1. Dr. Arif Baradia Ortho III
Grand Round
Dr. Arif Baradia Ortho III

2. Pott’s disease
This entity was first described by Percivall Pott. He noted this as a painful kyphotic deformity of the spine associated with paraplegia.
Tuberculosis of the spine is one of the oldest diseases afflicting humans. Evidences of spinal tuberculosis have been found in Egyptian mummies dating back to 3400 BC

3. Three percent are suffering from skeletal TB,
50% of these suffer from spinal lesion and almost 50% are from pediatric group. An estimated 2 million or more patients have active spinal tuberculosis.

4. Regional Distribution1
Cervical
12% 2
cervicodorsal 5% 3
Dorsal
42% 4
Dorsolumbar 5
Lumbar
26% 6
Lumbosacral 3%

5. Pathophysiology
Pott disease is usually secondary to an extraspinal source of infection.
The basic lesion is a combination of osteomyelitis and arthritis.
The area usually affected is the anterior aspect of the vertebral body adjacent to the subchondral plate.
Tuberculosis may spread from that area to adjacent intervertebral disks.
In adults, disk disease is secondary to the spread of infection from the vertebral body.
In children, because the disk is vascularized, it can be a primary site.

6. Progressive bone destruction leads to vertebral collapse and kyphosis
Progressive bone destruction leads to vertebral collapse and kyphosis. The spinal canal can be narrowed by abscesses, granulation tissue, or direct dural invasion. This leads to spinal cord compression and neurologic deficits.
Kyphotic deformity occurs as a consequence of collapse in the anterior spine. Lesions in the thoracic spine have a greater tendency for kyphosis than those in the lumbar spine.
The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes.
Healing takes place by gradual fibrosis and calcification of the granulmatous tuberculous tissue. Eventually the fibrous tissue is ossified, with resulting bony ankylosis of the collapsed vertebrae.

7. Paravertebral abscess formation occurs in almost every case
Paravertebral abscess formation occurs in almost every case. With collapse of the vertebral body, tuberculous granulation tissue, caseous matter, and necrotic bone and bone marrow are extruded through the bony cortex and accumulate beneath the ALL.
These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion.
In the thoracic region, the longitudinal ligaments limit the abscess, which is seen in the radiogram as a fusiform radiopaque shadow at or just below the level of the involved vertebra.
Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels.

8. The lesion could be: Florid - invasive and destructive lesion.
Non destructive
Encysted disease
Carries sicca
Hypertrophied
Periosteal lesion.

9. Recently, two distinct patterns of spinal TB can be identified, the classic form, called spondylodiscitis (SPD) a
atypical form characterized by spondylitis without disk involvement (SPwD).
SPwD seems to be the most common pattern of spinal TB.

10. Anatomically the lesion could be
Paradiscal - destruction of adjacent end plates and diminution of disc space.
Appendeceal (Posterior) - involvement of pedicles, laminae, spinous process.
Central - Cystic or lytic, concertina collapse.
Anterior –longitudinal lig, Aneurysmal phenomenon
Synovitis in post facet

11. History Presentation depends on the following:
Stage of disease
Site
Presence of complications such as neurologic deficits, abscesses, or sinus tracts
The reported average duration of symptoms at the time of diagnosis is 3-4 months.
Back pain is the earliest and most common symptom.
Patients have usually had back pain for weeks prior to presentation.
Pain can be spinal or radicular.
Constitutional symptoms include fever and weight loss.

12. Neurologic abnormalities occur in 50% of cases and can include spinal cord compression with paraplegia, paresis, impaired sensation, nerve root pain, or cauda equina syndrome.
Cervical spine tuberculosis is a less common presentation is characterized by pain and stiffness.
Patients with lower cervical spine disease can present with dysphagia or stridor.
Symptoms can also include torticollis, hoarseness, and neurologic deficits.
The clinical presentation of spinal tuberculosis in patients infected with the human immunodeficiency virus (HIV) is similar to that of patients who are HIV negative; however, the relative proportion of individuals who are HIV positive seems to be higher.

