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Tuberculosis Presentation

H.A.M. Nazmul Ahasan is a professor of medicine at Popular Medical College who presented on tuberculosis (TB). His presentation included general information about TB, the diagnostic approach for pulmonary and extra-pulmonary TB, treatment modalities, and managing TB in special situations. TB remains one of the world's deadliest diseases, infecting one third of the global population. It is spread through the air via droplet nuclei expelled through coughing or sneezing. Diagnosis involves history, clinical examination, investigations like sputum smear, culture and nucleic acid tests, imaging and biopsy of affected tissues.

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Mohiuddin Ahmed
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0% found this document useful (0 votes)
177 views181 pages

Tuberculosis Presentation

H.A.M. Nazmul Ahasan is a professor of medicine at Popular Medical College who presented on tuberculosis (TB). His presentation included general information about TB, the diagnostic approach for pulmonary and extra-pulmonary TB, treatment modalities, and managing TB in special situations. TB remains one of the world's deadliest diseases, infecting one third of the global population. It is spread through the air via droplet nuclei expelled through coughing or sneezing. Diagnosis involves history, clinical examination, investigations like sputum smear, culture and nucleic acid tests, imaging and biopsy of affected tissues.

Uploaded by

Mohiuddin Ahmed
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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H.A.M.

Nazmul Ahasan
Professor of Medicine
Popular Medical College
MY PRESENTATION INCLUDES :
• General information about TB

• Diagnostic Approach of both P.TB and


extra pulmonary TB

• Modalities of Treatment

• Mx of TB in special situation.
History
until mid-18th century ,many believed TB was
hereditary
1865 Jean Antoine 1882 Robert Koch
Villemin proved TB was discovered
contagious M. tuberculosis, the
bacterium that causes TB
Epidemiology

 Tuberculosis (TB) is one of the world's deadliest diseases.

One Third of the world's population , is infected with TB and rank as a 2nd
leading cause of death from an infectious disease worldwide after the HIV.

In 2017, 10.0 million people around the world become sick with TB disease

There were 1.3 million TB related deaths worldwide.

TB is a leading killer of people who are HIV infected.


Definition
• Tuberculosis (TB) is a air borne potentially fatal
contagious disease that can affect almost any part
of the body but is mainly an infection of the lungs.
• Neo-latin word :
"Tubercle"
-Round nodule /Swelling
"Osis"
- Condition
Pulmonary tuberculosis (PTB)
• Refers to disease involving the lung
parenchyma.
• A patient with both pulmonary and extra-
pulmonary TB constitutes a case of PTB
• Miliary TB is
classified as PTB
because there are
lesions in the lungs
Extra - Pulmonary Tuberculosis (EPTB)

• Refers to TB disease of organs other than the lungs.


• Therefore the following constitute a case of EPTB:
- Tuberculous intra thoracic lymphadenopathy
(mediastinal and/or hilar)
- Tuberculous pleural effusion ,without radiographic
abnormalities in the lungs.
- Extrathoracic TB
EPTB- contd…
• Usually results from haematogenous
dissemination.
• Sometimes direct extension from an adjacent
organ.
• It can occur at any age
• Can involve any organ of the body.
Classification of Mycobacteria:
• Mycobacterium tuberculosis complex: which can
cause tuberculosis in humans and other organisms.

• Mycobacterium leprae causes leprosy

• Atypical mycobacteria are all other mycobacteria


which can cause pulmonary disease resembling
tuberculosis, lymphadenitis, skin disease or
disseminated disease.
Oraganism
• TB is caused by 4 main mycobacterial species
collectively termed Mycobacterium tuberculosis
complex (MTB):
 Mycobacterium tuberculosis
 Mycobacterium bovis (reservoir cattle)
 Mycobacterium africanum (reservoir human)
 Mycobacterium microti
Imporatant Properties of M. Tuberculosis

• M. tuberculosis is an obligate aerobe;


this explains its predilection for causing
disease in highly oxygenated tissues such
as the upper lobe of the lung
TB Transmission
• TB is spread person to person
through the air via droplet nuclei

• M. tuberculosis may be expelled


when an infectious person:
– Coughs
– Sneezes
– Speaks
– Sings

• Transmission occurs when another


person inhales droplet nuclei
• M.BOVIS infection arise mainly
drinking non sterilised milk from
infected cows. 15
TB Transmission

Dots in air represent droplet nuclei containing


M. tuberculosis
16
17
PATHOGENESIS OF
TUBERCULOSIS
By Droplet inhalation the organism lodge in the alveoli.

Recruitment of macrophage and lymphocyte

Macrophage undergo transformation into epitheloid cell and


langhans cell which aggregates with lymphocyte to form
classical tubercular granuloma.

