dr. Rajasekaran dr. Rajasekaran dr. Rajasekaran s
Management of Spinal TB
Chemotherapy
Multidrug antitubercular treatment (ATT) is the mainstay of
treatment in both complicated and uncomplicated TB.65-68
Multidrug ATT is essential, as varying categories of bacilli
exist in a lesion. They may exist as intracellular, extracellular,
dormant, or rapidly multiplying forms and each has different
growth and metabolic properties.69 In addition, multidrug ATT
reduces instances of drug resistance.70 The duration of chemotherapy for spinal TB has been long debated, and the WHO
recommends 9 months of treatment where 4 drugs—isoniazid,
nature in underprivileged sections of developing countries,
TB is now an international concern, as it has its footprints
spread all over the world due to the global migration Epidemiology
The incidence of extrapulmonary TB (EPTB) is low at 3%, but
there has been no significant reduction in incidence of EPTB
when compared to pulmonary TB (PTB).7 Skeletal TB (STB)
contributes to around 10% of EPTB, and spinal TB has been the Clinical Presentation of Spinal TB
The clinical picture of spinal TB is extremely variegated.
Spinal TB usually is insidious in onset and the disease progresses at a slow pace.22 The diagnostic period, since onset
of symptoms, may vary from 2 weeks to several years. The
manifestation of spinal TB depends on the severity and duration of the disease, site of the disease, and the presence of
complications such as abscess, sinuses, deformity, and neurological deficit.23 Spinal TB can either be complicated or
uncomplicated. In complicated TB, patients present with deformity, instability, and neurological deficit. Uncomplicated
spinal TB is one in which diagnosis is made prior to development of such complication Pathophysiology of Spinal TB
TB is caused by Mycobacterium tuberculosis complex, which
has around 60 species. Among them only Mycobacterium
tuberculosis (the most common), Mycobacterium bovis, Mycobacterium microti, and Mycobacterium africanum are known to
affect humans.16 It is a slow-growing fastidious, aerobic bacillus. The primary site of infections can be in the lungs, lymph
nodes of the mediastinum, mesentery, gastrointestinal tract,
genitourinary system, or any other viscera. The bacilli tend to
remain dormant for prolonged periods and multiplies every 15
to 20 hours in aerobic conditions whenever favorable. Spinal
infection is always secondary and is caused by hematogenous
dissemination of the bacillus from a primary focus.17,Cold Abscess
Cold abscess lacks inflammatory features and initially forms in
the infective focus. Later, it takes the path of least resistance
along the natural fascial and neurovascular planes as depic
dr. Rajasekaran dr. Rajasekaran dr. Rajasekaran s
Management of Spinal TB
Chemotherapy
Multidrug antitubercular treatment (ATT) is the mainstay of
treatment in both complicated and uncomplicated TB.65-68
Multidrug ATT is essential, as varying categories of bacilli
exist in a lesion. They may exist as intracellular, extracellular,
dormant, or rapidly multiplying forms and each has different
growth and metabolic properties.69 In addition, multidrug ATT
reduces instances of drug resistance.70 The duration of chemotherapy for spinal TB has been long debated, and the WHO
recommends 9 months of treatment where 4 drugs—isoniazid,
nature in underprivileged sections of developing countries,
TB is now an international concern, as it has its footprints
spread all over the world due to the global migration Epidemiology
The incidence of extrapulmonary TB (EPTB) is low at 3%, but
there has been no significant reduction in incidence of EPTB
when compared to pulmonary TB (PTB).7 Skeletal TB (STB)
contributes to around 10% of EPTB, and spinal TB has been the Clinical Presentation of Spinal TB
The clinical picture of spinal TB is extremely variegated.