14. Natural course of disease
53% died within 10 yrs of onset
Early stage of healing– focus surrounded by sclerotic bone Ivory vertebra
Early radiological sign of healing– sharpening of fuzzy paradiscal margins & reappearance and minrralization of tuberculae
Several vertebrae destroyed– fibrous tissue
Disc space destroyed bony ankylosis/bone block formation

15. Lab Studies
Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95% of patients who are non–HIV-positive.
Erythrocyte sedimentation rate (ESR) may be markedly elevated .
The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent
Culture – LJ medium/BacTec
The polymerase chain reaction
A brucella complement fixation test

16. IFN- Release Assays (IGRAs)
Recently, two in vitro assays that measure T cell release of IFN- in response to stimulation with the highly tuberculosis-specific antigens ESAT-6 and CFP-10 have become commercially available.

17. Microbiology studies to confirm diagnosis: positive in only about 50% of the cases.

18. X Ray appearances
Lytic destruction of anterior portion of vertebral body
Increased anterior wedging
Collapse of vertebral body
Reactive sclerosis on a progressive lytic process
Enlarged psoas shadow with or without calcification
Vertebral end plates are osteoporotic.
Intervertebral disks may be shrunk or destroyed.
Vertebral bodies show variable degrees of destruction.
Fusiform paravertebral shadows suggest abscess formation.
Bone lesions may occur at more than one level.

19. X Ray appearances Discovertebral lesions, detected in 93% of patients,
Localized fluffy osseous destruction with surrounding osteoporosis is the earliest signs.
concentric collapse and may look like A.V.N.
Local lytic lesion may cause problem of diagnosis from neoplasic lesion.
destruction of adjacent vertebrae, Konstram (K) angle appears and shows the progress on follow up.
Skipped lesion (10% cases) can be diagnosed on suspicion and in correct size film.

21. X-ray of the thoracolumbar spine (Lateral view) showing wedge collapse of L1 and L2 vertebral bodies.

22. X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles.

23. Clinico-radiological Classification
stage
features
Usual duration I
Pre-destructive
Straightening, spasm, hyperemia in scinti
<3 mo II
Early-destructive
Diminished space paradiscal erosion Knuckle <10
2-4 mo
III
Mild kyphos
2-3 verte k:10-30
3-9 mo IV
Moderate kyphos
>3 verte K:30-60
6-24 mo V
Severe kyphos
>3 verte K:>60
>2 years

24. CT scanning
CT scanning provides much better bony detail of irregular lytic lesions, sclerosis, disk collapse, and disruption of bone circumference.
Low-contrast resolution provides a better assessment of soft tissue, particularly in epidural and paraspinal areas.
It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses.
In contrast to pyogenic disease, calcification is common in tuberculous lesions.

25. MRI
MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
MRI findings useful to differentiate tuberculous spondylitis from pyogenic spondylitis include thin and smooth enhancement of the abscess wall and well-defined paraspinal abnormal signal,
whereas thick and irregular enhancement of abscess wall and ill-defined paraspinal abnormal signal are suggestive of pyogenic spondylitis.
contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis.
most effective for demonstrating neural compression.

27. Myelography Spinal tumor syndrome Multiple vertebral lesions
Patients not recovered after decompression
Block present : second decompression
Block not present : intrinsic damage 1.Ischemic infarction
2.Interstitial gliosis
3.atrophy
4. tuberculous myelitis Myelomalacia

29. Differentials Pyogenic infections Typhoid spine Brucella Spondylitis
Mycotic Spondylitis
Syphilitic
Tumorous condition
Primary malignant tumor
Multiple Myeloma
Lymphomas
Secondary
Histocytosis-X
Spinal Osteochondrosis
Spondylolisthesis
Hydatid disease

30. Complications of tuberculosis
Paraplegia
Cold abscess
Sinuses
Secondary infection
Amyloid disease
Fatality

31. Tb spine with PARAPLEGIA
INCIDENCE 10-30%
Dorsal spine (MC)
Motor functions affected before /greater than sensory
Sense of position & vibration last to disappear

32. Patho of Tuberculoses Paraplegia
Inflammatory Edema –vascular stasis,toxin
Extradural Mass – Tuberculous ostetis abscess
Bony Disorder – Sequestra, Internal Gibbus
Meningeal changes – ‘dura as rule not involved’
Extradural grnulation -- contract, cicatrization peridural fibrosis  paraplegia

