POTT’S POTT’S SPINE

VERTEBRAL ANATOMY

Centre portion of each intervertebral disc is filled with gel like elastic substance(NUCLEUS PULPOSUS) which along with sturdy elastic collagen fibres(ANNULUS FIBROSUS)transmits stress from vertebra to vertebra

Annulus fibrosus enhances rotational stability of spine and helps to resist compressive forces

EMBRYOLOGY OF VERTEBRAL COLUMN

Formed from sclerotome portions of somites(derived from paraxial mesoderm)

Each sclerotome-loosely arranged cells cranially & densely packed cells caudally.

Some of the densely packed cells move cranially opposite the centre of myotome

INTERVERTEBRAL DISC

Remainin densely packed cells fuse with loosely arranged cells of immediately caudal sclerotome

MESENCHYMAL CENTRUM(primordium of body of vertebra)

Nerves lie in close relation to IVD and intersegmental arteries lie on each side of vertebral bodies.

Notochord persists and enlarges only in the region of IVD…..contributes to formn of NUCLEUS PULPOSUS which later gets surrounded by circular fibres of ANNULUS FIBROSUS

NP+AF

INTERVERTEBRAL DISC

Resegmentation of sclerotomes into definitive vertebrae causes myotomes to bridge the IVD…gives them the capacity to move the spine

FORMS

Spinous and transverse processes develop from chondrification centres(which appear at 6th week of embryonic life) in vertebral arch.

Ossification in vertebral arches-8th week At birth-each vertebra has 3 bony parts

connected by cartilageBony halves fuse during 1st 3-5yrs

Five secondary ossificn centres appear in vertebrae after pubrty

All secondary centres unite with rest of vertebrae-25yrs

POTT’S POTT’S SPINE

Dr SREEDEVI PK

TUBERCULOSIS OF SPINE

Vertebral TB-M.C form of skeletal TB(50% of all cases of TB of bones&joints)

M.C-1st 3 decades Equal in both sexes Any one/several vertebrae M.C-Lowr thoracic & lumbar spine

Infectious exudate may spread anteriorly beneath anterior longitudinal

ligament~>neighbouring vertebrae

Advances&destroys epiphyseal cortex,intervertebral disc&adj vertebrae

Infection begins in cancellous area of vertebral

body(Central/anterior/epiphyseal in location)

Note:infection of posterior bony arch and tyransverse process is unusual

Granulation tissue develops posteriorly-encircles & compresses spinal cord & nerve roots(more likely in thoracic spine ‘cause of small calibre of spinal canal here)

Posterior element involvt of C2(axial CT image showing reactive sclerosis)

COURSE……

ANTERIORLY……………

Exudate forms&netrates periosteum,accumulating beneath anterior longit.ligament(ALL)

Penetrates the ligament

Abscess

Migrates in various directions.Abscess tracks along lines of least resistance(along fascial planes,blood vessels & nerves

CERVICAL………

Collects behind

prevertebral fascia

Spreads laterally to sterno mastoid(a point at postr

edge))

Protrudes fwd..bulge

into pharynx

May gravitate to

mediastinum

Trachea,esophagus,pleural cavity

THORACIC

Remains locally confined as a bulbous mass for a long time

Back-pressre against spinal

cord

PARAPLEGIA

Exudate may spread laterally to extrapleural space-induces NON SPECIFIC PLEURAL EFFUSION

If exudate penetrates ALL, occupies mediastinum OR gravitates through diaphragm

to the LUMBAR ASPECT Rarely,thoracic cold abscess may track

backward b/w transverse processes&follow intercostal nerve-erupts on chest wall.

LUMBAR…..

A

•Tuberculous exudate enters PSOAS SHEATH

•Appears below inguinal ligament on medial aspect of thigh

B

•May spread laterally beneath iliac fascia

•Emerges at iliac crest at the anterior superior iliac spine

C

•Follows great vessels….may erupt alongside femoral vessels in triangle of Scarpa or in gluteal region

•Or forms an abscess abpve iliac crest posteriorly

REGIONAL DISTRIBUTION….

DORSAL-42% LUMBAR-26% DORSOLUMBAR-12% CERVICAL-12% CERVICODORSAL-5% LUMBOSACRAL-3%

Route of spread TB of spine is always secondary.

Bacteria reach spine via hematogenous route from lungs or lymph nodes.