Spinal TB usually is insidious in onset and the disease progresses at a slow pace.22 The diagnostic period, since onset
of symptoms, may vary from 2 weeks to several years. The
manifestation of spinal TB depends on the severity and duration of the disease, site of the disease, and the presence of
complications such as abscess, sinuses, deformity, and neurological deficit.23 Spinal TB can either be complicated or
uncomplicated. In complicated TB, patients present with deformity, instability, and neurological deficit. Uncomplicated
spinal TB is one in which diagnosis is made prior to development of such complication Pathophysiology of Spinal TB
TB is caused by Mycobacterium tuberculosis complex, which
has around 60 species. Among them only Mycobacterium
tuberculosis (the most common), Mycobacterium bovis, Mycobacterium microti, and Mycobacterium africanum are known to
affect humans.16 It is a slow-growing fastidious, aerobic bacillus. The primary site of infections can be in the lungs, lymph
nodes of the mediastinum, mesentery, gastrointestinal tract,
genitourinary system, or any other viscera. The bacilli tend to
remain dormant for prolonged periods and multiplies every 15
to 20 hours in aerobic conditions whenever favorable. Spinal
infection is always secondary and is caused by hematogenous
dissemination of the bacillus from a primary focus.17,Cold Abscess
Cold abscess lacks inflammatory features and initially forms in
the infective focus. Later, it takes the path of least resistance
along the natural fascial and neurovascular planes as depic
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...
POTT’S SPINE-1676656384.pptx
1.
2. POTT’S SPINE
Tubercular spondylitis has been documented
in ancient mummies from Egypt and Peru
and is one of the oldest demonstrated
disease.Percival Pott presented the classic
description of spinal TB in 1779.
Spinal TB constitutes about 50% of all cases
of osteoarticular TB.
MC site: Lower thoracic and lumber region
followed by middle thoracic and cervical
vertebrae.
5. ANATOMY
Vertebre develops from the sclerotome on
either side of notochord
Each pair of sclerotome (common blood
supply) form Lower half of one vertebra
and upper half of one below it along with
intervening disc.
Therefore ,infections via the arteries
involve the embryological section.
6. SPINAL TUBERCULOSIS
Pathology
• Spinal tuberculosis is usually a secondary infection from
a primary site in the lung or genitourinary system.
• Spread to the spine is hematogenous in most instances.
• Delayed hypersensitivity immune reaction.
• Initially : a pre-pus inflammatory reaction with
Langerhan’s giant cells, epithelioid cells, and
ymphocytes.
• The granulation tissue proliferates, producing thrombosis
of vessels.
7. SPINAL TUBERCULOSIS
• Tissue necrosis and breakdown of inflammatory cells
result in a paraspinal abscess.
• The pus may be localized, or it may track along tissue
planes.
• Progressive necrosis of bone leads to a kyphotic
deformity.
• Typically, the infection begins in the anterior aspect of the
vertebral body adjacent to the disk.
8. • The infection then spreads to the adjacent vertebral
bodies under the longitudinal ligaments.
• Noncontiguous (skip) lesions are also seen
occasionally
9. Pathogenesis Of Spinal
Tuberculosis
Five stages by Kumar KA (1988)
Stage
Stage
Stage
of
of
of
Implantation
early destruction
advanced destruction and
collapse
Stage of
Stage of
neurological involvement
residual deformity
11. PARADISCAL
Commonest type
Spread through arterial supply
Bacteria lodge in the contiguous areas of two
adjacent vertebrae granulomatous
inflammation leading to erosion of vertebral
margins loss of nutrition of intervertebral
disc Disc degeneration
When the intervertebral discs have been
completely destroyed,the adjacent bodies
fuse with each other.
12.
13. CENTRAL LESIONS
Body of single vertebra is affected.
Starts in the centre of the vertebral body.
Infection at this site probably reaches through
Batson’s venous or branches of post.vertebral
artry.
Lytic area develops in the centre of vertebral body
leading to balooning of vertebral body
mimicking tumour
Later stages-concentric collapse resembling
Verebra Plana.
Disc space is not/minimally affected
14.
15.
16.
