POTT'S SPINE

1. DR HARDIK PAWAR
TUBERCULOSIS OF
SPINE
“Yakshma”

2.  common in INDIA
 1-3% -osseous involvement
 >50% affects spinal column
- commonest form of skeletal TB.
 Dorsal spine - most commonly involved
 Most Common – first 3 decades.

3.  TB :Oldest recognized disease of mankind.
 India –Rigveda and Atharvaveda (3500-1800 b.c.) -
“Yakshma”
 Greco-ROMAN – PHTHISIS / CONSUMPTION
 French phsician Laennae
 Pale-pathological evidence of TB of bones, joints
and spine in prehistoric humans.

4. Percival Pott
presented the classic
description of spinal
tuberculosis in 1779.

5. Robert Koch
discovered
Mycobacterium
tuberculosis in 1882.

6. Tuberculosis (TB) - leading cause of death
worldwide from a single infectious disease
agent.
The registered number of new cases of TB
worldwide roughly correlates with economic
conditions.

7. The highest incidences : Africa, Asia, and
Latin America

8. 8 million people get TB every year, of whom
95% live in developing countries.
 An estimated 2 million people having active
spinal tb in d world
TB is increasing Day by day and there are
strains emerging which are resistant to
antibiotics

9. INDIA
1/5th
of total world
population of TB patients.
6 million radiologically
proven cases.
1 to 3% of all involve
skeletal system.

10. Thoracic vertebrae-
12
2nd
to 8th
are typical
and the remaining 5
are atypical
Identified by
presence of costal
facets on the sides
of vertebral bodies.

11. BLOOD SUPPLY:
 1 anterior spinal artery
 2 posterior spinal arteries
 Radicular arteries reinforce
these.
 2 segmental arteries on
each side supply each
vertebra.
 Prevertebral venous plexus
( Brescet-Batson)
communicates freely with
veins of brain, abdomen,
pelvis & lower limbs

12. GENERAL
1. Malnutrition
2. Poor sanitation
3. Living in crowded areas
4. Close contact with TB patients
5. Repeated pregnancies
6. Exanthematous fevers
7. Immuno deficiency states
 LOCAL – TRAUMA , MOVEMENTS ,
INCREASED
LOADS , DECREASED VASCULARITY

13. CAUSATIVE ORGANISM
Mycobacterium
tuberculosis.
SIZE – 3x0.3 um
Gram positive AFB
Hematogenous
dissemination from
primary focus
Bone & joints TB develop
generally 2-3 yrs after
the primary focus
PATHOLOGYPATHOLOGY

14. 1. TB bacilli phagocytosed1. TB bacilli phagocytosed
by mononuclear cellsby mononuclear cells
2.2. Epitheloid cell formationEpitheloid cell formation
3.Langhans giant cell formed by fusion3.Langhans giant cell formed by fusion
epitheliod cells. Formed only if caseationepitheliod cells. Formed only if caseation
necrosis has occurrednecrosis has occurred
PATHOLOGYPATHOLOGY

15. 4.Lymphocytes form a4.Lymphocytes form a
ring around the lesionring around the lesion
5.Tubercle formation5.Tubercle formation
 Epitheloid cells-characteristic of TB.
 Presence of caseation necrosis almost diagnostic of
TB
PATHOLOGYPATHOLOGY

16. PATHOGENESISPATHOGENESIS
STEP 1STEP 1
Bacilli from primary
focus through
bloodstream reach
DISC SPACE

17. STEP 2STEP 2
Once infected, soft
nucleus centre &
fibrous annula wall
weaken, decay &
collapse.
This causes the disc
space to close ,
squeezing down on
nerve root causing
pain.