Numerous granuloma aggregate to form primary lesion’’


Ghon focus”. when its involve the hilar lymph node it,s
called’’ Ghon complex”.
Reparative process encase the p.complex in a
fibrous capsule limiting the spread of bacilli

Lymphatic and haematogenous spread may


occur before immunity is established,however
secondary foci in other organ including lymph
node, serous membrane, meninges, bones, liver,
kidney .
Granuloma
Macrophages undergo transformation into epitheloid and
Langhans cells which aggregate with the lymphocytes to form
tuberculous granuloma
 Primary TB: Refers to infection of a previously
uninfected individual.
Progressive primary disease may appear during
the course of initial illness or after a latent
period of weeks or month.

 Miliary TB: Blood borne dissemination gives


rise to milliary TB.
 Post primary TB : Refers to exogenous (new
infection) or endogenous (Reactivation of
dormant lesion) infection in a person who
has been sensitized by earlier exposure. its
most frequently pulmonary and occurs in
the apex of the lung.
Factors increasing the pulmonary TB
 Patient Related:
● AGE ::all age; sharp increase in infection rates from
childhood to adolescence

●SEX::Males>Females

●Close contacts of patients with smear +ve


pulmonary TB

●Overcrowding (eg-prisons)

● Smoking

● Primary infection <1 year previously

●CXR evidence of self healed TB


 Associated diseases :

● Immunosuppression -HIV ,high dose steroids


● Malignancy ( specially lymphoma and
leukaemia)
● Type 1 DM
● CKD
● GI disease associated with malnutrition
● Deficiency of vitamin A or D
● Recent measles
DIAGNOSTIC APPROACH
• HISTORY

• CLINICAL EXAMINATION

• INVESTIGATION
HISTORY
• Productive prolonged cough
(3 weeks or longer)
• Chest pain
• Coughing out of blood
• Low grade evening rise of
temperature
• Night sweats
• Fatigue
• Loss of appetite
• Weight loss
CLINICAL FINDINGS

• Raised temperature
• Patient may be cachectic
• Cervical and other lymphadenopathy
(when disseminated)
• May present with features of collapse(
rt middle lobe) ,consolidation,
cavitation , pleural effusion, meningitis
and pericarditis.
• Hepatosplenomegaly in disseminated
TB
CLINICAL FINDINGS
• May present with features of hypersensitivity
(ex. Erythema nodosum, Dactylitis, phlyctenular
conjunctivitis)

• Unresolved pneumonia
Investigations
1. CBC-Lymphocytosis
2. ESR is increased (positive value only)
3. CXR-
a) Ghon focus/ Primary complex TB
b) ill defined opacities usually in upper
lobes with or with out fibrosis,
c) cavitation, pleural effusion, consolidation
or pneumothorax.
• Patchy opacity with fibrosis mainly in the
upper lobe
CXR- pulmonary TB

Primary complex Patchy opacity with cavity

1- Ghon focus
2- Ghon complex
34
3. Sputum for AFB-on 2 sputum specimens (microscopic
examination)-
1.ON –the spot specimen
2.Early morning specimen on the following
morning
 Early morning specimen should be collected for gene
xpert
 If specimen comes from remote area,it must be within 5
days after collection

 The most cost effective tool for screening pulmonary TB suspects


is microscopic examination of their sputum by the Ziehl –Neelsen
method.

 >65% of pulmonary patients are smear +ve & will be detected by


this method.
35
• The Probability of detecting acid-fast bacilli is
proportional to the bacillary burden in the
sputum ( typically +ve when 5000-10,000
organisms/ml of sputum are present).

36
4. sputum for culture & sensitivity of AFB in

a) Solid media-delayed b) Liquid media- early


growth (Lowenstein growth (BACTEC
Jensen media) –requires media) – requires 1-3
4-6 week week

37
5. Skin test:
Tuberculin test ( Mantoux test)

38
Tuberculin test
 MT test has low
sensitivity/ specificity

 Useful only in primary


or deep seated
infection.

 A +ve MT test does not


differentiate TB
infection from TB
disease.

39
6. Nucleic acid amplification
:
 Gene xpert :
(cartridge-based nucleic
acid amplification test
for simultaneous rapid
tuberculosis diagnosis &
rapid antibiotic
sensitivity test )
 QuantiFERON TB
Gold : is a simple blood
test that detects
M.tuberculosis
Gene Xpert
7. Pleural biopsy for tubercular pleural effusion

8. FNAC & biopsy- to confirm extra pulmonary TB

9. Response to empirical antituberculous drugs


(usually seen after 5-10 days)

42
REFRESHMENT
Extra-pulmonary
Tuberculosis
Extrapulmonary Tuberculosis
 Less common than
Pul.Tuberculosis
 Involves relatively inaccesible
sites
 Fewer bacilli can cause much
greater damage.
 More diagnostic problem
than pul.tuberculosis
Severity Of TBM & Time Of Intervention
( CNS TB)
According to the severity of illness, patients with TBM
can be categorised into three clinical stages.
Stage 1 : patients are conscious & oriented with or
without signs of meningial irritation,but no focal
neurological deficit
Stage 2: patients with altered sensorium or focal
deficits &
Stage 3 : patients are comatose & with neurological
deficit
Brain abcess

