Grand Round 080911
Dr Arif Baradia Ortho III
Pottrsquos diseasebull This entity was first described by Percivall
Pott He noted this as a painful kyphotic deformity of the spine associated with paraplegia
bull 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
bull Three percent are suffering from skeletal TBbull 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
Regional Distribution 1 Cervical 12
2 cervicodorsal 5
3 Dorsal 42
4 Dorsolumbar 12
5 Lumbar 26
6 Lumbosacral 3
Pathophysiology
bull Pott disease is usually secondary to an extraspinal source of infection
bull The basic lesion is a combination of osteomyelitis and arthritis
bull The area usually affected is the anterior aspect of the vertebral body adjacent to the subchondral plate
bull 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
bull 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
bull 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
bull The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes
bull 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
bull 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
bull These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion
bull 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
bull Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels
The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion
bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a
bull atypical form characterized by spondylitis without disk involvement (SPwD)
bull 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 ndashlongitudinal lig Aneurysmal phenomenon
5 Synovitis in post facet
History
bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits
abscesses or sinus tractsbull The reported average duration of symptoms at the time
of diagnosis is 3-4 months bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to
presentation ndash Pain can be spinal or radicular
bull Constitutional symptoms include fever and weight loss
bull 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
bull 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
bull 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 diseasebull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic
bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy
paradiscal margins amp reappearance and minrralization of tuberculae
bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block
formation
Lab Studies
bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive
bull Erythrocyte sedimentation rate (ESR) may be markedly elevated
bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent
bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test
bull IFN- Release Assays (IGRAs)bull 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
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
Pottrsquos diseasebull This entity was first described by Percivall
Pott He noted this as a painful kyphotic deformity of the spine associated with paraplegia
bull 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
bull Three percent are suffering from skeletal TBbull 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
Regional Distribution 1 Cervical 12
2 cervicodorsal 5
3 Dorsal 42
4 Dorsolumbar 12
5 Lumbar 26
6 Lumbosacral 3
Pathophysiology
bull Pott disease is usually secondary to an extraspinal source of infection
bull The basic lesion is a combination of osteomyelitis and arthritis
bull The area usually affected is the anterior aspect of the vertebral body adjacent to the subchondral plate
bull 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
bull 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
bull 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
bull The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes
bull 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
bull 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
bull These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion
bull 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
bull Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels
The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion
bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a
bull atypical form characterized by spondylitis without disk involvement (SPwD)
bull 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 ndashlongitudinal lig Aneurysmal phenomenon
5 Synovitis in post facet
History
bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits
abscesses or sinus tractsbull The reported average duration of symptoms at the time
of diagnosis is 3-4 months bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to
presentation ndash Pain can be spinal or radicular
bull Constitutional symptoms include fever and weight loss
bull 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
bull 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
bull 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 diseasebull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic
bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy
paradiscal margins amp reappearance and minrralization of tuberculae
bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block
formation
Lab Studies
bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive
bull Erythrocyte sedimentation rate (ESR) may be markedly elevated
bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent
bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test
bull IFN- Release Assays (IGRAs)bull 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
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
bull Three percent are suffering from skeletal TBbull 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
Regional Distribution 1 Cervical 12
2 cervicodorsal 5
3 Dorsal 42
4 Dorsolumbar 12
5 Lumbar 26
6 Lumbosacral 3
Pathophysiology
bull Pott disease is usually secondary to an extraspinal source of infection
bull The basic lesion is a combination of osteomyelitis and arthritis
bull The area usually affected is the anterior aspect of the vertebral body adjacent to the subchondral plate
bull 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
bull 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
bull 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
bull The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes
bull 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
bull 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
bull These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion
bull 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
