Potts spine management part 2 ATT ALD

1. Potts spine management
continues
Dr Arjun kouloth
ORTHO RESIDENT
LHMC NEW DELHI

4. • Compression starts anterior to the spinal cord
over the anterior column, its earliest manifestation
as gradual increase in the spasticity ( exagerated
deep tendon reflexes and plantar rextensor)
• As compression increases over the anterior column
of cord , the patient starts losing motor power
gradually from partial motor weakness to complete
motor loss with signs of UMN lesion
• deficit increases sequentially as cord compression
increases

5. • lateral column is also affected partially, thus
producing some reduction of sensation (pain,
temperature and crude touch)
• even posterior column is also affected leading to
complete loss of sensation and disturbances of
sphincters.
• In long standing compression, the spasticity is
replaced by flaccidity and flexor spasm

6. CURRENT CONCEPT
• Uncomplicated spinal TB is predominantly a
medical disease
• Treat with ATT with for appropriate duration and
at adequate dosage
• Surgery is limited to prevent and treat
complications & has specific indications

7. Middle path regime
• Rest in hard bed
• Chemotherapy
ATT (18 MONTHS (18- 24 MONTHS)
• X-ray & ESR once in 6 Weeks
• MRI/ CT at 6 months interval .
• Gradual mobilization
3-9 weeks- back extention exercise 5-10 min 3-4 times
• Spinal brace--- 18 months-2 years

8. Role of rest, bracing, and ambulation in
the proven patients?
• In patient who were ambulatory at the time of
diagnosis are kept ambulatory.
• In patients with severe pain, short period of rest
may be useful.
• While patient not ambulatory at the time of
diagnosis, are provided with 3-4 weeks rest and
made ambulatory when clinically stable.
• Bracing is controversial: in cases to relieve pain and
to prevent progression of deformity.

9. Investigations to be sent
• Microscopy and culture for AFB
• Histopathological examination
• PCR based tests – Gene Xpert/ CBNAAT
• LPA
Culture media used
• MGIT- Mycobacterium Growth Indicator Tube
Liquid based, takes 10 to 14 days
• LJ- Lowenstein Jensen
Solid egg based, takes 6 weeks
• Stains used – Z N staining,Fluorochrome staining

11. CBNAAT
• The Xpert (GeneXpert) MTB/RIF test for TB
by detecting the presence of TB
bacteria(DNA),
• as well as testing for resistance to the drug
Rifampicin
• qualitative, nested real-time polymerase
chain reaction (PCR) in vitro diagnostic test.
• (95% sensitivity and 93% accuracy)

12. Limitations
• Assay is not indicated for
– Patients being treated with ATT/Monitor
bacteriologic cure /monitor response to therapy
• Negative test does not exclude the
possibility of isolating MTB-complex from
the pus sample
• Positive test does not necessarily
indicate -viable organisms
• does not differentiate b/w the species
of the MTB-complex

14. MORPHOLOGY OF MYCOBACTERIUM
TUBERCULOSIS
•Straight or slightly curved rod
•Occurring slightly in pairs or small clumps
•Are ‘ACID – FAST’ & ‘ALCOHOL FAST’ +
•Resist decolourization by 20% sulphuric acid &
absolute alcohol for 10 minutes

15. Why combination of ATT
• Cell wall lipids and peptidoglycans have very low
permeability to usual Abx.
• 10- 20 hrs for replication.
• Each colony, there is different types of bacilli with
diff growth kinetics and metabolic charecterstics.

16. ATT
Daily regimen(18-24 MONTHS)
HRZE 2 MONTHS
HRE 9- 18 MONTHS
• Frequency of Dosage: DAILY (7 day/week)
• Single daily dosage

18. First Line:
High efficacy – low toxicity – routinely used
• Streptomycin (S) 1947
• Isoniazid (H)1952
• Ethambutol (E) 1961
• Rifampicin (R) 1962
• Pyrazinamide (Z) 1970

19. Second Line:
Low antiTB efficacy and/or higher toxicity – reserve
drugs
Ethionamide (Eto), Prothionamide (Pto),
Cycloserine (Cs), Terizidone (Trd), Para-
aminosalicylic acid (PAS), Rifabutin, Rifapentine
• Fluoroquinolones: Ofloxacin (Ofx), Levofloxacin
(Lvx/Lfx), Moxifloxacin Mfx), ciprofloxacin (fx)
• Injectables: Kanamycin (Km), Amikacin (Am),
Capreomycin (Cm)