Ependedymal TB
tubercle
ruptures into
subarachnoid space &
causes arachnoiditis.
That causes vasculitis,
infarction
, infarction leads to
hemiplegia
Quadriplegia.
TB Meningitis
• Clinical features varies in different age groups, initially
nonspecific
• No single diagnostic method with high sensitivity & specificity
• CSF profile mimics with many infectious & non infectious
meningitis
• Nonspecific imaging characteristics, basal meningeal
enhancement, hydrocephalus, tuberculoma, infarcts .
Complications :
• Hydrocephalus
• Raised ICP
• Vasculitis
• Seizures
Granuloma

TB Granuloma in brain
TB in Eye
Lymph Node Tuberculosis
 Cervical involvement is the most common
 Haematogenous & lymphatic dissemination
 In developing countries, LNTB continues to be the
most common form of EPTB & lymphadenitis due to
non-tuberculous mycobacteria is seldom seen.
 Patients presented with cough & dysphagia
Cervical TB
Pleural Tuberculosis
• Pleural TB is the most
frequently occurring form
of extrapulmonary disease
in adult.
• Epidemiology: 4% of US
cases & 20% in other
countries where HIV
common.
• Origination : Rupture of
subpleural focus into the
pleural space with
inflammatory response.
• Although, tuberculosis is generally a chronic
disease, pleural TB most often manifests as an
acute illness.
• Presentation : Most patients with pleural
involvement complain of pleuritic chest pain
followed by non productive cough, dyspnea,
low grade fever, anorexia & weight loss.
Investigations
• Chest X-ray:
• Pleural fluid analysis :
- Appearance :straw colour
- Type of fluid: Exudate
- Glucose : 20-40mg/dl
- Predominant cell :
Lymphocyte
- pH : 7.3-7.4
- Acid fast smear : +
- culture : +
• Pleural biopsy : + (80%
cases)
Pericardial Tuberculosis
• Pericardial TB is a serious form of extrapulmonary TB associated with
substantial mortality
.
• The incidence ranges from 1-8%

• Pathogenesis: Direct extension from adjucent mediastinal or hilar


lymph node or hematogenous spread to pericardial sac.
• Presentation :
- Patient may have a fever,pleuritic & positional chest pani, pericardial
friction rub.

-Pericardial tamponade may occur causing dyspnea, raised JVP,


paradoxical pulse, muffled heart sound, & possibly hypotention
For Diagnosis :
• Radiological manifestation - Pericardial
effusion - Constructive pericarditis
• ECG : Changes are common.
• Pericardial fluid analysis
• Pericardial biopsy - more definitive
Tuberculous Peritonitis
Risk factors :
- Use of systemic corticosteroid
- Cirrhosis
- HIV infection
- DM
- Malignancy
- Continuous ambulatory peritoneal dialysis
Pathogenesis :
• Reactivation of latent tuberculous foci in the
peritoneum that were established from hematogenous
spread from a primary lung focus.
Tuberculous Peritonitis
Clinical Presentation :
- Ascites (most common)
- Abdominal pain
- Fever
- Anorexia
- Weight loss
• Investigation :
-Comple blood count
-Serum CA-125 :Increased
-Peritoneal fluid analysis
-Peritoneal biopsy : reveal caseating granulomas
in upto 100% of patients & positive for acid
fast bacilli in 74% of patients.
-Chest X-ray : show evidence of old TB in 20-30%
of patients
-
CT scan of abdomen:
*Peritoneal thickening
*Ascites with fine mobile septations lymphadenopathy
Abdominal Tuberculosis
Encompass TB of the : genital tract, peritoneum,
omentum, mesentery & its lymph nodes & other
intra abdominal organs like , liver, spleen &
pancreas
 Ascites is the commonest presentation
 Bowel disturbance (alternate constipation&
diarrhoea )
 Weight loss
Abdominal TB
Uncommon TB Presentation
• Less common abdominal TB presentation: colonic
ulcer / colitis
• Chronic anal fissure & anal tag
• Splenic tuberculosis presents as hypersplenism or
splenic abcess or as a solitary lesion .
Abdominal TB
Genitourinary TB : haematogenous dissemination
from an active site of infection results in GUTB

Cross section
Renal TB
of GUTB
Adrenal TB causing
hypoadrenalism like TB in Testes
Features.
Cervical TB
Female Genital TB :
 is secondary to tuberculosis infection
elsewhere
 Haematogenous or lymphatic spread is most
common
 An important cause of infertility
 Pateints presented with chronic lower
abdominal pain or pelvic pain, or alteration
in menstrual pattern.
Skeletal Tuberculosis
• Affects the spine & hip joint, knee joint, foot bones, elbow &
hand joints
Spinal tuberculosis is the most common
Lower thoracic & lumber vertebrae are the most common sites
of spinal TB followed by middle thoracic & cervical vertebrae
Associated paravertebral abcess may present