17. Anterior lesions— Infection starts in the anterior
part of vertebral body and spreads under
the ant. Longitudinal ligament.
Post/Appendiceal— Pedicle,lamina,spinous
process or transverse process of
vertebra are affected.
18.
19.
20. CLINICAL FEATURES
Constitutional symptoms,such as fever, night sweats,loss of
weight and appetite may occur before symptoms related to
spine.
1. Pain-can be Localised to the site(MC early
symptoms)
Radicular
worsen with activity and at night(night
cries)
2. Stiffness-Protective mechanism of body where paravertebral
muscle go into spasm to prevent movement at the affected
vertebra.
21. 3. Cold abcess- Patient may present the first time with
swelling(cold abcess) or due to its compression
effects:-
Retropharyngeal abscess --Dysphagia,dyspnea,
Hoarseness of voice
Mediastinal abscess --Dysphagia
Psoas abscess -- Flexion deformity of
hip
-No usual signs of inflammation like heat ,redness
etc.
-Follows paths of least resistance along facial
planes,blood vassels &nerves.
22. PRESENTATION OF COLD ABSCESSES
FROM DIFFERENT REGIONS OF SPINE
Cervical spine- Exudate collects behind prevertebral
facia and may protrude as Retropharyngeal abscess, It
may track down in mediastinum to enter into
trachea,esophagus or pleural cavity.It may spread
lateraly into sterno-cleido mastoid and form abscess in
neck.
Thoracic spine- It may confined locally and may appear
on X-ray as fusiform or bulbous paravertebral abscess
.It can compress spinal cord or penetrate the
ant.longitudinal ligament to form a mediastinal
abscess or pass downward through medial arcuate
ligament to form lumber abcess.
Lumber spine- Most commonly enters the psoas
sheathPsoas abscess,also abscess in scarpa’s
triangle,medial aspect of thigh
23. 4.Fallacious history of trauma- Trauma may draw
attention to a pre-existing lesion or may activate a
latent tubercular focus
5. Paraplegia-Rarely it is the presenting symptom.
6. Wedging :-
Dorsal spine : Line of weight bearing passes ant to
vertebrae.Ant wedging occurs.In late stages
leading to
kyphotic deformity
Cervical and lumber spine : Wedging is less due
lordotic curvature
7. Gibbus-If patient presents late
24. EXAMINATION
1. Gait- Patient walks with short steps to avoid
jerking the spine.In TB of cervical
spine,patient often supports his head with
both hands under the chin and twists his
whole body in order to look sideways.
2. Attitude and deformity :-
Cervical spine : Stiff,straight neck
Thoracic spine : Kyphus or gibbus,walks
very
carefully
Lumber spine : Loss of lumber lordosis
25. 3. Paravertebral swelling- Superficial cold abcess may
present as fullness or swelling on the back,along
the chest wall, usually fluctuant. It is important to
look for cold abcesses in not so obvious
locations,depending upon the region of spine
involved.
4. Neurological Examination- To determine if there is
any neurological compression and to determine
level and severity of neurological compression
5. General examination- For any active or healed
lesion,for any other systemic illnesses
like,diabetes,HT,jaundice etc.
27. INVESTIGATION
Radiological examination :-
1. Xray spine-AP,Lateral
2. CXR-for primary focus
3. Xray abd-KUB,if psoas abcess is
suspected or to find out Primary in abd.
The classic roentgen triad in spinal tuberculosis is
primary vertebral lesion, disc space narrowing and
paravertebral abscess.