21. WEIGHT BAND

22. PAEDIATRIC WEIGHT BAND

23. MONITORING THE TREATMENT
CLINICAL
• Regains weight and apetite by 6 weeks
• Spinal pain and muscle spasm reduces
HEMATOLOGICAL
• ESR Shows a demostrable change after 1 onth of att
and normalises by end of 3 months
RADIOGRAPHS
• Abscess shadow decreases and sclerosis of bone
begins by 2-4 months
• Complete bonty fusion occurs by 9 months
MRI signs of healing
• Resolution of marrow edema/ replacement of marrow
fat
• Complete resoluton of para vertibral abscess

25. INH (H)
• Tuberculocidal
• fast multiplying organisms
• Extracellular as well as intracellular – also acidic
and alkaline medium
• MOA: Inhibition of synthesis of mycolic acid
• Genes “InhA” and “KasA” are targetted.
• ADRs:
Peripheral neuropathy – numbness, parasthesia,
mental disturbance & convulsion
• Prophylactic pyridoxine (10 mg/day) –
• Hepatitis – elderly and alcoholics

26. RIFAMPICIN
• Bactericidal to M. TB and many other gm+ve and –ve
bacteria – Staph. aureus, E. coli, M. Leprae,
Pseudomonas, Proteus etc
• Efficacy same as INH – Better than all anti-TB drugs
• Acts on all subpopulation – mainly slowly and
intermittently dividing
• Both extra and intracellular organisms
• Sterilizing and resistance preventing

27. • MOA: Interrupts RNA synthesis
• Resistance: Primary resistance 1 in 10 7
• Developes rapidly and due to mutation of rboB
gene
• Well distributed – penetrates intracellularly,
cavities, caseous masees and placenta
ADR
• HEPATOTOXICITY
• FLUE LIKE SYMPTOMS

28. PYRAZINAMIDE
• Similar to INH – developed parallelly
• Weak bactericidal – more active in acidic medium
– intracellular and inflammatory areas
• Highly active in first 2 months – kills residual
intracellular bacilli – sterilizing
• Advantage: Shortening of duration of treatment
and reduces risk of relapse.
• Resistance: when used alone – mutation of pncA
gene

29. • Kinetics: well absorbed orally, wide distribution,
good CNS penetration (meningeal TB)
ADRs:
Dose related hepatotoxicity – less among Indians
(>30 mg/kg )
• Contraindicated in liver diseases
Hyperuricaemia – gout
• Abdominal distress, athralgia, flushing,rashes,
fever, loss of diabetes control

30. ETHAMBUTOL
• Tubererculostatic : effective against MAC fast
multiplying bacilli With HRZ regimen – sputum
conversion hastens and prevents resistance
MOA : inhibits arabinosyl transferase – mycolic acid
incorporation to cell wall prevented
• Resistance: slowly – mutation of embAB – no cross
resistance to other drugs
• Kinetics:low CNS penetration,
ADR: COLOR BLINDNESS, RETROBULBAR NEURITIS
HYPERURECEMIA

31. STREPTOMYCIN
• First clinically useful anti-TB drug - aminoglycoside
Tuberculocidal – less effective than INH or Rifampicin
• Only on extracellular bacilli – poor penetration
• MOA: Inhibition of protein synthesis
• Resistance: rapidly and relapse – stop in resistance
Ototoxicity: Most common – vestibular and cochlear
damage
Cochlear damage – base to apex and high to low
frequency sounds (permanent deafness)
Nephrotoxicity: Tubular damage

32. • 15 mg/kg (12–18 mg/kg) daily
• Maximum daily dose 1000 mg
• Patients aged over 50 years may not tolerate
the daily dose of Streptomycin more than 750
mg
• Similarly, patients weighing less than 50 kg
may not tolerate doses above 500-750 mg
daily

33. • H and R are most potent bactericidal against all
population
• Z best on intracellular bacilli and those in inflamed
sites and sterilizing activity
• S is active against rapidly multiplying extracellular
• E is bacteriostatic – prevent resistance and hasten
sputum conversion

35. Second line drugs:
Injectable AMINOGLYCOSIDES
• Kanamycin Km), amikacin (Am), capreomycin (Cm)
• Ethionamide (Eto)
• prothionamide (Pto)
• cycloserine (Cs)
• terizidone (Trd)
• PAS
• rifabutin, rifapentine
• bedaquilline

36. fluroquinolones
• Ofx, Lfx, Mfx – bactericidal
• Active against – MAC, M fortuitum and other
atypical ones
• Mfx > Lfx > Ofx
• Penetrates cell and kill mycobacteria in
macrophages
• Uses : Drug resistant TB (Lfx is standard in MDR TB)

37. When to suspect for drug resistance?
Suspicion for resistance
• Lack of clinical or radiological improvement
• Appearance of new lesion
• Dehiscence of previous scar
• Increase in bone destruction after 3-5 months.
Predisposition for drug resistance:
• Contact with known MDR-TB.
• Previous treatment for TB.
• Poor adherence or premature stopping of
treatment in the past.