C/F : definite pattern of deformity,


pain, circumferential reduction of
movements,night cries .
Extra spinal osteoarticular finger
Pott’s Disease
Bone TB

Chronic Osteomeylitis
Milliary TB
Disseminated Tuberculosis
 Disseminated TB refers to involvement of two or
more non-contigous sites
 Milliary TB
 Cryptic TB : elderly person, mostly afebrile, no other
symptoms
 Diagnosed based on CXR ( small milliary shodows,
diffuse uniform distribution)
 Haematogenous examination, LFT
 Bronchoalveolar lavage
Chest Xray
Skin Tuberculosis
• Tubercular skin infection is exogenous through contact or internally
from another infectious site.
• Incidence is 1.5% which is low as compared to others.
• Types of Skin TB :
a) Primary :
- TB chancre
- Miliary TB
b) Secondary :
- Scrofuloderma
- Lupus vulgaris
-Orificial tuberculosis
-Tubercular gumma
- Tuberculosis verrucosa
• Clinical Feature :
* Characteristic lesion plaque, border
composed of soft reddish brown papules.
* Gelatinous consistency.
* Elevated, infiltrated, discoid with areas of
atrophy.
* Central healing with scarring while
periphery continues to spread

• Confirmation : by Tuberculin skin test.


Skin TB
TB In Breast
Tubercular mastitis can occur as a primary
disease or secondary to tuberculosi
elsewhere.
• Primary TB mastitis is extremely rare
• Direct inoculation through skin abrasions or
duct openings in the nipple
Breast TB
Tuberculosis in ENT :
TB in larynx, pharynx, oral cavity, & salivary glands
• In paranasal sinuses & nasopharynx & the Ear

TB in nose TB of larynx
Management of Pulmonary
Tuberculosis
Table :Case definition of
treatment history
New -A patient who has never received anti -TB drugs; or
A patient who received anti-TB drugs for less than on
month.

Relapse Relapse patients have previously been treated for TB,


were declared cured or treatment completed at the en
of their most recent course of treatment, and are now
diagnosed with a recurrent episode of TB (either a true
relapse or a new episode of TB caused by re-infection)

Treatment after failure: Treatment after failure patients are those who have
previously been treated for TB and whose treatment
failed at the end of their most recent course of
treatment.
Treatment patients have previously been treated for TB and were
after loss to declared lost to follow up at the end of their most recent
follow course of treatment.(These were previously known as
up/default treatment after default patients)

Transfer in A patient already registered for treatment in DOTS centre and


who is subsequently transferred to another registration unit .

Others Other previously treated patients are those who have


previously been treated for TB but whose outcome after their
most recent course of treatment is unknown or
undocumented.
Treatment of TB:Based on historical
Perspective-

Tuberculosis is an ancient Diseases…


By the dawn of the 19th century, tuberculosis
—or consumption—had killed one in seven of
all people that had ever lived. Throughout
much of the 1800s, consumptive patients
sought "the cure" in sanatoriums, where it
was believed that rest and a healthful climate
could change the course of the disease.
TB sanatorium
TB sanatorium
-When streptomycin and INH was discovered,
clinical trials started with these drugs for the
treatment of Pulmonary Tuberculosis began.

But resistance was evident following 2


to 3 months of mono therapy with a
single drug..
Combined drug regimen:
-So in 1960 Professor sir
John Crofton, a TB expert at the
university of
Edinburgh ,proposed that
combination of
Streptomycin,PAS,Isoniazid
should be used..-known as
‘Edinburgh Method’
for tuberculosis treatment.Since
then the incidence
of tuberculosis in Edinburgh 
declined rapidly.
Aims of treatment:
-To cure the patient of TB.

-To prevent death from acive TB or it’s late effects(disability).

-To prevent relapse of TB.

-To decrease transmission of TB to others.

-To prevent the development of acquired drug resistance.


Basic principals of TB treatment:
-Appropriate combination of drugs to kill
different bacterial populations.

-Drugs are given for the required duration to


kill the susceptible bacilli.