On an avg. 2.5 to 3.8 vertebrae are involved
30. Radiographs: General Features
Features of Pott’s on radiograph include
•
–
–
–
–
–
–
–
Signs of infection with lytic lucencies in anterior portion of vertebrae
Disk space narrowing
Erosions of the endplate
Sclerosis resulting from chronic infection
Compression fracture
Continuous vertebral body collapse
Kyphosis; gibbous (severe kyphosis)
• Atypical features
–
–
–
–
–
Soft tissue swelling from paraspinal abscesses, +/‐ calcification
Involvement of only one vertebral body
Involvement of several vertebral bodies without intervertebral discitis
Bowing of rib cage secondary to collapse of multiple vertebral bodies
Destruction of lateral or posterior aspects of vertebral bodies
31. 1. Paradiscal : Reduction in disc space- Initialy
there is demineralization with indistinct bony
margins-gradually disc space narrowing
occurs.The disc space may eventualy
disappear leading to wedging.
Lateral X-ray is better for evaluation of disc
space.
Takes 3-5 months for bony destruction to
become visible on X-ray
More than 30 % of mineral must be removed
from bone for a radiolucent lesion to be
visible
32. Tuberculous spondylitis. Lateral radiograph demonstrates
obliteration of the disk space (straight arrow) with destruction of
the adjacent end plates (curved arrow) and anterior wedging.
33. There is narrowing of the disk space at L4-5,
with end plates indistinctly outlined. CT
section through the disk space clearly
shows destructive changes of the disk and
vertebral end plate characteristic of
infection
34. RADIOLOGICAL EXAMINATION
2. Central : Lytic area in the centre of vertebral body which
enlarges and baloons out like tumour.Disc space is
preserved.
3. Anterior : Shallow excavation on anterior or lateral
surface of vertebral body.
4.TB of posterior elements is usually not detected in early
stages in radiographs.
Late Stages --Kyphotic deformity,lateral shift and
scoliosis,if one side of vertebrae is completely destroyed
Hemivertebrae
Signs of healing—bone density improves,sclerosis, fusion
of contiguous vertebrae.
Skip lesions as involvement of non contiguous vertebrae (7
– 10 % cases).
35. X-ray dorsolumbar spine showing vertebra plana of T10 vertebra.
Disc space is well maintained.
36. Subligamentous spread of spinal tuberculosis. Lateral radiograph
demonstrates erosion of the anterior margin of the vertebral
body (arrow) caused by an adjacent soft-tissue abscess.
37. Destruction of the right side of the vertebral body and the neural arch, with
the remainder of the body maintaining its shape. The lower disc space is
narrowed on the right side; the upper space is almost normal and there is a
small paravertebral abscess.
38.
39. Evidence of cold abcess on X-rays
Paravertebral abcess : Paravertebral soft tissue
shadow corresponding to the site of affected
vertebrae in AP view can
Fusiform [bird nest abcess] : L>W,seen in dorsal
spine area.
Globular or tense : W>L,pus under pressure a/w
paraplegia
Widened mediastinum : Abscess from dorsal
spine may present as widened mediastinum
40. Aneurysmal phenomena : Concave erosions
along the margins of vertebral bodies
produced by long standing tense
paravertebral abcess,usually in dorsal spine
Retropharyngeal abcess : In cervical spine
TB,seen on lateral view : increase in soft
tissue thickness (>4mm) in front of C3
vertebral body.
Psoas Abcess : In dorso-lumber and lumber
TB,psoas shadow on X-ray of abd may
show a bulge.
43. CT SCAN
CT demonstrates abnormalities earlier than plain radiography. It is of great
value in the demonstration small paravertebral abscess,not otherwise
seen on plain X-ray or any calcification within the cold abscess or
visualizing epidural lesions containing bone fragments.
44. A CT scan showing destruction of the neural arch on both sides,
as well as of the vertebral body. Arrows, anterior spinal abscess
45.
46. Tuberculous spondylitis. Axial
CT scan demonstrates lytic
destruction of the vertebral
body (black arrow) with an
adjoining soft-tissue abscess
(white arrow).
Calcified psoas abscess.
Axial CT scan demonstrates
bilateral tuberculous psoas
abscesses with peripheral
calcification (arrows).