TYPES OF VERTEBRAL TB

1) PARADISCAL – COMMONEST TYPE. BETWEEN THE TWO CONTIGUOUS AREAS OF TWO ADJACENT VERTEBRAE.

2) CENTRAL- BODY OF SINGLE VERTEBRA IS AFFETED.

3) ANTERIOR- INFECTION IS LOCALISED TO THE ANTERIOR PORTION OF THE VERTEBRAE.

4)POSTERIOR-POSTERIOR COMPLEX i.e PEDICLE,LAMIINA,SPINOUS OR TRANSVERSE PROCESS ARE INVOLVED.

5)APPENDICEAL-RARE, INVOLVES TRANSVERSE PROCESS.

COLD ABSCESS

Collection of pus and tubercular debris from diseased vertebrae.

Can travel in any direction.

Spread beneath the anterior longitudinal ligament- pre vertebral abscess.

Spread posteriorly and cause pressure over the spinal cord.

Spread through the sides of the vertebra –

para vertebral abscess.

Sometimes penetrates the anterior longitudinal ligament – lines of least resistance i.e. fascial planes,vessels,nerves

CLINICAL PICTURE

ACTIVE STAGE Constitutional symptoms antedate local spinal

involvement……anorexia,nausea,weakness,weight loss,night sweats,afternoon or evenin rise of temp

Frequently iniated by an exanthem or trauma. Spine- -Stiff and painful on movt. - Pain is localised to site of

involvement/referred dependin on specific nerve root irritation

- Localised KYPHOTIC deformity. (Tender to percussion)

Vertebral muscle spasm+ Night cries…..movt b/w inflamed surfaces. Cold abscess maybe + Pressure effects-dysphagia(mediastinal) Dyspnoea

Hoarseness(retropharyngeal) Restricted hip

extensn(Psoas abscess)

GIBBUS DEFORMITY IN TB

If any suspicion of TB spine……….. Palpate spinous processes by

sliding finger from cervical spine to sacrum…….so that even a small knuckle kyphosis (step/prominence) is not missed…………..thus making the diagnosis before gross vertebral destruction has occurred.

Stiffness,weakness&awkwardness of lower extremities herald onset of PARAPLEGIA.

CHARACTERISTICS OF SPECIFIC SPINAL INVOLVEMENT

CERVICAL Pain over cervical vertbrae/referred to

occiput/upper extremities Pain aggravated by pressure on top of head Neck rigidity Deformity-normal lordosis is reduced &

head is supported in hands Paralysis of arms before legs Occasionally death due to dislocation

LOW CERVICAL & UPPER THORACIC Pain along brachial plexus or intercostal

nerves Marked rigidity with angular kyphosis Abscess-

retropharyngeal,supraclavicular,mediastinal. Cord symptoms L.C Arms affected first Horners syndrome Neck rigidity-head&neck turn as one

THORACIC&THORACOLUMBAR Pain referred to lower extremities(esp

lateral aspect of thighs) Girdle pain Marked angular kyphosis Iliac or psoas abscess

LUMBOSACRAL Referred pain to lower extremities Deformity slight Psoas abscess Flexion of hips

ABSCESSES & SINUSES….. Cervical&dorsal-Can present away from

vertebral column:- Paraspinal regions,posterior/anterior

cervical triangles,along brachial pkexus in axilla,along intercostal spaces on chest wall.

Dorsolumbar&lumbar-Abscess freq tracks down psoas sheath……palpable in iliac fossa,lumbar triangle,upper part of thigh below inguinal ligmt,knee

Psoas abscess-Pseudo-hip flexion deformity(No limitation of internal & external rotation of hip jt when tested in position of flexion deformity)

- Can present as a lump in iliac foss - HEALED STAGE- -Not ill- -Regains lost weight- -No evening rise of temp- -No spinal pain/tenderness- -ESR falls

-Radiological E/O bone healing in serial Xrays

-But deformity persists

Bony ankylosis of L3-L4 resulting in kyphosis in an old case of TB spondylitis

INVESTIGATIONS………

BLOOD-Hb-anemia TC –lymphocytosis ESR raised S.proteins-Hypoproteinemia Mantoux-helpful in children<2-3yrs….not

diagnostic though

X-RAY APPEARANCES

Depending on site of lesion TB spine………..