-Drugs are given in the correct dosage to


achieve the therapeutic effect.
General management
 Improved dietary measure.
 Contact tracing and their
management with
chemoprophylaxis.
 Improved housing condition
 Education and motivation of the
patient
Anti-Tuberculous Chemotherapy
• First line of anti-TB drugs: • Second line of anti-TB
drugs:
Bactericidal:
Bactericidal:
-Isoniazide (H)
-Rifampicin( R ) -PAS
-Pyrazinamide(Z)
-Cycloserine
-Streptomycin(S)
-Ethionamide
-Ciprofloxacin
Bacteriostatic:
-Ethambutol(E)
Bacteriostatic:
-Thiocetazone
Treatment phases:

Effective chemotherapy consists of 2


phases-

1. The initial or intensive phase


2. The continuation phase
TB Type of patient Treatment Treatment
Diagnostic regimen regimen
category
Intensive Continuation
Phase (Daily) phase
(Daily)
I -New smear positive PTB
-New smear negative PTB (HRZE) for 2 (HR) for 4
-New extrapulmonary TB months months
-New concomitant/ associated
HIV/AIDS

II
4
-Sputum smear positive PTB 4FDC+
with history of treatment of Levofloxacin
more than one month
-Relapse
-Treatment failure after Cat.1
-Treatment after loss to follow
up
-others
RETREATMENT OF TB
• In case of Pulmonary positive and extra
pulmonary TB -4FDC+ LEVOFLOXACIN for 6month.
• In case of pulmonary negative cases- 4FDC FOR
6MONTH
• In case of TB meningitis ,bone TB, neurologicalTB,-
4FDC+ LEVOFLOXACIN for 12 month.
• Above these cases if rifampicin is resistant-start
the treatment of MDR-TB
Category I :
Pre-treatment Intensive phase Continuation
weight (kg) phase

Daily (first
Number 2
of 4FDC Daily( Next 4
months)
tablets months)
Number of 2FDC
tablets

30-37 2 2
38-54 3 3
55-70 4 4
>70 5 5
CATEGORY-2
• 4FDC as like before
• Levofloxacin:ONCE daily
Levofloxacin

wt <33kg 33-50kg 51-70kg >70

10mg/kg 750mg 750mg 1000mg


DURATION OF TREATMENT
• Duration of Anti-TB therapy in smear positive,
negative
and extra-pulmonary TB will be 6 months in case of
Cat-I.
Except in case of:
-CNS TB
-Bone TB

Duration of Anti-TB drug in case of CNS TB and


Bone TB will be 18 months.
Duration of Anti-TB in Cat-II is as I told before
Daily dose and important side effects of
commonly used drugs
Drugs Clinical Dose Important side
setting effects
Rifampicin Children 10-20 mg/Kg -Hypersensitivity
(R) -Hepatitis
Adult 450 mg/day -Skin rashes
<50Kg 600 mg/day -Drug Fever
>50Kg -Vasculitis
-Nausea, Vomiting
-Abdominal Pain
Isoniazid Children 10 mg/Kg -Polyneuropathy
(INH) -Hypersensitivity
Adult 300mg/day -Skin rashes
Continued..

Drugs Clinical Setting Dose Important side


effects
Ethambutol Children&Adult 25mg/Kg -Optic neuritis
(E) Initial 8 weeks -Hypersensitivity
Subsequesntly 15mg/Kg

Pyrazinamid Children and 20-35mg/Kg -Hepatitis


e (Z) Adult -Hypersensitivity
-Gout
Streptomyci Children 30mg/Kg -Vertigo
n (S) 0.75gm -Hypersensitivity
Adult 1 gm -Deafness
<50Kg Nephrotoxicity
>50Kg
Chemoprophylaxis:
(INH 5mg/Kg orally daily for 1 year)
• Indications:

-Non-BCG vaccinated tuberculin positive children


under 3
years

-Immunosuppressed patients -Adolescents with


high degrees of tuberculin sensitivity

-Infants of highly infectious patients


Some important facts to consider:

1)Patient should also be given pyridoxine 20mg/day to


prevent Isoniazid induced peripheral neuropathy

2)The consultant should counsel the patient about the


harmless orange coloration of urine.

3)The patient should be adviced to consult with the doctor


if any rash,visual disturbance,jaundice (high colored
urine,yellow discoloration of skin sclera and mucous
membrane) appears.
Follow up of treatment
• IN case of new pt:
• one early morning sputum should be examined at
the end of month 2\3 ,5 and 6 after the start of
tratment.

• If sputum is positive at the end of 2nd month

Don’t continue with the intensive phase of treatment


but be started on the continuation phase of Rx.
CONTINUED
• IN these pt sputum sample should sent for gene Xpert and
Mx as like.

• If the sputum is positive at the month of 5 or 6 outcome


will be recorded as Rx failure.

• If the gene Xpert is positive at any point of treatment


outcome should be” failure” and wiill be registerd as DR TB.

• EVERY PT Should be weighed and give FDC as like.


Follow up continued
• Smear negative pulmonary TB
At the end of 2nd month of treatment one
sputum sample should be examined to ensure that they
remain negative.If positive pt should be declared as
“treatment Failure”.and referred for gene Xpert.