18. STEP 3STEP 3
The infection spreads
to vertebral bodies
above & below the
disc.

19. STEP 4STEP 4
The bones weakened
by the infection,
crumble under the
weight of the human
body.

20. STEP 5STEP 5
The deformed
spinal column
compresses spinal
cord producing
functional
impairment.

21. STEP 6STEP 6
Over time, the
deformed vertebrae
heal & fuse.
This may further
compress nerve
roots, causing pain
& neurodeficit

22. Disease itself
Ischemic necrosis due
to peri /endarteritis
Osteoporosis due
to hyperemia
DESTRUCTION OF VERTEBRA
Progressive deformity
Collapse
KYPHOSIS
GIBBUS

23. Cold abscess
Formed by collection of products of
liquefaction and reactive exudation
Composed of mainly serum,leucocytes,caseous
material, bone debris and TB bacilli.
Tracks away along neighbouring vessels and
nerves to reach surface
May burst to form sinus.

24. Caseous exudative
type
• more in children
• more destruction
• more exudation
• abscess formation.
Granular type
• more in adults
• less destructive
• insidious onset/course
• abscess formation rare

25. Cervical (12%)
Cervicodorsal (5%)
Dorsal (42%)
Dorso-lumbar (12%)
Lumbar (26%)
Lumbo-sacral (3%)

26. 1. PARADISCAL (due to arterial spread)
2. CENTRAL (due to venous spread)
3. ANTERIOR (due to subperiosteal spread)
4. APPENDICAL
5. ARTICULAR TYPE

27. 7%
12%
20%
Skip lesions
Other bone TB
Visceral TB

28.  Common in 1st
3 decades
 Male=Female
 Slight BACK pain and stiffness are the
earliest complaints
 PRSSURE SYMPTOMS – due to clod abscess

29. Constitutional symptoms:
(40% cases)
 Malaise
 Loss of appetite/weight
 Night sweats
 Evening rise of
temperature.
Specific features:
 Pain/night cries
 Stiffness
 Deformity - Gibbus
 Restricted ROM
 Enlarged Lymph Nodes
 Abscess
 Neuro-deficit 20%
ACTIVE STAGE:

30. Clinical featuresClinical features PercentagePercentage
1.Kyphosis 80-85%80-85%
2.Neurodeficit 20-30%20-30%
3.Palpable cold abscess 15-20%15-20%
4.Radiological
perivertebral abscess
15-20 %15-20 %
5.Extra spinal foci 10-15%10-15%
6.Skipped lesions 05%05%

31. NEUROLOGICAL Deficit:
20-40% cases: Neurodeficit
Mainly seen in adults due to
• Inelasticity of Prevertebral fascia.
• Loss of flexibility of spine.
• Degenerative changes like OA.

32. NEUROLOGICAL DEFICIT (tuli 1985, kumar 1988)
• Four grades
StageStage Clinical featuresClinical features
I [Negligible] Patient unaware of Neuro-deficit,
physician detects extensor
planter or ankle clonus
II
[Mild]
Patient aware of deficit but manages
to walk with/without support+signs of
spasticity.
III
[ Moderate]
Non ambulatory because of
paralysis in extension sensory deficit
less than 50%
IV
[Severe]
3+paralysis in flexion sensory deficit
more than 50%

33.  Classification of causes (Hodgsons)
Extrinsic causesExtrinsic causes Rare causesRare causesIntrinsic causesIntrinsic causes
•Prolong stretching of
cord over deformity
•Tuberculous
meningomyelitis
•Infective
thrombosis/end arteritis
•Pathological dislocation
• Syringomylic changes
•Spinal tumor syndrome
•Posterior element TB

34. Extrinsic causesExtrinsic causes
In Active disease In Healed disease
• Inflammatory edema
•Abscess (fluid/caseous)
• Granulation sequestrated
bone/ disc
• Pathological subluxation/
• Internal gibbus
• Dural fibrosis
• Sequestra from
vertebral body
• Canal Stenosis
•TB debris

35.  Griffith seddon classified TB PARAPLEGIA
 Early onset
paraplegia (within
2yrs)
inflammatory edema,
granulation tissue,
caseous tissue and
rarely ischemic lesion
of cord
ACTIVE disease
Good prognosis
 Late onset (more
than 2 yrs of onset)
recrudescence of
disease or
mechanical
compression of cord
- Caseous tissue,
debris,
sequestra,
internal gibbus,
stenosis of canal,
deformity
HEALED DISEASE
POOR PROGNOSIS

36.  CBC-
• Hb%
• Lymphocytosis
• DC:-lymphocyte-monocyte ratio.
High lymphocyte & low monocytes count
suggest good resistance. if ratio is 5:1,it is
favorable ratio.
 ESR :
• Raised in active stage of disease
• Normal ESR over a period of 3 months suggest pt
is in stage of repair.

