spinal TB is paucibacillary)
Not routine.
Only if smear positive
No recommended as a routine test for extrapulmonary TB which tends to be paucibacillary.
For drug resistance testing (PCR based0
We always involve a infection disease specialist.
Duration is controversial.
We typically dive 9-12 months depending on clinical and radiological response
And surgery is reserved for complications
First complication is neurological deficit
What is internal gibbus? Angulation of disease spine - formation of a bony ridge on the anterior wall of the spinal canal
Extensive destruction of column and you anticipate a severe deformity
Circumferential distraction with dislocation/translation
Progressive kyphosis on serial imaging
Childhood tuberculosis with spine at risk signs
Surgery is indicated where there is anticipation that the destruction is severe enough to cause severe deformity or instability, potentially threatening the spinal cord.
This is a 25 y old lady with severe vertebral body destruction, 5 VB are destroyed, with normal neurology. Surprisingly this patient was also ambulatory.
15 year old boy. D9 tuberculosis. Not much deformity. Treated with antibiotics.
Progressive collapse over 4 months to 56 deg, complete collapse of D9 VB. Toppling sign.
Causes of worsening of destruction despite antibiotics and bracing.
Patient was compliant with antibiotics.
Drug resistance?
Paradoxical reaction?
PVCR one VB.
Correction from 56 deg to 14 deg
Another patient who presented with both significant neurological deficit and severe column destruction.
was operated with a P+A surgery. First...posterior...second.. High thoracotomy approach third rib bed.
Avoid early MRI scans (3-4 months)
May show radiological worsening. Paradoxical reactions. Immune reaction to dying bacilli.
Go by clinical response.
There is a nonunion with opening of the pseudo on extension film
Fusion and column reconstruction performed
This is a 58 yr old lady who was diagnosed with T11 tuberculosis on HPE, cultures were negative. The initial VB height loss was minimal. 6 mo later, she develop 2 VB loss, progressive kyphosis and became non ambulatory and was treated with surgery. Such progressive destruction could be because of drug resistance (which was almost non existent during the MRC trials, non compliance with antibiotics as these have to be taken for over 6 to 9 months, and a paradoxical reaction, which is typically seen in the first 3 months in 15% cases. It is also called the immune restoration syndrome which is due to exuberant inflammatory response against dying bacilli. (Especially seen in HIV patients who are on HAART and pregnancy).
This patient had multi-drug resistant tuberculosis strain.
Treated as tuberculosis, initially, worsened on treatment, neurology deteriorated. Therefore surgery was performed
Turned out to be Non Hodgkin’s lymphoma.
You may ask what is the ideal surgical approach?
The key or the mantra is to INDIVIDUALIZE.
Tuberculosis preferentially damages the anterior column and usually the spinal cord compression is from the ventral aspect of the spinal cord.
Several advantages
Ideal exposure.
Direct decompression of the spinal cord.
Least handling of the spinal cord.
Very good reconstruction of the column is possible
Avoids damaging posterior elements (which are usually intact in TB spondylodiscitis)
Disadvantages
Technical (requires experience with anterior approaches)
Patient selection is important as all patients may not tolerate thoraotomy.
Cervicothoracic region - anterior approach may be difficult (depend on location of the manubrium)
In addition, this patient has posterior column destruction.
Therefore, this was treated with a posterior approach.
Posterior element tuberculosis.
Direction of spinal cord compression was dorsal and hence posterior approach was chosen.
Large defect may not be amenable to reconstruction via the posterior approach alone, especially in the lumbar spine where the defects are large and the lumbar roots cannot be sacrificed.
Hence here A+P approach is chosen.