Potts spine

Moderator: Dr peeyush sharma

Presenter: Dr Pramod mahender

Potts 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

 One fifth of TB population is in India.

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.
Every day 1000 die of tuberculosis in
India.

Regional Distribution
1

Cervical

12%

cervicodorsal

5%

Dorsal

42%

Dorsolumbar

12%

Lumbar

26%

Lumbosacral

3%

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.

 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.

 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 anterior longitudinal ligament.
These cold abscesses gravitate along the fascial planes and
present externally at some distance from the site of the
original lesion.
In the lumbar region the abscess gravitates along the psoas
fascial sheath and usually points into the groin just below
the inguinal ligament.
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.

The lesion could be:

Florid - invasive and destructive lesion.
Non destructive - lesion suspected clinically but
identifiable by modern investigations like CT scan
or M.R.I.
Encysted disease
Carries sicca
Hypertrophied
Periosteal lesion.

 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.

Anatomically the lesion could be

1. Paradiscal - destruction of
adjacent end plates and
diminution of disc space.
2. Appendeceal (Posterior) involvement of pedicles,
laminae, spinous process.
3. Central - Cystic or lytic,
concertina collapse.
4. Anterior longitudinal lig,
Aneurysmal phenomenon
5. Synovitis in post facet

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.

 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.

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

Lab Studies
Tuberculin skin test (purified protein derivative
[PPD]) demonstrates a positive finding in 84-95%
of patients who are nonHIV-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
The polymerase chain reaction
A brucella complement fixation test

 IFN- Release Assays (IGRAs)

Recently, two in vitro assays that measure T
cell release of IFN- in response to
stimulation with the highly tuberculosisspecific antigens ESAT-6 and CFP-10 have
become commercially available.

 Microbiology studies to confirm diagnosis:

Obtain bone tissue or abscess samples to
stain for acid-fast bacilli (AFB), and isolate
organisms for culture and susceptibility. CTguided procedures can be used to guide
percutaneous sampling of affected bone or
soft tissue structures. These study findings
may be positive in only about 50% of the
cases.

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.

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.

X-ray of the thoracolumbar spine (Lateral view) showing

wedge collapse of L1 and L2 vertebral bodies.

X-ray of the spine in a child showing complete

destruction of D12 and L1 vertebral bodies leaving
only the pedicles.

Kumars clinico-radiological
Classification
stage
PreI

features
Straightening, spasm,
hyperemia in scinti

Usual duration

II

Earlydestructive

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

Severe
kyphos

>3 verte K:>60

>2 years

destructive

<3 mo

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.

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.

Myelography

Spinal tumor syndrome

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

Differentials

1. Pyogenic infections
2. Typhoid spine
3. Brucella Spondylitis
4. Mycotic Spondylitis
5. Syphilitic
6. Tumorous condition
7. Primary malignant tumor
8. Multiple Myeloma
9. Lymphomas
10.Secondary
11.Histocytosis-X
12.Spinal Osteochondrosis
13.Spondylolisthesis
14.Hydatid disease

Complications of tuberculosis
1.
2.
3.
4.
5.
6.

Paraplegia
Cold abscess
Sinuses
Secondary infection
Amyloid disease
Fatality

Tb spine with PARAPLEGIA

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

Patho of Tuberculoses Paraplegia

1. Inflammatory Edema vascular stasis,toxin
2. Extradural Mass Tuberculous ostetis+
abscess
3. Bony Disorder Sequestra, Internal Gibbus
4. Meningeal changes dura as rule not
involved
Extradural grnulation -- contract,
cicatrization peridural fibrosis
paraplegia

5. Infarction of spinal cord

- Ant spinal
artery
Endarteritis,Periarteritis,Thrombosis
6. Changes in Spinal cordMyelomalacic,Syringomyelic
change,Atrophy upto 50%dec in dia-good
functions

Seddons 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.

Kumars classification of
tuberculous paraplegia
1

Negligible

Clinical features
Unaware of neural deficit,
Plantar extensor/ Ankle clonus

Mild

Walk with support

Moderate Nonambulatory,

stage

Paralysis in extention,sensory loss

<50%
4

Severe

3+ paralysis in flexion/sensory
loss>50%/ Sphinters involved

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

BASIC PRINCIPLES OF
MANAGEMENT

Early diagnosis
Expeditious medical treatment
Aggressive surgical approach
Prevent deformity
Expect good outcome

 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.

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--- 18 months-2 years

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--- 18 months-2 years

Drugs in middle path

phase

duration

drug

Intensive 5-6
months

INH
Rifampicin
300ofloxacin400-600mg /
400mg streptomycin

Continua 7-8
tion
months

-do

3-4mth Pyrazinamide
1500mg
4-5mth Rifampicin

Prophyla 4-5
ctic
months

-do

Ethambutol 1200mg

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

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

Decompression
+/- fusion

Failed response,Too advanced

Debridement+/fusion

Failed response after 3-6

months,Doubtful
diagnosis,Instability

Debridement +/DECOMP+/fusion

Recrudescence of disease

Debridement+/fusion

Prevent severe Kyphosis

Anterior
transpostion

Severe Kyphosis +neural deficit

Laminectomy

STS,secondary stenosis,
posterior disease

APPROACH
1. Cervical spine Anterior retropharyngeal
(smith-Robinsons)
Anterior approach Anterior/Medial
border of sternocleidomastoid
2. Dorsal spine (D1 to L1)
1 Transthoraccic transpleural
2 Anterolateral decompression(D2 L1)
3. Lumbar spine Anterolateral(Lumbovertebrotomy)
Extraperitoneal Ant. approach

Tulis recommended approch

Cervical spine T1 Anterior approch
Dorsal spine DL junction Antrolateral
approch
Lumbar spine &Lumboscral junction
Extraperitoneal Transverse Vertebrotomy

Surgical technique
Costotransversectomy in tense paravertebral
abscess
remove transverse process
rib 2 inchs

Anterolateral decompression

Posterior part of rib

Transverse process
Pedicle
Part of the vertebral body
Griffith Seddon Roaf -- prone position

Tuli
--right lateral position
Advantage:- 1 avoid venous congestion
2 avoid excessive bleeding
3 permits freer respiration
4 better look at site

Posterior Spinal Arthrodesis

By Albee & Hibbs
Albee tibial graft inserted longitudinally in
to the split spinous vertebral process
Hibbs overlapping numerous small osseous flap
from contiguous laminae spinous
process & articular facets
Indications 1 mechanical instability
2 to stabilise craniovertebral region
3 as part of panvertebral operation

DYNAMIC CAGE
:Govender&Prabhoo

SYNTHES PLATE WITH

SAPCER

Yilmaz C, Selek HY, et al. Anterior instrumentation

for the Treatment of Spinal Tuberculosis. J Bone and
Joint Surg 1999; 81-A : 1261-67

we feel that every attempt should be

made to minimize this deformity with
some form of instrumentation
wherever indicated, and preferably
anteriorly.

Thank

you
Thank you