1) PARADISCAL-M.C2) CENTRAL3) ANTERIOR4) APPENDICEAL

Earliest radiological finding-narrowing of disc space

Loss of definition of paradiscal margins Bones look rarefied and osteopenic(40% Ca

loss-radiolucent signs) Observed before osseous destructive

changes Trabecular destruction-atleast 3-5 months

from beginning of infectious process

Late changes-Anterior wedge compression in anterior vertebral involvement

Central vertebral body collapse(CONCERTINA COLLAPSE) in central involvement.

Destruction of posterior elements in posterior affection.

Soft tissue swelling&calcificn-highly predictive of TB

Healing stages-vertebral body&posterior elements dense(sclerosis)

Collapsed vertebral body L1-L3

Cervical-b/w vertebral bodies&pharynx(retropharyngeal)-birdnest shadow

Upper thoracic-V-shapd/bulbous/heart shaped shadow&widened mediastinum

Low thoracic&thoracolumbar-fusiform shadow occupy site of psoas shadow. Increased density and lessening of size of shadow indicates calcification and healing

Axial CT-vertebral body destruction,paravertebral abscess ext into spinal canal

MODERN IMAGING TECHNIQUES

CT SCAN• Assessmt of destructive lesions of vertebral

column• Paravertebral soft tissue swellings• Degree of neural compromise• Specially useful in-1) posterior spinal disease2)CraNiovertebral&cervicodorsal TB3)Sacroiliac joint TB• Suspected areas of disease should be localized

before taking CT

ISOTOPE BONE SCAN-Localises diseased area by demonstratin a hot spot even when lesions<5mm

Note:atleaqst 30-40% calcium must be removed from a particlr area for radiolucent changes to become visible

Anterior wedging and erosion of T9

Axial CT image showing vertebral body destruction&adj soft tissue mass

MRI• Diagnosis of TB in rare sites incl

posterior elements,vertebral appendages&sacroiliac jt

• Excellent modality to judge health of spinal cord…detects cord compression.

ULTRASOUND ECHOGRAPHSTo diagnose presence & size of

tuberculous abscess in lumbar vertebral disease.

GALLIUM SCAN-For disseminated TB BIOPSY-By percutaneous technique with

CT guidance………biopsy mateial subjected to culture

BIOPSY & CULTURE-MOST DEFINITIVE DIAGNOSTIC TEST

Radiological & MRI e/o healing lags behind biological healing processes in spinal TB.

X-rays,MRI-Upto 5months of starting multidrugtherapy may actually show deterioration in most pts.

If images don’t show improvement whwn repeated>6 months after onset of Rx….consider alternate diagnosis/therapeutically refractory disease.

Rarely-healing accomp by fat replacemt of healed area

COMPLICATIONS

1) PARAPLEGIA2) COLD ABSCESS3) SINUSES4) SECONDARY INFECTION5) FATALITY

DIFFERENTIAL DIAGNOSIS

Pyogenic infections Typhoid spine Brucella spondylitis Mycotic spondylituis Syphilitic infection Tumorous conditions Primary malignant tumors Multiple myeloma

Lymphomas Secondary neoplastic deposits HistiocytosisX Local developmental abnormalities of

spine Spinal osteochondrosis Traumatic conditions Osteoporotic conditions Spondylolisthesis

MANAGEMENT

AIMS OF Rx Halt progression of destruction and

deformity Prevent and overcome paraplegia.Treatment should be

prolonged ….and a cautious attitude

maintained for many years…as

recrudescence of disease can occur even

years later!!

GENERAL SUPPORTIVE

CHEMOTHERAPY

SURGERY

CHEMOTHERAPY

Isoniazid(INH)-most effective anti-TB drug INH-5mg/kg/day……300mg usually(adults) 10-15mg/kg/day……………...children. S/E-peripheral neuropathy,anemia,hepatitis

Pyridoxine 50mg to be supplemented daily

MONITOR LFT

Ethambutol-25mg/kg/day X 60days 15mg/kg single dose

thereafter.S/E-Visual disturbances……avoid in

childrenPERIODIC

OPHTHALMIC CHECK

UPS

Streptomycin Adults 0.75-1g/day X 60days 1g/day 2-3times weekly thereafter Children 15-25mg/kg/day INTRAMUSCULARS/E-Ototoxicity,nephrotoxicity AVOID IN RENAL

INSUFFICIENCY

RIFAMPICIN Adult-600mg Children-10mg/kg/day Oral single daily dose given ½ hr before

breakfast Relatively mild toxic effects Colors urine&othr body fluids bright

orange

***COMBINATION CHEMOTHERAPY*** Delays emergence of drug resistant

strains of bacilli. Rx regimen- HRE X 6MONTH….If at the end of 6months,clinical &

radiological response satisfactory, IE X 12-18MONTHS

Failure to respond to first line drugs……(due to bacterial resistance/allergic intolerance/toxic effects)…..use SECOND LINE DRUGS

Cycloserine,Ethionamide,Kanamycin,Amikacin,Thiocetazone

Failure to respond despite adq chemotherapy with radiological e/o progression of disease or neurological involvement emerges.