33. 5. Infarction of spinal cord - Ant spinal artery
Endarteritis,Periarteritis,Thrombosis
6. Changes in Spinal cord-
Myelomalacic,Syringomyelic change,Atrophy –upto 50%decrease in diameter -good functions

34. Seddon’s Classification:
GROUP A_-Early onset - This comes up in active stage of the disease within first 2 years. Compressive Agents are inflammatory edema, granulation, abscess, casseous material, sequestra and rarely ischaemic lesion. GROUP B -Late onset- Usually after 2 years of onset of the disease.
due to recurrence or by mechanical pressure. This can be better divided into paraplegia with active disease and with healed disease. Active disease - Caseous material, debris, sequestrated disc or bone, internal gibbus, stenosis and deformity can cause compression. Healed disease - Usually internal gibbus and acute kyphotic deformity can also give late onset paraplegia. Usually there is a continuous traction, compression leading to paraplegia.

35. Evolution of treatment
Pre-antitubercular era
Artificial abscess- Pott in 1779
Laminectomy & laminotomy : chipault(1896 )
Costo-transversectomy: Menard in 1896
Posterior mediastinotomy
Calves operation 1917
Lateral rhachiotomy of carpener 1933
Anterlateral decompression of Dott& Alexander:1947

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

37. Studies performed by the British Medical Research Council indicate that tuberculous spondylitis of the thoracolumbar spine should be treated with combination chemotherapy for 6-9 months. According to a 1994 recommendation by the US Centers for Disease Control and Prevention, this is the treatment of choice.

38. What is Middle path regime?
Admission rest in bed
Chemotherapy
X-ray & ESR once in 3 months
MRI/ CT at 6 months interval for 2 years
Craniovertebral ,cervicodorsal, lumbosacral& sacroiliac joints
Gradual mobilization
3-9 weeks- back extention exercise 5-10 min 3-4 times
Spinal brace months-2 years

39. Abcesses – aspirate near surface
Instille 1gm Streptomycin +/- INH in sol
Sinus heals 6-12 weeks
Neural complications if responds 3-4 weeks :- surgery unnecssary
Excisional surgery for posterior spinal disease
Operative debridement for patients –if no arrest after 3-6 months- spinal arthrodesis (recommended)
Post op--Spinal brace months-2 years

40. Drugs in middle path phase duration drug Intensive 5-6 months
INH mg
Rifampicin
ofloxacin mg / streptomycin
Continuation
7-8 months
-do
3-4mth Pyrazinamide mg
4-5mth Rifampicin
Prophylactic
4-5 months
Ethambutol 1200mg

43. Surgical indications
No sign of Neurological recovery after trial of 3-4 weeks therapy
Neurological complication during treatment
Neuro deficit becoming worse
Recurrence of neuro complication
Prevertebral cervical abscesses,neurological signs& difficulty in deglutition& respiration
Advanced cases Sphincter involvement,
flaccid paralysis,
Severe flexor spasms

44. Other indications Recurrent paraplegia
Painful paraplegia– d/t root compression,etc
Posterior spinal disease--involving the post elements of vertb
Spinal tumor syndrome resulting in cord compression
Rapid onset paraplegia due to thrombosis,trauma etc
Severe paraplegia
Secondary to cervical disease and
cauda equina paralysis

45. 1
Decompression +/- fusion
Failed response,Too advanced 2
Debridement+/- fusion
Failed response after 3-6 months,Doubtful diagnosis,Instability 3
Debridement +/-DECOMP+/- fusion
Recrudescence of disease 4
Prevent severe Kyphosis 5
Anterior transpostion
Severe Kyphosis +neural deficit 6
Laminectomy
secondary stenosis, posterior disease

46. APPROACH Cervical spine – Anterior retropharyngeal (smith-Robinson’s)
Anterior approach – Anterior/Medial border of sternocleidomastoid
2. Thoracic spine (T1 to L1) –
1 Transthoraccic transpleural
2 Anterolateral decompression(T2 – L1)
3. Lumbar spine – Anterolateral(Lumbovertebrotomy)
Extraperitoneal Ant. approach

47. DYNAMIC CAGE :Govender&Prabhoo

48. SYNTHES PLATE WITH SPACER