bull Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels
The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion
bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a
bull atypical form characterized by spondylitis without disk involvement (SPwD)
bull 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 ndashlongitudinal lig Aneurysmal phenomenon
5 Synovitis in post facet
History
bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits
abscesses or sinus tractsbull The reported average duration of symptoms at the time
of diagnosis is 3-4 months bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to
presentation ndash Pain can be spinal or radicular
bull Constitutional symptoms include fever and weight loss
bull 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
bull 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
bull 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 diseasebull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic
bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy
paradiscal margins amp reappearance and minrralization of tuberculae
bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block
formation
Lab Studies
bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive
bull Erythrocyte sedimentation rate (ESR) may be markedly elevated
bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent
bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test
bull IFN- Release Assays (IGRAs)bull 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
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
Regional Distribution 1 Cervical 12
2 cervicodorsal 5
3 Dorsal 42
4 Dorsolumbar 12
5 Lumbar 26
6 Lumbosacral 3
Pathophysiology
bull Pott disease is usually secondary to an extraspinal source of infection
bull The basic lesion is a combination of osteomyelitis and arthritis
bull The area usually affected is the anterior aspect of the vertebral body adjacent to the subchondral plate
bull 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
bull 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
bull 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
bull The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes
bull 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
bull 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
bull These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion
bull 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
bull Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels
The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion
bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a
bull atypical form characterized by spondylitis without disk involvement (SPwD)
bull 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 ndashlongitudinal lig Aneurysmal phenomenon
5 Synovitis in post facet
History
bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits
abscesses or sinus tractsbull The reported average duration of symptoms at the time
of diagnosis is 3-4 months bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to
presentation ndash Pain can be spinal or radicular
bull Constitutional symptoms include fever and weight loss
bull 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
bull 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
bull 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 diseasebull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic
bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy
paradiscal margins amp reappearance and minrralization of tuberculae
bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block
formation
Lab Studies
bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive
bull Erythrocyte sedimentation rate (ESR) may be markedly elevated
bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent
bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test
bull IFN- Release Assays (IGRAs)bull 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
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
Pathophysiology
bull Pott disease is usually secondary to an extraspinal source of infection
bull The basic lesion is a combination of osteomyelitis and arthritis
bull The area usually affected is the anterior aspect of the vertebral body adjacent to the subchondral plate
bull 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
bull 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
bull 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
bull The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes
bull 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
bull 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
bull These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion
bull 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
bull Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels
The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion
bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a
bull atypical form characterized by spondylitis without disk involvement (SPwD)
bull 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 ndashlongitudinal lig Aneurysmal phenomenon
5 Synovitis in post facet
History
bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits
abscesses or sinus tractsbull The reported average duration of symptoms at the time
of diagnosis is 3-4 months bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to
presentation ndash Pain can be spinal or radicular
bull Constitutional symptoms include fever and weight loss
bull 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
bull 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
bull 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 diseasebull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic
bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy
paradiscal margins amp reappearance and minrralization of tuberculae
bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block
formation
Lab Studies
bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive
bull Erythrocyte sedimentation rate (ESR) may be markedly elevated
bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent
bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test
bull IFN- Release Assays (IGRAs)bull 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
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
bull 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
bull 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
bull The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes
bull 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