38. How to confirm for first line drug resistance?
Gene Xpert
fully automated molecular assay - real time PCR.
• Detects MTB and resistance to Rifampicin.
• < 2 hours.
• Since TB is paucibacillary disease it may not be able
to detect MDR in many cases.
LPA- line probe assay
• can detect MTB and resistance towards Rifampicin
and Isoniazid within 2-3 days

39. DST- Drug Sensitivity Test
• culture based method
• Growth of organism is inhibited in culture
containing various anti tubercular drugs.
Culture being a slow method, takes weeks or
months to get the results.

40. Multi Drug Resistant Tuberculosis
Mycobacterium are resistant to both
>Isoniazid
>Rifampicin
It was found that only 3 % of all New Tuberculosis
cases that arise world wide every year are
estimated to be MDR

41. Epidemiology of MDR
• 43% of global MDR TB cases had previous
treatment
• 15% of previously treated patients have MDR
which is five times higher than the global
average of 3% in new patients
• when a first course of treatment containing 6
months of rifampicin fails, 50–94% of
patients have MDR-TB

42. SITES OF MDR
• Predominantly Lung substantial reports reveal
occurrence at extra pulmonary sites viz bones
skin and soft tissue ,lymph nodes,CNS ETC
• Extra-pulmonary MDR TB more in HIV + PTS.

43. Clinical factors promoting resistance
• Delayed diagnosis and isolation
• Inappropriate drug regimen
Inadequate initial therapy/course of
treatment
 Inappropriate treatment modifications
 Adding single drug to a failing regimen
 Inappropriate use of chemoprophylaxis
• Poor adherence and incomplete F/Up
• Failure to isolate MDR TB patients
• Over the counter anti TB drugs/Faked drugs

44. XDR TB
• MDR plus resistance to a
FQ and
one second line injectable drugs
(amikacin,capreomycin,kanamycin)

45. GENERAL GUIDELINES FOR MANAGEMENT OF MDR/XDR
• Treatment has to be individualised
• regimen -depending upon culture sensitivity tests.
• Intermittent therapy should not be used
• use of drugs to which there is demonstrated in vitro
resistance is not encouraged because there is little or no
efficacy of these drugs
• A good response does not justify continuation of an
inadequate regimen
• Resistance to RIF is associated in most cases with cross
resistance to rifabutin and in all cases to rifapentine

46. • Bactericidal drugs with proven efficacy should be
used
• Cultures should be done monthly
• Two years of total treatment after conversion of
cultures to negative is usually recommended
• Occasional patients with limited disease are cured
after 18 months

47. Treatment MDR
• PKCEEL X 6-9 MONTHS.
• CEEL X 12-18 MONTHS
Pyrazinamide
Kanamycin
cycloserine
Ethambutol
Ethionamide
Levofx

49. TDR TB
resistance to all available drugs.No treatment
options presently available

50. HIV:EFFECTS ON TB
• Atypical presentation
• Extra pulmonary : 4x
• Smear negative / Normal CXR 20%
• Increases risk of progression to AIDS or death
• significantly increased plasma HIV viremia
• Generalized immune activation due to TB :
increased CD4 : targets for HIV
• Increased expression of HIV coreceptors CCR5 &
CXCR4 in TB-HIV
• INH chemoprophylaxis is recommended for HIV+
with a positive tuberculin skin test

51. HIV:EFFECTS ON TB

52. • Increasing degrees of immunodeficiency,
extrapulmonary TB , with or without pulmonary
involvement, is more common, and found in the
majority of TB patients with CD4+ counts <200
cells/ µ L.
• TB can be a severe systemic disease with high
fevers, rapid progression, and sepsis syndrome.
• ATT same regimen as HIV-

53. TB- Immune Reconstitution Inflammatory Syndrome
Patient initially have improvement in symptoms
and/or radiological findings.
• But there occurs a paradoxical deterioration of the
same at the primary /new sites during or after TB
treatment
• absence of any other cause of this deterioration.
• MC presenting symptoms are recurrent fever,
enlarged lymph nodes,worsening dyspnea.
• Sites involved are lymph nodes and lungs
irrespective of the primary sites.
• resolve spontaneously .