37. Mantoux test
 10 mm: everyone
 5 mm: HIV infected
 Evidence of old disease
 Close contacts of infectious
cases
 in doubtful cases in
children a negative
Mantoux test rules out TB.

38.  Sputum examination :
for AFB

39. Aspiration of abscess :
smears & culture of pus
CULTURE=GOLD STANDARD
SOLID MEDIA: 3-8 weeks
Lowenstein Jensen (egg Based)
Middlebrook 7H11(agar based)
LIQUID BROTH:
1-3 weeks

40.  BACTEC media: for faster culture (within 1-2wks)
Bactec 460 Bactec9000MB Bactec mgit960b

41. ELISPOT (Enzyme-linked immunospot)
 T-cell based assay from blood
 1 tube of blood needed
 Useful in outbreaks for contact investigations
 showed greater sensitivity than PPD

42. IgM & IgG antibodies:
IgM indicates recent infection.
IgG indicates past infection.
Disadv: high sensitivity but low specificity
PCR:
Tissue PCR more specific
BIOPSY:
CT guided
C-Arm guided
Percutaneous

43. Plain radiography signs :
 Reduced disc space
 Blurred paradiscal
margins
 Destruction of bodies
 Loss of trabecular
pattern
 Increased Prevertebral
soft tissue shadow
 Subluxation/dislocation
 Decreased Lordosis/
kyphosis

44.  Posterior element
involvement
(5%)
 Skip lesions
(7%)

45. Paradiscal lesion:
Commonest lesion
Spread through arterial
supply
Reduced disc space
(earliest sign)
Loss of vertebral
margins.
Increased Prevertebral
soft tissue shadow

46. Reduced disc space in
Koch due to
 Atrophy of disc tissue
due to lack of nutrition
(due to aseptic necrosis
of end plates)
 Prolapse of nucleus
pulposus into soft
necrotic vertebral bodies

47. Central type of lesion: (TB
of the Centrum)
Spread through Batson’s
venous plexus/ branches
of posterior vertebral
artery.
Minimal disc space
reduction
At the end concentric
collapse.

48. Anterior type lesion:
Starts beneath the
anterior longitudinal
ligament & periosteum
Collapse & disc space
reduction is usually
minimal & occurs late
Erosion is primarily
mechanical
Appendicial type
lesion :lesion :
 Rare
 Isolated infection of
pedicles/ lamina/
transverse process/
spinous process
 Erosions
 Para vertebral shadows
 Intact disc space

49. Skipped lesion :
More than one TB
lesion present in
vertebral column
with one or more
healthy vertebrae in
between the 2
lesions.
7% on routine X-rays.
More frequently
detected on CT/MRI

50. Lateral shift and scoliosis:
Reasons-
More destruction of vertebral body on one
side
Kyphotic deformity :
Due to collapse of bone
Forward angulation – 1-2 knuckle
3 – gibbus
large no round kyphosis

51. Healing is indicated by
1. Decreased soft tissue
shadow
2. Disappearance of
erosion
3. Return of normal
density
(mineralization)
4. Bony ankylosis

52. Figure a – Separation of the facet joint. The facet
joint dislocates at the apex of the curve
Figure b – Posterior retropulsion.
Figure c – Lateral translation.
Figure d – Toppling sign.