bull 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
bull These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion
bull 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
bull Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels
The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion
bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a
bull atypical form characterized by spondylitis without disk involvement (SPwD)
bull 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 ndashlongitudinal lig Aneurysmal phenomenon
5 Synovitis in post facet
History
bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits
abscesses or sinus tractsbull The reported average duration of symptoms at the time
of diagnosis is 3-4 months bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to
presentation ndash Pain can be spinal or radicular
bull Constitutional symptoms include fever and weight loss
bull 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
bull 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
bull 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 diseasebull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic
bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy
paradiscal margins amp reappearance and minrralization of tuberculae
bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block
formation
Lab Studies
bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive
bull Erythrocyte sedimentation rate (ESR) may be markedly elevated
bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent
bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test
bull IFN- Release Assays (IGRAs)bull 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
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
bull 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
bull These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion
bull 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
bull Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels
The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion
bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a
bull atypical form characterized by spondylitis without disk involvement (SPwD)
bull 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 ndashlongitudinal lig Aneurysmal phenomenon
5 Synovitis in post facet
History
bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits
abscesses or sinus tractsbull The reported average duration of symptoms at the time
of diagnosis is 3-4 months bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to
presentation ndash Pain can be spinal or radicular
bull Constitutional symptoms include fever and weight loss
bull 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
bull 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
bull 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 diseasebull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic
bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy
paradiscal margins amp reappearance and minrralization of tuberculae
bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block
formation
Lab Studies
bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive
bull Erythrocyte sedimentation rate (ESR) may be markedly elevated
bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent
bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test
bull IFN- Release Assays (IGRAs)bull 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
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
The lesion could bebull Florid - invasive and destructive lesion bull Non destructivebull Encysted disease bull Carries sicca bull Hypertrophied bull Periosteal lesion
bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a
bull atypical form characterized by spondylitis without disk involvement (SPwD)
bull 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 ndashlongitudinal lig Aneurysmal phenomenon
5 Synovitis in post facet
History
bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits
abscesses or sinus tractsbull The reported average duration of symptoms at the time
of diagnosis is 3-4 months bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to
presentation ndash Pain can be spinal or radicular
bull Constitutional symptoms include fever and weight loss
bull 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
bull 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
bull 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 diseasebull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic
bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy
paradiscal margins amp reappearance and minrralization of tuberculae
bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block
formation
Lab Studies
bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive
bull Erythrocyte sedimentation rate (ESR) may be markedly elevated
bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent
bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test
bull IFN- Release Assays (IGRAs)bull 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
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
bull Recently two distinct patterns of spinal TB can be identified the classic form called spondylodiscitis (SPD) a
bull atypical form characterized by spondylitis without disk involvement (SPwD)
bull 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 ndashlongitudinal lig Aneurysmal phenomenon
5 Synovitis in post facet
History
bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits
abscesses or sinus tractsbull The reported average duration of symptoms at the time
of diagnosis is 3-4 months bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to
presentation ndash Pain can be spinal or radicular
bull Constitutional symptoms include fever and weight loss
bull 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
bull 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
bull 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 diseasebull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic
bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy
paradiscal margins amp reappearance and minrralization of tuberculae
bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block
formation
Lab Studies
bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive
bull Erythrocyte sedimentation rate (ESR) may be markedly elevated
bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent
bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test
bull IFN- Release Assays (IGRAs)bull 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
