1. CLINICAL MANAGEMENT OF TUBERCULOSIS
OF ADULT, CHILDREN AND SPEACIAL GROUP
Dr. Noor Aliza Bt. Md. Tarekh
Chest Physician, HSAJB
2. History
• One of the oldest diseases known to
affect humans - tuberculous spinal
disease found in Egyptian mummies.
• First recognised in 4000 B.C
• “White plague”/ “consumption” in Europe
16th century.
• Spread worldwide 17th century.
3. GLOBAL PERSPECTIVE
• TB is leading cause of death
due to an infectious disease
in adults
• TB kills 2 million people every
year
• Declared global emergency
by WHO in 1993
4. Introduction
• Caused by bacteria belonging to M.
tuberculosis complex
• Usually affects lungs (80-85%) but
other organs may be involved
• Curable in all cases if properly
treated
5. Aetiologic Agent
• M. tuberculosis – most frequent
agent of human disease
• M. bovis – once an important
cause of tuberculosis transmitted
by unpasteurised milk
• M. africanum – West Africa
• M. microti – does not cause
disease in humans
7. CMI + tubercleCMI + tubercle
formationformation
dropletsdroplets
nucleinuclei
organismorganism
replicationreplication
macrophagemacrophage
lysislysis
lymphatic and bloodlymphatic and blood
spreadspread
miliarymiliary
further multiplicationfurther multiplication
latent (LTBI)latent (LTBI)
Not controlNot control
Ghon focus/ ranke compleGhon focus/ ranke comple
Person at risk
Specific immunity is usually
adequate to limit further
multiplication of the bacilli; the
host remains asymptomatic, and
the lesions heal.
Host defences
weakening
A droplet nucleus, passes
down the bronchial tree
and implants in a
respiratory bronchiole /
alveolus beyond the
mucociliary system.
DepositionDeposition
Tubercle bacilli
multiply in the
alveoli.
Within 2-10 weeks, the immune system
produces special immune cells called
macrophages that surround the tubercle
bacilli. The cells form a hard shell that
keeps the bacilli contained and under
control. ( TB Infection ).
If the immune system cannot keep the bacilli
under control, the bacilli begin to multiply
rapidly (TB disease).
This process can occur in
different places in the body,
such as the lungs, kidneys,
brain, or bone
Droplet nuclei containing tubercle bacilli are inhaled, enter the lungs.
8. Through lymph nodes
and lymphatics
BLOOD
STREAM
Acute
spread
Chronic
spread
Miliary
tuberculosis
Tuberculous
meningitis
Bones
Joints
Kidneys
Etc
Direct from
lung lesion
9. TB Infection VsTB Disease
TB Infection
( Latent TB Infection )
TB Disease
M. Tuberculosis in the body
Tuberculin skin test reaction usually positive
No symptoms Symptoms such as cough, fever,
weight loss
CXR usually normal CXR usually abnormal
Sputum smears & cultures -ve Sputum smears & cultures tve
Not Infectious & not a case of TB Often Infectious before treatment
& a case of TB
18. Physical Findings
• Limited use
• May not have any
abnormalities during
auscultation
• May have crackles or signs of
consolidation
19. Diagnosis of TB
• High index of suspicion needed
• Symptoms and signs depend on organs
involved
• For pulmonary TB:
• Sputum AFB D/S x 3
• Chest radiograph
• Mantoux test
• Sputum MTB C & S or BACTEC
20.
21.
22. Diagnostic Procedures
• Bronchochoscopy ( BAL )
• Gastric lavage
• Lumbar puncture ( PCR )
• Pleural, pericardial, peritoneal biopsy
• Bone marrow and liver biopsy
23. Indications forAFBCulture
• For bacteriological confirmation of
TB
• When we suspect a h/o being
treated for TB before
• Any foreigners where we are not
certain of previous history
• Any history of irregularities in
treatment
• Treatment failures
• Relapse TB
24. Aims of Treatment
• To cure patients and render
them non- infectious
• To reduce morbility and
PREVENT mortality
• To prevent relapse and
emergence of resistant of
tubercle bacilli (MDR TB).