53. Multiple vertebral
involvement:
1.Immunocompromized
2. DM
3.Hemoglobinopathies

54. CT SCAN
• Patterns of bony destruction.
• Calcifications in abscess
(pathognomic for Tb)
• Regions which are difficult to
visualize on plain films, like :
1. Cranio-vertebral junction (CVJ)
2. Cervico-dorsal region,
3. Sacrum
4. Sacro-iliac joints.
5. Posterior spinal tuberculosis
because lesions less than 1.5cm
are usually missed due to
overlapping of shadows on x rays.
MRI
• Lack of ionizing radiation, high
contrast resolution & 3D imaging.
• Detect marrow infiltration in
vertebral bodies, leading to early
diagnosis.
• Changes of discitis
• Assessment of extradural
abscesses / subligamentous
spread.
• Skip lesions
• Spinal cord involvement.
• Spinal arachanoiditis.

55. • MRI :diagnosis of TB of
Dfficult & rare sites,
Disease of posterior elements
Vertebral appendages
Epidural exiension
Infections of sacroiliac region.
Follow up
USG : to diagnose the
presence of tubercular
abscesses in Dorso-lumbar
vertebral disease.

56. LOCATION OF PARAVERTEBRAL ABSCESS

57. Angle of Kyphosis

59. BONE SCAN (Technitium (Tc) - 99 m )
• Increased uptake in up to 60 per cent patients with active
tuberculosis.
• >= 5mm lesion size can be detected.
• Avascular segments and abscesses show a cold spot due to
decreased uptake.
• Highly sensitive but nonspecific.
• Aid to localise the site of active disease and to detect
multilevel involvement.

60. 1. Pyogenic infections
2. Typhoid spine
3. Brucella spondylitis
4. Mycotic spondylitis
5. Syphilitic infection of
spine
6. Tumorous conditions-
hemangioma, GCT,
aneurysmal bone cyst
7. Primary malignant
tumor
8. Multiple myeloma
9. Lymphomas
10. Secondary neoplastic
deposits
11. Histiocytosis X
12. Spinal osteochondrosis
13. Traumatic conditions
14. Hydatid cyst

61. EVOLUTION OF TREATMENT:
Undergone tremendous revolutionary
changes.
Ancient Indians used herbal preparation
SIPURDA.
Pott & Charcot applied Hot iron to drain pus

62. Hippocrates advocated
traction & other means
to correct deformity

63. BASIC PRINCIPLES OF
MANAGEMENT
• Early diagnosis
• Expeditious medical treatment
• Aggressive surgical approach
• Prevent deformity
• Expect good outcome

64. Sanatorium treatment

65. Surgery was not attempted due to fear of
secondary infection and death
Most of operative procedures were
developed for either for treatment or for
prevention of paralysis in TB spine
Principle was more direct approach to
diseased part.

66. Surgeries done in Preantitubercular Era:
• Laminectomy & laminotomy : Chipault (1896 )
• Costotransversectomy Menard (1896)
• Posterior mediastinotomy
• Calves operation (aspiration without sinus
formation) (1917)
• Lateral rhachiotomy Capener (1933 )
• Anterolateral decompression Dott &
Alexander(1947)

67. Results of Surgeries done in
Preantitubercular Era:
Serious sinus formation
Pseudoarthrosis (4-26%)
Recurrence of lesion
Neurological deterioration
Death

68. Antitubercular drugs (AKT)
 Black picture has taken a dramatic turn for
the better with discovery of Antitubercular
drugs (AKT)
1943- PAS
1944- Streptomycin
1951- INH (MAGIC BULLET)
1970- RIFAMPIN & SHORT COURSE RX-
EVOLUTION OF TREATMENTEVOLUTION OF TREATMENT

69. Simultaneously under cover of AKT
direct surgical attack was popularized
those days
Attention was mainly paid on Thoracic
spine cases
No direct reference was made to the
treatment of cervical disease
EVOLUTION OF TREATMENTEVOLUTION OF TREATMENT

70. Rest
Braces
High protein diet
Multivitamins, hematinics
Hygiene
Bed sore care
Chest/ urinary tract care
Improve Immune status
Treat other comorbid conditions.