54. • All HIV-TB coinfection cases to be initiated on
ATT ,Followed by ART irrespective of CD4
count.

55. Goals of surgical treatment
DECOMPRESSION
• Debridement and drainage of large abscesses
• Decompression of spinal cord and neural structures
(both bony and soft tissue compression)
DEFORMITY
• Kyphosis correction
STABILITY
• Reconstruction of the anterior column( weight
bearing)
• Stabilization of the spine with intrumentation

56. Absolute Indications of surgery
1. No progressive recovery after fair trial of
conservative treatment (4-6 weeks)
2. Neurological complications develops during
conservative treatment
3. Worsening of neurological deficit during t/t
4. Recurrence of neurological complications
5. Pressure effects (deglutition/respiration)
6. Advanced cases of neurological involvement
(Sphincter disturbances, flaccid paralysis or
severe flexor spasm)

57. APPROACH
Cervical spine –
• Anterior retropharyngeal (smith-Robinson’s)
•Anterior approach – Anterior/Medial border of
sternocleidomastoid.
Dorsal spine (D1 to L1) –
•Transthoracic transpleural
•Anterolateral decompression(D2 – L1)
Lumbar spine –
•Anterolateral(Lumbovertebrotomy)
•Extraperitoneal Ant. Approach

58. Tuli’s recommended approch
• Cervical spine –T1
Anterior approch
• Dorsal spine –DL junction
Antrolateral approch
• Lumbar spine &Lumboscral junction
Extraperitoneal Transverse Vertebrotomy

59. Griffith et al -- prone position
Tuli --- Right lateral position
Advantage:-
1. avoid venous congestion
2 . avoid excessive bleeding
3. permits free respiration
4. Lung & mediastinal contents fall anteriorly
Parts to remove :
• Posterior part of rib (~8cm from the TP)
• Transverse process (TP)
• Pedicle
• Part of the vertebral body
ANTEROLATERAL DECOMPRESSION

60. • The skin flap along with the deep fascia is elevated
and retracted medially up to the midline
• ribs articulating with the diseased vertebrae serve
as the guide to the placement of the incision
semicircular incision (convex
laterally)
from the midline about 6 cm proximal to
the center of the diseased area, it is
curved distally and laterally to a point
about 9 cm from the midline and
continues distally and medially to the
midline about 6 cm distal to the center).

61. • paraspinal muscles divided transversely from its
lateral border coming up to the bases of the TP of
the diseased vertebrae
• Medial parts of 2 to 4 ribs, which are articulating
with the diseased vertebrae, and their TP are
exposed subperiosteally.
• Subperiosteal exposure of ribs from medial to
lateral direction at the upper border of ribs, and
lateral to medial direction at the lower border of
ribs.
• transverse processes are resected from their base

62. • Two to 4 ribs, about 8 cm from the TPs are cut.
• If there is a paravertebral abscess--- liftes up the
periosteum and the ALL from the anterior and
lateral surfaces of vertebral bodies and discs.
• frank abscess (if present) would open out at this
stage and suction done
• liquid pus, semi-solid caseous material, small
sequestra and necrotic debris can be dislodged
with the finger and are removed by suction
• Excision of 3 to 4 ribs provides a good exposure in
severe kyphosis and crowding of rib

64. SPINAL BRACES
• Spinal braces are mostly used for ambulation of
cases of spinal tuberculosis
• Taylor brace may control a simple kyphotic
deformity but has little control on a scoliotic
deformity
• Milwaukee brace or a Jewett brace : tb lesions in
the dorsal spine throughout the growing age if the
number of vertebrae involved is more than 2, or
there is panvertebral disease, or radiologically
there is wedging

67. • Anterior spinal hyperextension (ASH) brace
has been found to be more acceptable by
young girl
• upper dorsal spine involving D1 to D3
vertebrae, there is no simple brace to control
the spine effectively.
• bracing is to extend the usual spinal brace
upwards with the attachment of cervical collar.
SOMI brace
• cervical spine from cervical first to cervical
seventh vertebrae

69. lower lumbar (third lumbar and below)
and lumbosacral region a Goldthwaite
brace or a lumbar corset