25. PRINCIPLES OF TB TREATMENT
CORRECT COMBINATION
CORRECT DOSAGES
CORRECT DURATION
APPROPRIATENESS TO PATIENT
26. Deciding To InitiateTreatment
Should be based on clinical,
pathological, and radiographic
findings; and the results of
microscopic examination of acid-fast
bacilli (AFB)--stained sputum
(smears) (as well as other
appropriately collected diagnostic
specimens and cultures for
mycobacteria.
31. Intensive Phase
• Inj. Streptomycin ( S )
• T. Isoniazid ( H )
• CAP .Rifampicin ( R )
• T. Pyrazinamide ( Z )
• T. Pyridoxine ( VIT.B6 )
• T. Ethambutol ( E)
Daily for two months
32. Intermittent Phase
• Inj. Streptomycin 3/4 - 1 g
• T. Isoniazid ( 13 - 17 mg /Kg
body wt)
• C. Rifampicin 600 mg.
• T. Pyridoxin ( Vit B6 ) 10 mg.
Biweekly for four months.
33. WHO RECOMMENDATION
(According to treatment categories)
From the public health perspective the highest TB
control programme priority is the identification and cure
of the infectious cases i.e those patients with sputum smear positive
PTB.
In settings of resource constraint, it is
necessary for rational resource allocation to prioritize
TB treatment categories according to the cost- effective
of treatment of each categories.
Treatment categories are therefore ranked from 1 (highest priority )
to IV (lowest priority).
34. CATEGORY I
NEW SMEAR POSITIVE PTB 2EHRZ(SHRZ) 6HE
NEW SMEAR NEGATIVE WITH 2EHRZ(SHRZ) 4HR
EXTENSIVE LESION 2EHRZ(SHRZ) 4H3R3
CATEGORY II
SPUTUM SMEAR POSITIVE
RELAPSE 2SHRZE/1EHRZ 5H3R3E3
RX. FAILURE 2SHRZE/ 1EHRZ 5HRE
RX.INTERRUPTION
CATEGORY III
NEW SMEAR NEGATIVE PTB 2HRZ 6HE
NEW LESS SEVERE FORMS 2HRZ 4HR
EXTRA PTB 2HRZ 4H3R3
CATEGORY IV
CHRONIC CASES
(sputum positive after supervised rx) NOT APPLICABLE
ALTERNATIVE TB RX
INITIAL PHASE CONT.PHASE
DAILY OR 3X/WEEK
TREATMENT BY CATEGORY
(WHO guidelines)
35.
36. Notes:
• Initiate treatment with 4 drugs on high index
of suspicion
• Repeat smear and culture at 2 months
• Lengthened if culture still positive at 2
months/ cavitations to 9 months
• EMB is discontinued when drug testing
showed no resistance
• PZA is discontinued after 56 doses
37. Treatment Flow Chart
INITIATION OF TREATMENT
56 DOSES DAILY (8 WEEKS/2 MONTHS)
* baseline investigations
BIWEEKLY TREATMENT
16 DOSES (8WEEKS/2MONTHS)
*sputum D/S ,CXR
BIWEEKLY TREATMENT
16 DOSES(8 WEEKS/2 MONTHS)
*sputum D/S, CXR
FOLLOW UP 3/12, 6/12 AND 9/12
*sputum D/S X3,sputum culture AFB, liver function test, renal profile
blood sugar, pregnancy test, sr. uric acid,visual test and HIV if indicated.
39. COMPLICATIONSOF DRUG THERAPY
ADVERSE REACTION TO TB DRUGS
DRUG RESISTANCE
MODIFICATION TO SUIT PATIENT’S NEEDS
RELAPSE
IMMUNOLOGICAL REBOUND
40. OUTCOMEOFTREATMENT
• CURE ( SPUTUM CONVERSION RATE )
• COMPLETED TREATMENT
• INTERUPTTED TREATMENT
• RELAPSED
• DEATH
• LOST TO FOLLOW UP
• TREATMENT FAILURE
– NON COMPLIANCE
– RESISTANT TB
41. TREATMENTFAILURE
Patient who remains or becomes
again smear-positive at five months
or later during treatment.