47. Current Trends In Imaging
ROLE OF CT SCAN
CT IMAGING shows focus of
-
-
-
-
-
Bone
Early
Level
Infection
Erosions
Of Lesion
Amount Of Bone Destruction
Posterior Element Lesions
48. CT: Features
Features on CT
• Soft tissue findings
‐ Abscess with calcification is diagnostic of spinal TB; CT is
excellent modality to visualize soft tissue calcifications
• Pattern and severity of bony destruction
‐ Pattern of vertebral body destruction‐ framentary, osteolytic,
localized and sclerotic, and subperiosteal
• Used to guide needle in percutaneous needle biopsy of
paraspinal abscess
49. MRIInvestigation of choice to evaluate the type and
extent of compression of cord,to know the
spread of disease under the anterior or
post.ligament, most effective to demonstrate
neural compression,helps to differentiate
between TB and pyogenic infection :-
TB – Thin and smooth enhancement of the
abcess wall
Pyogenic – Thick and irregular
MRI is more sensitive than x-ray and more specific
than CT in the diagnosis of spinal tuberculosis.
50. CORD CHANGES
Conventional radiograph-no information
CT –inadequate assesment
MRI -gives invaluable information
Cord oedema or focal myelomalacia is seen as hyperintense signal and It can
also diagnose extraosseous extradural granuloma.
51. Current Trends In Imaging
ROLE OF MRI SCAN
MR IMAGING IDENTIFIES
-
-
Cord compression / changes
Soft tissue shadows and
intraosseus abscesses
Skip lesions
-
- Sub ligamentous spread of
infection and epidural extension
The Imaging Method Of Choice
-
52. MRI: Features
•
•
•
Highly sensitive and specific for
Provides early detection
spinal TB
Best to distinguish exact
tissue involvement
extent of spinal cord and soft
• Features
–
–
–
Edema of vertebrae and disk space
Signs of spinal compromise i.e. cord compression
Note: Poorly visualizes calcification in abscesses
53. MRI: Spinal Cord Involvement
PACS, BIDMC
Sagittal T2W (Images 1-3)and axial T1W (Image 4)
High intensity activity in T12 to L3 vertebrae indicative of infection (*) (*). Complete destruction of
vertebral bodies with osseous retropulsion into the spinal canal, causing cauda equina (*). On axial
view, note destruction of vertebral body with loss of circular shape(*).
4
3
2
1
55. ‘Gibbus formation’ in the thoraco-lumbar region of a patient with spinal
tuberculosis (left). The magnetic resonance shows spinal tuberculosis at
T10–T12. Spinal tuberculosis causes the destruction, collapse of vertebrae
and angulation of vertebral column
56. X-ray of cervical region which shows spinal tuberculosis of cervical six
to seven vertebrae and a retropharyngeal abscess (left). T1-weighted
image of an MRI of same patient, which shows destruction of C6–C7
vertebrae
59. Current Trends In Imaging
ROLE OF BONE SCAN
Helps in detection of
early lesions when
radiologically normal
Helpful in diagnosing
skip lesions/ involvement
of other bones
95% sensitivity
61. MYELOGRAPHY
To determine the level of obstruction
May be indicated in cases with ‘spinal tumour syndrom’