• Extra pulmonary TB: Pt should be assessed clinically. If not


be improved clinically pt should be assesed for DR
Treatment of
EXTRAPULMONARY TUBERCULOSIS
GENERAL PRINCIPLES OF
EXTRAPULMONARY TUBERCULOSIS
 Treatment regimen as Pulmonary TB
 A 6-month course is recommended for most sites of
extrapulmonary TB
 TB MENINGITIS needs at least 9-12 month treatment
course
 Prolong therapy for extrapulmonary TB that is slow to
respond
 Adjuvant corticosteroids use is recommended for TB
PERICARDITIS and TB MENINGITIS
MANAGEMENT OF TB MENINGITIS
• Duration of Anti TB regimen :
- 6(2+4) months in most guideline
- 12(2+10) months recommended by American
Thoracic Society, Infectious disease society
of America, CDC etc
- we practice extending the regimen for 2 years
- Pyrazinamide must be present in the regimen
• Steroid use: significantly reduces mortality and
disabilities
• MDR TB context
RECOMMENDED STEROID REGIMEN IN
TUBERCULOSIS MENINGITIS
CHILDREN
 Prednisolone 2 to 4 mg/kg/day , tapered over four weeks
ADULT
 Prednisolone 60 mg/day , tapered gradually over six weeks
 Dexamethasone
- i.v. for the first three weeks (initially 0.4mg/kg/day,
tapering to 0.1mg/kg/day)
- followed by oral form 4 mg/day , tapered over three to
four weeks at the rate of 1 mg/day each week
Role of Surgery in
TB MENINGITIS
indications: -hydrocephalus
-tuberculous brain abscess
-vertebral tuberculosis with
cord compression
• Surgical intervention should not be delayed : -in
patients with stupor and coma (stage III)
- still marked progressive neurologic impairment
even under chemotherapy
TREATMENT OF SKELETAL TB
o Medical treatment alone is usually adequate
o Surgery can be a useful adjunct to medical
therapy for :
- abscess drainage
- debridement of infected material
- decompression and stabilization of
vital structures such as the spinal
cord.
Advanced neurological
deficits

Neurological deficits
progressing while on therapy
Recommendatio
n of Surgery in
Spine TB Diagnosis still in doubt after a
thorough evaluation

Kyohosis at the time of


presentation
Management of Abdominal TB
 Cat 1 anti TB drugs
 Duration 12 months
 40 mg/day for 6 weeks
 Surgery in case of:
- intestinal obstruction
- severe haemorrhage
- acute abdomen
- intra-abdominal abscess
• 8 month regimen containing
Isoniazide,Rifampicin and
Ethambutol for first 2
months followed by
Isoniazide and Rifampicin Management
for 6 months
• Residual lymph nodes after
of TB
completion of treatment Lymphadeniti
should be observed closely.
Any increase in size or
s
appearance of symptoms
calls for excisional biopsy for
histopathology and culture.
Difficulties in managing
lymph node tuberculosis

1. Appearance of freshly involved nodes,


2. Enlargement of the existing nodes,
3. Development of fluctuation,
4. Appearance of sinus tracts,
5. Residual lymphadenopathy after
completion of treatment
6. Relapse
 Recommended as a adjunctive therapy
for during the first eleven weeks of
treatment.

 The recommended regimens :


- for adults : prednisolone
60 mg/day x 4 weeks,
ATS,CDC and 30 mg/day x 4 weeks,
IDSA guidelines 15 mg/day x 2 weeks, then
for cortico- 5 mg/day for 1 week
- for children : prednisolone
steroids in TB
1 mg/kg/day x 4 weeks,
pericarditis with a decreasing dose over
time as described for adults

PERI- Generally reserved for
recurrent effusions or for
CARDIECTOMY continued elevation of
central venous pressure
after four to six weeks of
anti-TB and steroid therapy.

 More easily accomplished


and has a lower mortality if
performed in the early
stages, but poorly tolerated
and unsuccessful in end-
stage constrictive disease.
Corticosteroids in
TB
Usually not given except in certain circumstances:
 Tubercular pleural effusion: to prevent pleural
thickening
 Tubercular pericardial effusion: to prevent
constrictive pericarditis
 TB meningitis: to prevent adhesion of meninges
 In severe cases of TB: to prolong life so that anti-TB
drugs can act
TUBERCULOSIS I N SPECIAL SITUATIONS
Pregnancy With Tuberculosis
Treatment During Pregnancy
• Risk to mother and fetus is far greater from
untreated TB than from the drugs used to
treat TB
– Increased risk of spontaneous abortion
– Increase in perinatal mortality
– Increased maternal morbidity
– Congenital TB
 Isoniazid (INH), rifampicin and
ethambutol are known to be
safe for administration during
pregnancy

 Pregnant and postpartum


women are at increased
risk of INH induced
hepatitis
 Supplement with pyridoxine 50mg/day

 Monitor for signs of hepatotoxicity


during pregnancy and immediate
post-partum

 SM induced ototoxicity to the fetus


has been reported irrespective of
period of gestation. Therefore Cat-
II in pregnancy would be:
3HRZE/5HRE.
Women taking OCP:
• Rifampicin reduces the efficacy of
estrogen thus increases risk of pregnancy.