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
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 ndashlongitudinal lig Aneurysmal phenomenon
5 Synovitis in post facet
History
bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits
abscesses or sinus tractsbull The reported average duration of symptoms at the time
of diagnosis is 3-4 months bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to
presentation ndash Pain can be spinal or radicular
bull Constitutional symptoms include fever and weight loss
bull 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
bull 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
bull 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 diseasebull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic
bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy
paradiscal margins amp reappearance and minrralization of tuberculae
bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block
formation
Lab Studies
bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive
bull Erythrocyte sedimentation rate (ESR) may be markedly elevated
bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent
bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test
bull IFN- Release Assays (IGRAs)bull 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
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
History
bull Presentation depends on the following ndash Stage of disease ndash Site ndash Presence of complications such as neurologic deficits
abscesses or sinus tractsbull The reported average duration of symptoms at the time
of diagnosis is 3-4 months bull Back pain is the earliest and most common symptom ndash Patients have usually had back pain for weeks prior to
presentation ndash Pain can be spinal or radicular
bull Constitutional symptoms include fever and weight loss
bull 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
bull 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
bull 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 diseasebull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic
bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy
paradiscal margins amp reappearance and minrralization of tuberculae
bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block
formation
Lab Studies
bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive
bull Erythrocyte sedimentation rate (ESR) may be markedly elevated
bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent
bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test
bull IFN- Release Assays (IGRAs)bull 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
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
bull 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
bull 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
bull 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 diseasebull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic
bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy
paradiscal margins amp reappearance and minrralization of tuberculae
bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block
formation
Lab Studies
bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive
bull Erythrocyte sedimentation rate (ESR) may be markedly elevated
bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent
bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test
bull IFN- Release Assays (IGRAs)bull 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
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
Natural course of diseasebull 53 died within 10 yrs of onsetbull Early stage of healingndash focus surrounded by sclerotic
bone Ivory vertebrabull Early radiological sign of healingndash sharpening of fuzzy
paradiscal margins amp reappearance and minrralization of tuberculae
bull Several vertebrae destroyedndash fibrous tissuebull Disc space destroyed bony ankylosisbone block
formation
Lab Studies
bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive
bull Erythrocyte sedimentation rate (ESR) may be markedly elevated
bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent
bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test
bull IFN- Release Assays (IGRAs)bull 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
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
Lab Studies
bull Tuberculin skin test (purified protein derivative [PPD]) demonstrates a positive finding in 84-95 of patients who are nonndashHIV-positive
bull Erythrocyte sedimentation rate (ESR) may be markedly elevated
bull The enzyme-linked immunosorbent assay (ELISA) has a reported sensitivity of 60 to 80 per cent
bull Culture ndash LJ mediumBacTecbull The polymerase chain reaction bull A brucella complement fixation test
bull IFN- Release Assays (IGRAs)bull 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
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
bull IFN- Release Assays (IGRAs)bull 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
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
bull Microbiology studies to confirm diagnosis positive in only about 50 of the cases
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
X Ray appearances
bull Lytic destruction of anterior portion of vertebral body bull Increased anterior wedging bull Collapse of vertebral body bull Reactive sclerosis on a progressive lytic process bull Enlarged psoas shadow with or without calcificationbull Vertebral end plates are osteoporotic bull Intervertebral disks may be shrunk or destroyed bull Vertebral bodies show variable degrees of destruction bull Fusiform paravertebral shadows suggest abscess
formation bull Bone lesions may occur at more than one level
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
X Ray appearances
Discovertebral lesions detected in 93 of patients bull Localized fluffy osseous destruction with surrounding
osteoporosis is the earliest signs bull concentric collapse and may look like AVN bull Local lytic lesion may cause problem of diagnosis from
neoplasic lesion bull destruction of adjacent vertebrae Konstram (K) angle
appears and shows the progress on follow up bull 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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
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 T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
X-ray of the spine in a child showing complete destruction of T12 and L1 vertebral bodies leaving only the pedicles
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
Clinico-radiological Classification
stage features Usual duration