In cases of multiple vertebral lesion
When pt has not recovered after decompression
62. FNAC : Especially of cold abcess,ZN Stain,C/S
Biopsy : May be required in cases of doubtful
diagnosis
Other Investigation : To support the diag:-
Increased ESR,Decreased Hb,relative
lymphocytosis,Mantoux
63. The Sero-immunological and
Biochemical Investigations
POLYMERASE CHAIN REACTION
- Simple and widely used
- Highly sensitive but less specific
ROLE OF IgM AND OTHERS
- Low specificity and sensitivity
- Of low predictive value in spinal TB
extra-pulmonary diseases
and other
65. Even though, classical clinical and
radiological features have been described
in the literature, spinal tuberculosis does
mimic other lesions
Can be
MISSED, MISTAKEN or MISDIAGNOSED
69. TREATMENT
Before availability of ATT,mortality rate was 30
% or severe crippling deformities
Aim of treatment is to achieve healing of
disease & to prevent,detect early and
promptly any complication like paraplegia
Rest: Bed rest for pain relief and to prevent
further collapse and dislocation of diseased
vertebrae.in children body cast is used.For
cervical spineMinerva jacket&coller
70. Building up of patient’s resistance : High protein diet.
ATT : This remains the cornstone of management,
completed by rest,nutritional support and splinting,
as necessary.However, there is difference of opinion
reg.the duration of drug therapy.Short course
chemotherapy for nine months has shown good
results in patients with disease coused by
succeptible microorganisms.
Antibiotics : For persistently draining sinuses which
get secondary infection.
Bed soar care and to treat other comorbid conditions.
71. Mobilisation : Gradual as improvement begins
sit & walk,the spine is supported with
coller(cervical),brace (dorso-lumber spine)
Cold abcesses may subside with ATT,if
present superficially may need
aspration(antigravity insertion of needle
through a zig-zag tract) or
evacuation(wound closed without a drain)
Sinuses: Mostly heal within 6-12 weeks.If no
improvement Excision of tract
72. Pott Disease: Treatment
•
•
Various imaging modalities are useful in determining extent of disease.
Treatment options then depend on the degree of spinal destruction.
Oguz et al.- http://www.springerlink.com.ezp-
prod1.hul.harvard.edu/content/h482j21x5548q078/fulltext.pdf
Most practicing
clinicians simply
define Pott’s as
EARLY or LATE
disease.
GATA Classification
73. Anti Tubercular Drugs
Specific anti-tuberculous drugs have
revolutionized the outcome of spinal
tuberculosis which is now considered
curable
to be
It has to be realized that surgical treatment
cannot replace chemotherapy
74. Anti Tubercular Drugs
One in 20 new cases of tuberculosis is
considered to be multidrug-resistant
Therefore, in spinal tuberculosis, 3 months
of intensive chemotherapy with 4 drugs
followed by 12-15 months of maintenance
therapy with two drugs is necessary
75. The Role of Empirical Treatment
Always an attempt should be made to prove the
diagnosis before therapy is initiated
However, young patients with classical clinico-
radiological features and high ESR may be
empirically started on ATT
If empirical therapy is initiated, meticulous
monitoring to ensure sustained improvement is
necessary
77. Controversial Surgeries
LAMINECTOMY
Is CONTRAINDICATED in spinal tuberculosis
because the disease is present anteriorly and by
doing a posterior decompression, the spine
becomes completely unstable
It is only indicated in cases of posterior element
disease and spinal tumour syndrome
81. Limited Surgeries In
Tuberculosis of Spine
COSTO-
TRANSVERSECTOMY
Excision of portion of
a rib and the
articulating
transverse process
82. Conventional Limited Surgeries
ANTERO-LATERAL
DECOMPRESSION
First described by
Capener (1933).
Only operation in which
decompression of the
cord is performed by
removing the actual
cause of compression
Lateral
Rachotomy
by Capener
83. Conventional Radical Surgery
Hodgson et al.( 1960)
Developed the concept of
radical excision of the
diseased vertebral bodies
and their replacement by
bone grafts in all cases
spinal tuberculosis
of
84. INDICATION FOR SURGERY
1. Doubtful diagnosis where open biopsy is necessary
2. Failure to respond to ATT
3. Radiological evidence of progression of bony lesion or paraspinal
abcess shadow.
4. Imminent vertebral collapse.
5. Instability of spine and subluxation or dislocation of vertebral body.
86. Absolute Indications
Paraplegia during conservative treatment
Paraplegia worsening during treatment
Complete motor loss for 1 month despite
conservative treatment
Paraplegia with uncontrolled spasticity
Severe and rapid onset paraplegia
Severe flaccid paraplegia/ sensory loss
87. Relative indications Rare indications
Recurrent
paraplegia
Paraplegia
Painful and
paraplegia
Paraplegia
Posterior element
disease
Spinal tumor
syndrome
Severe cervical
lesion c paraplegia
1. 1.
in elderly
spastic
2. 2.