71. Non neurological cases of
Spinal TB
BROAD TREATMENT REGIMENS
Radical surgery
Conservative t/t with
chemotherapy only
Middle path
regimen

72. Bactericidal drugs DoseDose
1.Isoniazid 5mg/kg5mg/kg
2. Rifampicin 10-15 mg/kg10-15 mg/kg
3. Streptomycin 20mg/kg20mg/kg
4. Pyrazinamide 20-25 mg/kg20-25 mg/kg
Bacteriostatic drugs DoseDose
11. Ethambutol 25mg/kg (x 2mnths)25mg/kg (x 2mnths)
Then 15mg/kgThen 15mg/kg

73. • Amikacin, Kanamycin,capriomycin
• Ciprofloxacin, Ofloxacin, Levofloxacin
• Rifabutin
• Clarithromycin
• Clofazimine
• Ethionamide
• Cycloserine

74.  INH +RMP+ETM+ PZN for first 3 months
 INH + RMP +PZN for 9 months
 INH + RMP for next 6 months
Entire duration of chemotherapy lasts for 16-18
months
10 mg pyridoxine for prevention of peripheral
neuropathy

75.  Rationale
“All spine TB cases do not require surgery and
only those who do not respond to conservative
measures should be operated”

76. Treatment is on non-operative lines with
AKT, rest & spinal braces
1.Rest: in hard bed or plaster of Paris bed( in
children)
2.Drugs :
INH +Rifampicin +ETB FOR 4 months
INH + PZA FOR 4 MONTHS
INH + RMP FOR 4 MONTHS
INH FOR LAST 4 MONTHS
TOTAL DURATION 16 months.

77. supportive therapy-
 multivitamins,
 hematinics if necessary &
 high protein diet.
3.Radiographs & ESR: at 3-6 months interval
4.Gradual mobilisation:
with the help of spinal braces
5. Abscess are aspirated
6. Sinus excision
7. decompression

78. Indications of surgery in middle path regime:
1. No progressive recovery after a fair trial of
conservative t/t (3-4 wks)
2. Neurological complication develops during
conservative treatment
3. Worsening of Neuro-deficit during t/t
4. Recurrence of neurological complications
5. Pressure effects (deglutition/respiratory)
6. Advanced cases of neurological involvement
(sphincter disturbances, flaccid paralysis, or severe
flexor spasms)

79. TUBERCULOUS PARA/QUADRIPLEGIATUBERCULOUS PARA/QUADRIPLEGIA
AKT + REST (3-6 WKS)AKT + REST (3-6 WKS)
PROGRESSIVE RECOVERY NO IMPROVEMENTPROGRESSIVE RECOVERY NO IMPROVEMENT
CT AKT SURGERYCT AKT SURGERY
PROGRESSIVE RECOVERY NO IMPROVEMENTPROGRESSIVE RECOVERY NO IMPROVEMENT
MRI/ MYELOGRAMMRI/ MYELOGRAM
(REPEAT)(REPEAT)

80. MRI/ MYELOGRAMMRI/ MYELOGRAM
NO COMPRESSION COMPRESSION PRESENTNO COMPRESSION COMPRESSION PRESENT
INTRISIC DAMAGE TO CORD REPEAT SURGERYINTRISIC DAMAGE TO CORD REPEAT SURGERY
Ct AKT + REHABILITATIONCt AKT + REHABILITATION
NO RECOVERY IMPROVEMENTNO RECOVERY IMPROVEMENT
Ct AKTCt AKT

81.  In patients without neurological deficit
 IN in TB paraplegia

82.  1. Abscess drainage by anatomical level
cervical spine - retropharyngeal
- post triangle of neck
- supraclivicular region
dorsal spine – costotransversectomy
MENARD
LUMBAR spine – paravertebral

83.  2. HONG KONG PROCEDURE
RADICAL DEBRIDEMENT AND ARTHRODESIS
 3. ANTEROLATERAL DECOMPRESSION
 4. POSTERIOR SPINAL ARTHRODESIS
ALBESS PROCEDURE
HIBB’S PROCEDURE