I Pre-destructive
Straightening spasm hyperemia in scinti
lt3 mo
II Early-destructive
Diminished space paradiscal erosion Knuckle lt10
2-4 mo
III Mild kyphos 2-3 verte k10-30 3-9 mo
IV Moderate kyphos
gt3 verte K30-60 6-24 mo
V Severe kyphos
gt3 verte Kgt60 gt2 years
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
CT scanning
bull CT scanning provides much better bony detail of irregular lytic lesions sclerosis disk collapse and disruption of bone circumference
bull Low-contrast resolution provides a better assessment of soft tissue particularly in epidural and paraspinal areas
bull It detects early lesions and is more effective for defining the shape and calcification of soft tissue abscesses
bull In contrast to pyogenic disease calcification is common in tuberculous lesions
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
MRI
bull MRI is the criterion standard for evaluating disk space infection and osteomyelitis of the spine
bull 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
bull contrast-enhanced MRI appears to be important in the differentiation of these two types of spondylitis
bull most effective for demonstrating neural compression
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
Myelographybull Spinal tumor syndromebull Multiple vertebral lesionsbull Patients not recovered after
decompression 1 Block present second decompression2 Block not present intrinsic damage
1Ischemic infarction 2Interstitial gliosis
3atrophy 4 tuberculous myelitis
5Myelomalacia
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
Differentials 1 Pyogenic infections2 Typhoid spine3 Brucella Spondylitis4 Mycotic Spondylitis5 Syphilitic6 Tumorous condition7 Primary malignant tumor 8 Multiple Myeloma9 Lymphomas10Secondary11Histocytosis-X12Spinal Osteochondrosis13Spondylolisthesis14Hydatid disease
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
Complications of tuberculosis
1 Paraplegia 2 Cold abscess3 Sinuses4 Secondary infection5 Amyloid disease6 Fatality
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
Tb spine with PARAPLEGIA
bull INCIDENCE 10-30bull Dorsal spine (MC)bull Motor functions affected before greater than
sensorybull Sense of position amp vibration last to disappear
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
Patho of Tuberculoses Paraplegia1 Inflammatory Edema ndashvascular stasistoxin2 Extradural Mass ndash Tuberculous ostetis+
abscess3 Bony Disorder ndash Sequestra Internal Gibbus4 Meningeal changes ndash lsquodura as rule not
involvedrsquoExtradural grnulation --
contract cicatrization peridural fibrosis paraplegia
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
5 Infarction of spinal cord - Ant spinal artery
EndarteritisPeriarteritisThrombosis6 Changes in Spinal cord-
MyelomalacicSyringomyelic changeAtrophy ndashupto 50decrease in diameter -good functions
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
Seddonrsquos Classificationbull
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 ndash 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
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
Evolution of treatment Pre-antitubercular erabull Artificial abscess- Pott in 1779bull Laminectomy amp laminotomy chipault(1896
)bull Costo-transversectomy Menard in 1896bull Posterior mediastinotomybull Calves operation 1917bull Lateral rhachiotomy of carpener 1933bull Anterlateral decompression of Dottamp
Alexander1947
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
BASIC PRINCIPLES OFMANAGEMENT
10487291048729
bull Early diagnosisbull Expeditious medical treatmentbull Aggressive surgical approachbull Prevent deformitybull Expect good outcome
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
bull 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 regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
What is Middle path regimebull Admission rest in bed bull Chemotherapy bull X-ray amp ESR once in 3 monthsbull MRI CT at 6 months interval for 2 yearsbull Craniovertebral cervicodorsal lumbosacralamp
sacroiliac jointsbull Gradual mobilizationbull 3-9 weeks- back extention exercise 5-10 min 3-4
timesbull Spinal brace--- 18 months-2 years
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
bull Abcesses ndash aspirate near surface bull Instille 1gm Streptomycin +- INH in solbull Sinus heals 6-12 weeksbull Neural complications if responds 3-4 weeks -
surgery unnecssarybull Excisional surgery for posterior spinal diseasebull Operative debridement for patients ndashif no arrest
after 3-6 months- spinal arthrodesis (recommended)
bull Post op--Spinal brace--- 18 months-2 years
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
Drugs in middle path
phase duration drug
Intensive 5-6 months
INH 300-400mg
Rifampicin ofloxacin400-600mg streptomycin
Continuation
7-8 months
-do 3-4mth Pyrazinamide 1500mg4-5mth Rifampicin
Prophylactic
4-5 months
-do Ethambutol 1200mg
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
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 abscessesneurological
signsamp difficulty in deglutitionamp respiration6 Advanced cases- Sphincter involvement
flaccid paralysisSevere flexor spasms
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
Other indicationsbull Recurrent paraplegiabull Painful paraplegiandash dt root compressionetcbull Posterior spinal disease--involving the post
elements of vertbbull Spinal tumor syndrome resulting in cord
compressionbull Rapid onset paraplegia due to thrombosistrauma
etcbull Severe paraplegiabull Secondary to cervical disease and bull cauda equina paralysis
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
1 Decompression +- fusion
Failed responseToo advanced
2 Debridement+- fusion
Failed response after 3-6 monthsDoubtful diagnosisInstability
3 Debridement +-DECOMP+- fusion
Recrudescence of disease
4 Debridement+- fusion
Prevent severe Kyphosis
5 Anterior transpostion
Severe Kyphosis +neural deficit
6 Laminectomy secondary stenosis posterior disease
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
APPROACH1 Cervical spine ndash Anterior retropharyngeal
(smith-Robinsonrsquos) Anterior approach ndash AnteriorMedial
border of sternocleidomastoid2 Thoracic spine (T1 to L1) ndash
1 Transthoraccic transpleural 2 Anterolateral decompression(T2 ndash
L1)3 Lumbar spine ndash Anterolateral(Lumbovertebrotomy) Extraperitoneal Ant approach
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
DYNAMIC CAGE GovenderampPrabhoo
SYNTHES PLATE WITHSPACER
SYNTHES PLATE WITHSPACER
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