– POOR COMPLIANCE
– INAPROPRIATE TREATMENT
– DRUG RESISTANCE
43. MECHANISMSOF TOXICITY
• DOSE RELATED OR HYPERSENSITIVITY
• HIGH DUE TO MULTIPLE DRUGS USE
• MAJOR DETERMINANTS ARE :
- DOSE
- MODE OF ADMINISTRATION
- AGE
- GENETIC STATUS
- NUTRITIONAL STATUS
- CONCOMITANT
THERAPY -
HEPATIC/RENAL FUNCTION
44. STREPTOMYCIN
• Is not absorbed by GIT
• Bactericidal
• Plasma half life 2-3 hrs, prolonged in
new-born,elderly ,renal patients
• Given by deep I/m injection
• Contraindication:
-Hypersensitivity
-Auditory nerve
impairment -Myasthenia
gravis
• Dosage : 15mg/kg.
52. Approach to Mx of A/E of TB drugs
1. Monitoring
• Before treatment
° clinical features – drug history: OCP, PI
warfarin
- liver & renal disease
° baseline Ix – LFT, RFT, FBC, visual acquity
• During treatment
monitored for adverse effects of anti TB
53. 2. Management
• minor adverse effects
adverse effects management
GIT upset give drug last thing at
anorexia/nausea night
Joint pain aspirin/NSAID
Burning sensation pyridoxine 100mg daily
in the feet
orange/red urine reassurance
Mild skin rash reassurance and
and pruritis symptomatic Rx
54. • major adverse effects
° hypersensitivity reaction
° drug induced hepatitis
° renal impairment
° reversible visual impairment – ETH
° irreversible eight CN damage – SM
° thrombocytopenia, shock - RFP
62. Hypersensitivity reaction
Skin rash Steven-Johnson syndrome
Hypersensitivity Drug
least likely Isoniazid
Rifampicin
Pyrazinamide
Ethambutol
most likely Streptomycin
63. Management
• stop all anti TB drugs until the reaction
has subsided
• symptomatic Rx
• once the reaction has subsided the drug
or drugs responsible for the reaction
must be identified:
→ a challenge dose for hypersensitivity
64. A challenge dose for hypersensitivity
anti TB regimen
skin rash
a challenge dose of each
drug of the regimen
° dose: 1/10 of the therapeutic dose daily
° start with the drug that are least likely to cause
the reaction
° challenge should be done for one drug at a time
rash after 1st
yes no
do not proceed continued in full dosage
± desensitization
65. Drug Challenge Dose(mg)
D1 D2 D3
INH 50 300 300
RFP 75 300 full dose
PZA 250 1000 full dose
ETM 100 500 full dose
SM 125 500 full dose
66. Desensitization
Reaction occurs with the 1st
dose desensitizing
• only done if one is unable to devise a suitable
regimen of treatment without the offending drugs
• do not start desensitization doses when other
alternative and suitable drug combinations are
available
• done by giving initially small and slowly increasing
dosage of the offending drug
• the patient should observed for ↑ T and pruritis
67. Rapid desensitization
• dosage can be given by giving the drug more frequent
• generally begin with 1/10 – 1/100 of the therapeutic dose
and then doubled each time
• example: rapid desensitization for INH
Day suggested time dose(mg)
1 6 am 1
12 noon 2
6 pm 4
12 mn 8
2 6 am 15
12 noon 30
6 pm 60
12 mn 100
3 6 am 200
12 noon 200
4 & beyond 6 am 300
• same procedure with other drugs: SM, Rifam, PZA & EMB
70. • Management - rule out other possible causes
Drug induced hepatitis
LFT ( AST, ALT and ALP )
>3x 2-3x <2x
Pt well pt unwell monitor LFT repeat LFT after
Non-infec infec weeklyx2/52 after 2/52
then 3 weeks
Stop all Rx: SM,EMB,Qua continue Rx with
till LFT till LFT N continue Rx all drugs
with all drugs
LFT
N abN suggested Rx: 2SHE/10HE(S)
A challenge dose
71. Renal impairment
• INH, RFP, PZA
° eliminated by non renal routes
( hepatic / bile )
° can be given in normal dose to
patient with renal failure
72. ° several reports RFP
renal toxicity – tubulo-interstitial
nephritis
- interstitial fibrosis
- tubular necrosis
dramatic response after – stop RFP
- corticosteroid
° severe RF - ↓ INH 200mg daily to avoid
peripheral nephropathy
74. Extrapulmonary TB
Virtually any organ may be affected
• Lymph node
• Pleura
• Genitourinary tract
• Bones and joints
• Brain
• Peritoneum
• Skin
In order of
decreasing
frequency
76. TBLymphadenitis
• Painless swelling of lymph nodes
• Commonly affects cervical and
supraclavicular lymph nodes
• Lymph nodes may have sinuses
discharging caseous material
77. Tuberculous Lymphadenitis
Evaluation:
Diagnosis can be established by culture of M. tb
from lymph node biopsy or aspirate.