3.
3.
with
4.
complications (UTI) Cauda equinopathy
4.
88. Conventional Treatment: Tuli
Anti tubercular drugs are the most
important therapeutic measure
ATT must be continued for about 18
months( must include Isoniazide)
Patients with early disease can achieve
full clinical healing
Indications of surgery are mainly for
complications than for the disease control
89. The Middle Path Regimen of Tuli –
Surgical Indications
No neurological recovery after 4 weeks of ATT
Development of neurological deficit during the
course of chemotherapy
Recurrence of neurological deficit after initial
improvement
Worsening of neurological deficit while on
chemotherapy
Advanced case of neurological involvement
90. BRITISH MEDICAL RESEARCH COUNCIL
When appropriate facilities and expertise
are available radical surgeries have
definite advantage over non-operative
treatment
J Bone Joint Surg 60 (B), 61 (B) 64
However long term follow up of
surgeries showed considerable
(B) and 67
radical
loss of
(B)
correction and failure of the bone graft
leading to progression of kyphosis
Parthasarathy et al, Rajashekaran et al, Sundararaj
and Moon et al
et al
91. Current Trends In The Surgical
Management of Spinal Tuberculosis
Aims
Correction of kyphosis
Early fusion
Prevention of
Prevention of
progression of kyphosis
late onset paraplegia
92. Current Trends In The Surgical
Management of Spinal Tuberculosis
Debridement, anterior instrumentation and fusion
Anterior debridement and anterior column
reconstruction with bone grafting or CAGE
Debridement, posterior instrumentation and fusion
93. Anterior Debridement And
Reconstruction
Helps in neurological recovery and
produces early fusion
However, achieves only limited correction
of kyphosis and may not be able to
prevent progression
96. can be
Role of Posterior
Instrumentation And Fusion
Aggressive correction of
achieved
kyphosis
Prevents recurrence of kyphosis
Not beneficial without anterior
debridement and fusion
97. Combined Anterior Decompression And
Grafting / CAGE With Posterior
Bone
Instrumentation And Fusion
Single stage through
two approaches-
Combined anterior
and posterior
Single posterior
approach
98. Combined Anterior Decompression And
Bone Grafting / CAGE With Posterior
Instrumentation And Fusion
LIMITATIONS
-
-
Needs appropriate facilities and expertise
Intensive anaesthetic and postoperative
care
Secondary infection and implant failure
-
99.
100. PROCEDURES
1. Anteriolateral decompression with
interbody bone grafting.Grafts placed
anteriorly.
2. Costo transversectomy with dempression
3. Metallic implants& titanium cage filled with
cancellous bone when whole body is
destroyed.
4. Kyphotic deformity is prevented by ant
debridement,ant inerbody fusion&post
fusion.
101. Conclusion
Early diagnosis and treatment prevent
complications
Threat of MDR-TB
Intensive chemotherapy and
PCR / CT / MRI / Bone scan
diagnosis
More aggressive and radical
advocated:
monitoring
help in early
surgeries are
To
To
To
correct and prevent progression of kyphosis
achieve better healing and
lessen the chance of late onset paraplegia
103. Cold Abscess
Classic local signs of
acute infection (calor
rubor) not evoked
and
Pus accumulates
beneath anterior
longitudinal ligament and
extends along paths of
least resistance
104. Cold Abscess - cervical spine
Retropharyngeal abscess-
dysphagia, difficult phonation
Neck swelling- behind
sternomastoid in posterior
triangle of neck
Mediastinum
Axilla and cubital fossa (along
vessel and nerve)
Spinal canal
105. Cold Abscess - thoracic spine
Prevertebral-
posterior
mediastinum
Empyema- rupture
into pleura
Track along
intercostal nerves
106. Cold Abscess - thoracic spine
Extrapleural space-
Spreads laterally
Spinal canal- cord
compression
paraplegia
and
Bone School
107. Lower thoracic spine
Track down through lateral
arcuate ligament
Kidney bed
Anterior abdominal wall (via
nerve planes)
Medial arcuate ligament
Psoas sheath
Thigh swelling
108. Lumbar spine- Psoas Abscess
Psoas abscess can
travel along sciatic
nerve to pelvis,
gluteal region,
posterior aspect of
thigh and
region
popliteal
110. Mechanical Causes of
Progression of Kyphosis
Involvement of anterior
and middle column
produces progressive
kyphosis
Involvement of only the
middle or the posterior
column may not produce
kyphosis
Active continuous
growth of the posterior
column leads to
progression
111.