84. SURGERY INDICATIONS
1 Decompression (+/- fusion) Too advanced ds, failure to respond to
conservative therapy
2 Debridement + /- decompression +/- Recurrence of disease or of neural
fusion complication
3 Anterior transposition of cord Severe kyphosis (>60⁰) + neural deficits
(Extrapleural anterolateral approach)
4 Laminectomy Extradural granuloma / tuberculoma (STS), Old
healed disease presenting as secondary canal
stenosis / posterior spinal disease

85. SURGICAL APPROACHES :
WORKERS C1-C2 CERVICAL C7-D1 DORSAL DORSO- LUMBAR L5-S1
LUMBAR
Kirkaldy-Willis - Anterior Transpleural Anterolateral or Anterolateral Retroperitoneal Transperitoneal,
(1965) through bed of transpleural sympathectomy paramedian
3rd rib or ureter incision in
approach Trendelenburg
position
Hodgson Transoral / Through Transpleural via Anterior Bed of 11th rib Renal approach Transperitoneal in
(1969) transthyroi anterior or bed of 3rd rib transpleural extrapleural Trendelenburg
d posterior∆ /split sternal for decompression extraperitone position. Lower
extensive lesion al / left midline incision
transpleural
via bed of 9th
rib
Kemp et al - Anterior Anterior cervical Trans-sternal for Bed of 12th rib Retroperitoneal Retroperitoneal
(1973) D3-D4.Anterior approach through oblique
transpleural for renal incision
D5-D12
Smith & Anterior
Robinson
(1985)
Mc Afee et al Retrophary
(1987) ngeal extra-
mucosal
Anterior -
- -
- -
- -
- -
- -
Tuli et al Transoral Anterior Low anterior Anterolateral or Anterolateral Retroperitoneal Retroperitoneal or
(1988) for cervical transpleural approach Retropsoas
drainage transverse
vertebrotomy

86. Tuli’s recommended approach
• Cervical spine -T1
Anterior approach
• Dorsal spine -DL junction
Anterolateral approach
• Lumbar spine &Lumbosacral junction
Extraperitoneal Transverse Vertebrotomy

87. ANTERIOR APPROACH TO THE
CERVICAL SPINE (C2 to D1)
Smith & Robinson
• Oblique / transverse incision.
• Plane b/w SCM & carotid sheath laterally & T-O medially.
• Longitudinal incision in ALL open a perivertebral abscess, or
the diseased vertebrae may be exposed by reflecting the ALL
& the longus colli muscles.
Hodgson approach via posterior triangle by retracting SCM,
Carotid sheath, T & O anteriorly & to the opposite side.

88. SURGICAL APPROACHES TO
DORSAL SPINE
• Anterior transpleural transthoracic approach (Hodgson &
Stock, 1956)
• Anterolateral extrapleural approach (Griffiths, Seddon & Roaf,
1956)
• Posterolateral approach (Martin,1970)
{Dura is exposed by hemilaminectomy first &
then
extended laterally to remove the posterior ends of2 - 4ribs, corresponding transverse processes & the pedicles}.

89. TRANSTHORACIC TRANSPLEURAL
• Left sided incision preferable
• Incision is made along the rib which in the mid-axillary line, lies
opposite the centre of the lesion (i.e. usually 2 ribs higher than the
centre of the vertebral lesion).
• For severe kyphosis, a rib along the incision line should be removed.
• AJ-shapedparascapularincisionforC7-D8lesions,scapulauplift
& rib resection.
• After cutting the muscles & periosteum, rib is resected
subperiosteally.

90. • Semicircular incision
• For severe kyphosis, additional 3-4 transverse processes and
ribs have to be removed.
• Intercostal nerves serve as guide to the intervertebral
foramina & the pedicles.

91. ANTEROLATERAL DECOMPRESSION
• 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

92. • Semicircular incision
• For severe kyphosis, additional 3-4 transverse processes and
ribs have to be removed.
• Intercostal nerves serve as guide to the intervertebral
foramina & the pedicles.