SURGICAL INTERVENTION

SURGICAL TREATMENT

INDICATIONS1) Failure to respond to ATT2) Radiological e/o progression(enlargmt

of paraspinal abscess shadow)3) Imminent vertebral collapse4) Instability of spine5) Progressive neurological deficit

SURGICAL OBJECTIVES1) Excise infected tissue as completely as

possible2) Decompress intraspinal neural

elements3) Reduce spinal deformity4) Provide stability by spinal fusion

PRINCIPLES1) Removal of all diseased tissue by

thorough debridement2) Correction of deformity3) Interbody bone grafting & stabilization.4) Relief of pressure on intraspinal

contents.

WHAT IS DONE??????

Major focus of disease is removed Spinal deformity reduced Intraspinal neural elements

decompressed Bone defect obliterated Spinal stability provided by autogenous

bone grafts

PREOPERATIVELY, an ATT regimen is maintained(atleast 3months)…….

Severe destruction-external skeletal fixation with a HALO-PELVIC DEVICE.

Following removal of diseased focus,distraction aids in overcoming kyphosis.

Later…bone grafting

OPERATIVE AAPROACHES

Lesions of C4-C6-lateral approach or anterior approach

Lesions of C7-T4-posterior thoracoplasty approach by removing third rib on left side

Lesions below T40Spine is approached from left

Aorta –landmark Incision- Along a rib that’s

2ribs higher than the rib that arises at apex of kyphosis.

Surgical procedures

Lateral rhachotomy Costotrasversectomy Albee procedure-aims to unite the

spinous processes by a single cortical graft(s/c aspect of tibia)….fixed by sewing muscles over it.

Hibbs procedure-only local bone is used Combined procedure Circumduction fusion

POTT’S PARAPLEGIA

POTT’S PARAPLEGIA

Pott’s paraplegia can be due to – - inflammatory causes- oedema,abscess - mechanical causes-tubercular debris - intrinsic causes-pathological dislocation - spinal tumour d/s- extradural granuloma Most commonly occurs in TB of dorsal

spine because spinal canal is narrowest in this part

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.

Kumar’s classification oftuberculous paraplegiastage Clinical features

1 Negligible Unaware of neural deficit,Upgoing Plantar / Ankle clonus

2 Mild Walk with support

3 Moderate Nonambulatory,Paralysis in extention,sensory loss <50%

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

CLINICAL FEATURES OF PARAPLEGIA- - clumsiness - twitching - increased reflexes - clonus - positive Babinski’s sign

In Pott’s paraplegia , motor functions are affected first.

The paralysis follows the following stages-

muscle weakness, spasticity , incoordination, paraplegia in extension , flexor spasms,paraplegia in flexion and flaccid paraplegia lastly.

TREATMENT OF POTT’S PARAPLEGIA 1) ATT 2)SPINE PUT TO ABSOLUTE REST 3)PARALYSED LIMBS SHOULD BE TAKEN

CARE OF. 4)REPEATED NEUROLOGICAL

EXAMINATION TO CHECK FOR WORSENING.

Surgical indications1. No sign of Neurological recovery after trial of

3-4 weeks therapy2. Neurological complication during treatment3. Neuro deficit becoming worse4. Recurrence of neuro complication5. Prevertebral cervical abscesses,neurological

signs& difficulty in deglutition& respiration6. Advanced cases- Sphincter involvement,

flaccid paralysis,Severe flexor spasms

MIDDLE PATH REGIMEN

Widely accepted regimen for tb spine Admission,rest in bed or pop cast. Chemotherapy X-ray and ESR once in 3 months Gradual mobilisation in the absence of

neurological involvement. Spinal braces-18 months to 2 years.

Abscesses are aspirated out drained. Sinuses heal within 6-12 weeks If no neurological complications develop

and patient is responding to the 3-drug therapy , surgery is unnecessary.

Excisional surgery for posterior spinal disease.

Operational debridement for patients who do not show arrest of disease after 3-6 months of chemotheray.

Thank you

Thank you