112.
113. Deformity
Knuckle deformity: Wedging
adjacent vertebral bodies
of 1 or 2
Gibbus deformity: wedge collapse of
2-3 vertebral bodies anteriorly
Round kyphus deformity:
more than 3 vertebrae
wedging of
114. Pott’s Paraplegia
Paraplegia is the result of
interference
conductivity
tracts of the
with the
of the pyramidal
spinal cord and is
most often associated with
the tuberculosis of the dorsal
spine (10 – 30 %)
It can be early or late onset
115. Why paraplegia is common
dorsal spine?
in
Commonest site for tuberculosis
Thoracic kyphosis helps in squeezing
products into the canal
Cord : canal ratio is smaller
Spinal cord terminates below L1
1.
the
2.
3.
4.
Ant. Lon. Lig. Is loose in thoracic spine
whereas in lumbar pus enters the psoas
5.
116. Pott’s Paraplegia
EARLY ONSET PARAPLEGIA
Occurs when disease is active
Usually within 2 years of onset of
disease
Usually prognosis is good
the
LATE ONSET PARAPLEGIA
Paraplegia of healed disease
Occurs 2 years after the onset of
disease
Has poor prognosis
the
117. Causes of early onset paraplegia
Seddon-1935
A) Inflammatory causes:
1. Abscess/ inflammatory tissue
caseating mass
and
2. Spinal tumor syndrome (circumscribed
tuberculous mass)
3. Posterior spinal disease
4. Infective thrombosis
118. Causes of early onset
Seddon-1935
paraplegia
B) Mechanical causes:
Pathological subluxation/
dislocation
1.
Cord compression by sequestra/
loose fragments of bone/
granulation tissue/ debris/ disc
2.
119. Causes of late onset
Seddon-1935
paraplegia
A) Inflammatory causes:
Continued activity or
reactivation
B)
1.
Mechanical causes:
Cord stretched over internal
gibbus/ transverse ridge
Vascular and dural fibrosis
2.
120. Causes of Paraplegia
Extrinsic causes
1)
a)
In active disease:
Abscess
2)
a)
In healed disease
Transverse ridge
internal gibbus
/
Granulation tissue
b)
Fibrosis of dura
Sequestered
and disc
Pathological
subluxation /
dislocation
bone b)
c)
d)
121. Causes of Paraplegia
Intrinsic causes:
Tubercular
Rare causes:
Infective thrombosis
of the cord
Spinal tumor
syndrome
1.
1.
involvement of the
dura/
cord
meninges/ 2.
122. Pott’s Paraplegia
Classification - Kumar & Tuli
Stage Clinical features
I Negligible Patient unaware of neural deficit, physician detects
plantar extensor and/or ankle clonus.
II Mild Patient aware of deficit but manages to walk with
support, clumsiness of gait.
III Moderate Paralysis in extension, sensory deficit less than 50%
IV Severe III + flexor spasm/ paralysis in flexion/ flaccid/ sensory
deficit more than 50%/ sphincters involved.
Bone School @ Bangalore