93. ANTERO-LATERAL APPROACH TO
LUMBAR SPINE ( LUMBO-
VERTEBROTOMY)
• Left side approach
• Semicircular incision
• Expose and remove transverse process
subperiosteally.
• Preserve lumbar nerves

94. EXTRA PERITONEAL ANTERIOR
APPROACH TO LUMBAR SPINE
• 45 ⁰ right lateral position with a bridge centered over the area to be
exposed.
• Similar incision as nephroureterectomy or sympathectomy
• Strip peritoneum off posterior abdominal wall and kidney,
preserving ureter.
• Longitudinal incision along psoas fibers for abscess drainage
• Retract the sympathetic chain
• Double ligation of lumbar vessels.

95. EXTRA PERITONEAL APPROACH TO
LUMBO-SACRAL REGION
• Left side preferred ( left Common iliac vessels longer
& retracted easily).
• Lazy "S" incision
• Strip & reflect the parietal peritoneum along with
ureter & spermatic vessels towards right side.

96. TRANS PERITONEAL HYPOGASTRIC/
SUPRAPUBIC ANTERIOR APPROACH TO
LUMBO-SACRAL REGION
• Supine position
• Midline incision from umbilicus to pubis.
• Lumbo-sacral region identified distal to aortic bifurcation and left
common iliac vein.
• Longitudinal incision on parietal peritoneum over lumbo-sacral
region in midline.
• Avoid injury to sacral nerve & artery and sympathetic ganglion.

97. POSTERIOR SPINAL
ARTHRODESIS
• By- Albee & Hibbs
• Albee- Tibial graft inserted longitudinally in to the split
spinous processes across the diseased site.
• Hibbs- overlapping numerous small osseous flaps from
contiguous laminae , spinous processes & articular facets
• Indications-
1. Mechanical instability of spine in otherwise healed disease.
2. To stabilize the craniovertebral region (in certain cases of T.B.)
3. As a part of panvertebral operation

98. TREATMENT OF PARAPLEGIA IN
SEVERE KHYPHOSIS
• Griffiths et al (1956) :anterior transposition of cord through
laminectomy
• Rajasekaran (2002): posterior stabilization f/b anterior
debridement and bone grafting ( titanium cages) in active
stage of disease and vice versa for healed disease.
• Antero-lateral (Preferred approach) .

99. SURGICAL CORRECTION OF SEVERE
KYPHOTIC DEFORMITY
• Fundamentals of correction:
1. to perform an osteotomy on the concave side of the curve
and wedge it open ( secured with strong autogenous iliac
grafts) .
2. to remove a wedge on the convex side and close this wedge
( Harrington compression rods and hooks)

100.  Removal of Taylor's brace was subject to clinical &
radiological follow up ( usually 10-12 wks)
If patient neurologically
intact
 Taylor's brace applied
after 48 hrs.
 Patient kept ambulatory
If patient is having
Neurodeficit
 Regular neurocharting.
 Taylor's brace applied after
patient could sit up without
support
 Taylor's brace worn for period
of 3 months
 Patient kept ambulatory

101.  All patients evaluated at
3 mnths
6 mnths
9 mnths
12 mnths
Clinical Radiological
•Wt gain
•Pain relief
•Free ROM
•Resolution of abscesses
•Neurological recovery
EvaluationEvaluation
• Decreased soft tissue
shadow
• Disappearance of
erosion
• Return of mineralization
• Graft incorporation
• Bony ankylosis
15mnths
18 mnths

102.  First objective sign can be seen in 24 hrs-12
weeks after decompression.
 Time taken for near complete recovery
varies between 3-6 months
 No significant neural recovery occurs after
12-18 months.

103. Definition of favorable status-
 No residual neural impairment
 No sinus/ cold abscess.
 No impairment of physical activity due to
spinal disease/lesion.
 Presence of radiographic quiescent disease.

104.  Extradural granuloma
 Severe kyphosis
 Reactivation of lesion
Decreased nutrition
Resistant organisms
Compromised immuno-status

105. Treatment
Necessary surgery
Newer anti tubercular drugs
Supportive measures

106. Surgery has its distinct advantages.
necrotic biowaste is removed completely &
abscesses are drained
• Early relief from pain
• Early bony fusion
• Prevention & correction of deformity
• Confirmation of diagnosis by histopathology