• A higher doses of estrogen can be used


with rifampicin or another contraceptive
method may be used.

132
Breastfeeding Women With
Tuberculosis
Breastfeeding women with TB
• A WOMAN with TB who is breast feeding should receive a full
course of anti –TB drug.

• The mother and baby should stay together ,mother should use face
mask and breast feeding should be continued.

• Prophylactic Rx with INH should given to the baby for 6 month or at


least 3 months ahead(which one is longer)of the time the mother is
considered non infectious.

• BCG vaccination should be postponed untill the end of the isoniazid


prophylaxis.
Breastfeeding Women with TB

Should receive full course of anti-TB drugs.


Mother should use face mask.
Prophylactic Isoniazide should be given to
baby for 6 months or at least 3 months
ahead (which one is longer) of the time the
mother is considered non-infectious.
BCG vaccination should be postponed until
the end of the prophylaxis.
135
TB AND DIABETES MELLITUS
TB AND DIABETES MELLITUS
• Patients with DM are at increased risk of
TB- the relative risk is 3.5 times the normal
population.

• More in IDDM than NIDDM and those


with poorly controlled DM
• During the course of anti tb rx DM pt may
require rx with insulin.
• Strict BSL control required, Give insulins.
Possible failure of sulphonylureas with
Rifampicin co- administration.

• Pyrazinamide gives false + benedict test


in urine, as well as difficult BSL control,
sometimes..
TB with Renal Disease

139
The Renal Impaired TB Patient
 Patients with end stage renal disease
(ESRD) have increased risk for
progression to active TB disease.

 Risk is 10 – 25 times greater.

 Clinical presentation may be atypical.

 Diagnosis is mainly on clinical grounds.


Treatment option in Renal failure:
 Isoniazide, Rifampicin and pyrazinamide are
either eliminated almost entirely by biliary
excretion. So, these drugs can be given in
normal doses in renal failure.

 Streptomycin and Ethambutol are excreted


by the kidney and can be given in reduced
doses or intermittently.

Safest regimen is 2HRZ/4HR.


141
Treatment
• Increasing the dosing interval instead
of decreasing the dosage of drugs is
recommended.
• If CrCl <30ml/min., including
hemodialysis patients, administer
anti-TB treatment thrice weekly after
dialysis.
TB AND LIVER DISEASE
TB Treatment and Hepatitis
• Drug induced hepatitis:IF symptoms +
investigation goes favor of DIH…STOP all the
drug at least 2 weeks untill the hepatitis
resolved.
• In most cases pt can restart the same anti TB
drug without return of hepatitis.
• If hepatitis produce severe jaundice it is
advisable to avoid rifampicin and
pyrazinamide
TB Treatment and Hepatitis
• -Then suggested regimen will be
2SHE/10HE.
• A Severly ill pt with DIH may die without
anti TB drug.
• In this case the least hepatotoxic drug
streptomycin and Ethambutol can be
started..
• In case of extensive TB ofloxacin can be
considered.
Special Treatment Situations
acute viral hepatitis
• Tb rx should be deferred until the Viral hepatitis has
been resolved.
• When it is necessary we can treat by combination of
streptomycin and Ethambutol for 3 month.
• If hepatitis has resolved pt can receive a continuation
phase of 6 month Isoniazid and Rifampicin.
• If hepatitis is not fully resolved streptomycin and
ethambutol should be continued for a total 12
month.
Special Treatment Situations
Chronic liver disease

• Patient with liver disease should not receive


pyrazinamide.
• In this case regimen 2SHRE\6HR(Total 8
month).
TB and HIV infection
‘the cursed duet’
HIV TB pandemic
• TB is the leading opportunistic
infection in HIV infected patients.
• Often the first indicator of immune
deficiency (AIDS defining Illness)
• World wide 40 million HIV infected of
whom15 million are co infected with TB.
• HIV increases the likelihood of active TB
disease.
Opportunistic diseases in the course
of HIV-infection
Oral Candida-infection
Seroconversion:
Kaposi sarcoma
CD4+ Acute retroviral syndrome
Lymphoma
(cells/µL)
Pneumococcal pneumonia Dementia
800- Candida vaginitis Oral haircell-
leukoplacia
ITP
Cachexia
600- Toxoplasmosi
s PCP
HSV
400- Candida esophagitis
Cryptococcosis
TB MAC
200- CMV

50-
0-
0 2 4 8 10
Pulmonary vs extra-pulmonary TB:
HIV+ vs HIV-
TB diagnosis in HIV+ persons

 Microbiology

 Radiology

 TST

 IGRA
Treatment of TB/HIV
complicated by
Optimal regimen for treatment of co-infection
not defined.
Absorption of Anti-­TB drugs.
HAART & TB drug interactions.
Large pill burden.
Paradoxical reactions.
Antiretroviral therapy for HIV infection in
adults and adolescents