Demonstration of AFB in tissue or aspirate or
pathologic evidence of caseating granuloma is
consistent with TB.
Treatment:
Treatment follows pulmonary TB regimen.
Prolong treatment for a total of nine (9) months.
Even if lymph node excision is complete,
chemotherapy is indicated.
81. TB Pleura
• Penetration by tubercle bacilli into
pleural space
• Feature – pleural effusion,
empyema
• Tuberculous empyema – AFB
direct smear often positive and
usually requires surgical drainage
82. Pleural Tuberculosis
Evaluation:
In pleurocentesis, AFB stain of the fluid sediment
is seldom positive; culture is positive in a quarter
to third of cases.
Treatment:
Treatment follows pulmonary TB regimen. A total
of 9 months treatment.
84. Genitourinary TB
Symptoms – frequency, dysuria, haematuria, loin pain,
may be asymptomatic, discovered only
after severe renal destruction.
Evaluation:
Urinalysis has been reported to be abnormal in 90% of cases
(mostly gross or microscopic hematuria and/or pyuria). AFB
culture of three morning urine specimens will show M. tb in
90% of patients.
Treatment:
Treatment follows pulmonary TB regimen, and is usually
highly successful. Surgery is indicated only for intractable pain,
persistence of non-tuberculous infection from obstruction or
serious, persisting hematuria. Treatment should be continued
for nine to twelve months.
85. Genital TB
• Female – affects fallopian tubes and
endometrium
- may cause infertility,
pelvic pain,
menstrual abnormalities
• Male – affects epididymis, testes
and prostate
86.
87.
88. Testicular tuberculosis. Computed tomographic scan of the pelvis showing a large, irregular,
mixed solid and cystic left testicular mass (arrow).
89. Tuberculosisof theBonesand Joints
Skeletal TB occurs most commonly in the weight-bearing
joints. The spine is the most frequent site (also known as
Pott's disease), followed by the hip and knee. The most
common presenting symptoms are pain and difficulty with
locomotion.
Evaluation:
For skeletal TB should be X-ray films of the involved joint,
followed by specimen collection and culture. Biopsy will be
necessary to obtain tissue for confirmation of diagnosis.
Treatment:
Treatment follows the regimen for TB meningitis, treatment for
twelve (12) months for all individuals, regardless of immune
status.
90.
91. Osteoarticular tuberculosis. Radiograph of the right
knee showing a large effusion, osteopenia, joint
space narrowing, and lucencies in the distal femur.
Spinal tuberculosis. Magnetic resonance imaging of the spine revealing osteomyelitis
involving T10 and T11 vertebral bodies and disc space (A; arrow) and an adjacent
multiloculated paravertebral abscess (B; arrow).
92.
93. Gastrointestinal TB
• Any part of GI tract may be involved
• Spread via swallowing of sputum,
blood-borne or ingestion of
unpasteurised cow’s milk
• Terminal ileum and caecum most
common
• Features – abdominal pain,
diarrhoea, obstruction, palpable
mass
94. TuberculousPeritonitis
The disease presents with one of two manifestations:
1) ascites that leads to abdominal pain and distention with or
without gastrointestinal symptoms;
2) abdominal pain, with or without symptoms suggesting
intestinal obstruction.
Evaluate :
Culture of the ascitic fluid or peritoneal or open biopsy; the
diagnosis of "dry" tuberculous peritonitis is made, usually,
by laparotomy and biopsy that reveals caseating
granulomas with or without tissue stains positive for AFB.