• HIV/TB co infection
Irrespective of CD4 cell counts,
patients coinfected with HIV and
TB should be started on ART as
soon as possible after starting TB
treatment
Effect of TB on HIV

• Increases HIV replications – higher


viral load
• Decreases CD4 counts
• Higher risk of opportunistic
infections & death
• Exacerbates weight loss &
wasting
• Complicates treatment
regimens
Treatment in special populations:
Children
 Children

• Same as adults
• Doses based on weight
• Fewer problems with toxicity
• Harder to administer
• Harder to monitor
• Pills (crushed) vs. liquid
preparations
Complications of TB
MDR-TB
XDR-TB
Prevention
Prognosis
Chronic complications of
pulmonary tuberculosis:

A. Pulmonary-
1) Cor-pulmonale
2) Massive haemoptysis
3)Fibrosis / Emphysema
4) Lung / Pleural calcification
5) Bronchiectasis
6) Broncho pleural fistula
7) Atypical Mycobacterial infection
8) Aspergilloma
159
Chronic complications of
pulmonary tuberculosis:

B. Non-pulmonary
1) Laryngitis
2) Enteritis
3) Anorectal disease
4) Amyloidosis
5) Empyma necessitans
6) Poncet’s polyarthritis
160
DRUG RESISTANT TUBERCULOSIS

MDR-TB
XDR-TB
MDR-TB
• Multidrug resistant TB (MDR-TB) is defined as the
presence of M. tuberculosis resistant to at least INH
and Rifampicin, the 2 most potent anti-TB drugs with
or without other drug resistance.

• MDR-TB is a man made phenomenon due to


ineffective administration of effective drugs. ITS
realated with health care providers ,inadequate supply of
quality drugs,pt,s inadequate drug intake.
Targeting risk group for presumptive DR TB

• Failure of category 1 and 2


• All relapses
• All rx after loss to follow up
• Close contact to DR TB pt with symptoms
• All HIV infected persons
Standard Drug Regimen for MDR-TB

Intensive phase Continuation phase


(8 months) (12 months)

Kanamycin
Pyrazinamide Pyrazinamide
Levofloxacin Levofloxacin
Ethionamide Ethionamide
Cycloserine Cycloserine
Shorter Regimen for MDR-TB
(by WHO 2016)

Intensive phase Continuation phase


(4 months) (5 months)

Kanamycin
Clofazimine Clofazimine
Moxifloxacin Moxifloxacin
INH- high dose Pyrazinamide
Pyrazinamide Ethambutol
Ethambutol
XDR-TB

• Extensively drug resistant TB (XDR-TB)-


is defined as the presence of M. tuberculosis
resistant to Rifampicin & INH, in addition to

• a) any quinolone &

• b) at least one injectable second line agent


(amikacin, kanamycin, or capreomycin).
Treatment regimen for XDR-TB

• 12 (Capreomycin, Moxifloxacin, PAS,


Cycloserine, Amoxiclav, Clofazimine, Linezolid,
Pyrazinamide)

• 12 (Moxifloxacin, PAS, Cycloserine, Amoxiclav,


Clofazimine, Linezolid, Pyrazinamide)
Follow up
(in case of 6 month treatment regimen)
Monitoring of patients with sputum smear
positive pulmonary Tb is done sputum smear
examination
• At time of diagnosis
• At end of intensive phase (end of two months)
• In continuation phase
• At end of treatment
Prevention :
Control
Measures

Curative Preventive
component component

Stop
BCG
Case finding Treatment transmission of TB Education
vaccination
TB
DOTS
(Directly observed therapy short course)
DOTS CORNER
Objectives of dots
OBJECTIVES:
1.To prevent drug resistance
2.To prevent drop out cases
3.To prevent reinfection

Observed by:
• A health worker or
• Other trained person

Success rate:
• Nearly 80%
Preventive measures
1) BCG Vaccination:
it is a attenuated live bovine tubercular bacilli

Dose schedule: 1 dose of BCG vaccine is given


intradermally at birth
Preventive measures
2) Stop transmission of TB from one person to
another:
• maintain cough etiquette

• When a TB patient cougs, he/she should cover his


mouth and nose with a tissue and put the used
tissue in a bin.

• Use face mask


Preventive measures
3) TB education
• Take drugs regularly

• Improve dietary measure

• Avoid crowded places

• Well ventilated living space


Prognosis

• TB is a treatable and curable disease.


• Early diagnosis and proper treatment: complete recovery
of TB
• TB in immunocompromised person: prognosis is not good

Poor prognostic factors:


• TB with HIV
• TB with Hodgkin’s lymphoma
• End-stage renal disease
• Chronic lung disease
• Malnutrition
World TB Day
It’s Time...
...to keep the promises made at the UN HLM on TB
...for a world without TB
...to treat 40 million people affected by TB by 2022
...to know your TB status
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