Treatment:
Treatment is comparable to that for pulmonary tuberculosis
( nine to twelve months ).
96. Miliary Tuberculosis
• Due to haematogeneous spread of tubercle
bacilli
• Either 1° or reactivation of old disseminated
foci
• Symptoms – fever, night sweat, anorexia,
weakness
• Signs – hepatosplenomegaly,
lymphadenopathy
• Cryptic form – elderly characterised by mild
intermittent fever, anaemia and meningeal
involvement
97. Miliary Tuberculosis
Evaluation:
The diagnosis of disseminated TB is usually suspected
because of the presence of miliary infiltrates on chest x-ray.
Transbronchial biopsy is the most high-yield procedure to
obtain tissue. In other instances, hematogenous dissemination
is evidenced by tissue biopsy from other organs such as lymph
nodes, liver, or bone marrow.
Treatment:
Treatment follows the regimen for TB meningitis.
Use of corticosteroids:
Fulminant miliary TB may be associated with the Adult
Respiratory Distress Syndrome (ARDS) and disseminated
intravascular coagulation (DIC). In such cases, corticosteroid
treatment (prednisone 60-80 mg/day) is indicated.
100. TBMeningitis /Tuberculoma
• Features – headache, confusion,
altered sensorium, neck stiffness,
cranial nerve palsy
• Hydrocephalus is common
• Tuberculoma presents as space-
occupying lesion, seizures and
focal signs
101. TuberculousMeningitis
Evaluation:
Examination of the cerebral spinal fluid
(CSF).
CSF - pleocytosis (65% of cases have
white blood cell counts between
100-500) with lymphocytic
predominance, elevated protein
and low glucose are usual.
Acid fast bacilli (AFB) have been seen in
up to 37%.
.
102. TuberculousMeningitis
Treatment:
TB meningitis can be treated with isoniazid, rifampicin,
pyrazinamide and ethambutol in doses comparable to those
use in pulmonary TB for the first two (2) months, followed by
isoniazid and rifampicin in the continuation phase for 7 (in non-
immunocompromised individuals) to 10 additional months
(in children and immunocompromised individuals ).
Use of corticosteroids:
The use of corticosteroids in patients who are initially
confused, stuporous, or have focal neurologic deficits, dense
paraplegia or hemiplegia, or "CNS block". Cerebral edema
evidenced by CT scan is considered an indication for
corticosteroid therapy by some.
Prednisone is started at 40-60 mg daily. The dose is gradually
reduced after one or two weeks, using the patient's symptoms
as a guide. If the patient has responded to treatment, steroids
can usually be discontinued entirely after 4-6 weeks.
103.
104. Pericardial Tuberculosis
Pericardial TB is much more common in HIV-infected
individuals. Onset may be either subtle (dominated by
cardiovascular consequences of effusion) or abrupt
(fever and precordial pain).
Examination:
Fluid from pericardiocentesis will be similar to fluid
from tuberculous pleural effusion. A positive acid-fast
bacilli (AFB) smear is uncommon; a culture will be
positive in only 25-50% of cases. issues of immediate
treatment. Some physicians advocate primary surgical
intervention with a pericardial "window" and biopsy in
every case of suspected TB pericarditis.
105. Pericardial Tuberculosis
Treatment:
Treatment follows pulmonary TB regimen.
Use of corticosteroids:
Corticosteroid use is generally recommended.
If used, begin prednisone 60-80 mg daily, and
gradually decrease the dosage over a period of several
weeks as the effusion subsides.
Use of corticosteroids is not necessary if
pericardiectomy has been performed.
Pericardiectomy:
This procedure is indicated if there is constriction.
110. TB with HIV co-infection
In early stages the presentations of TB in TB-HIV
co-infection is the same as HIV negative but in late
stages extra pulmonary and dissemination are
common.
Diagnostic problems arise as other respiratory
diseases occur frequently and tuberculin test may
be negative.
WHO recommends standard short course
chemotherapy (DOTS or FDC) similar to that
recommended for HIV negative cases.
After initiating ATT or anti retroviral therapy (ART)
worsening of preexisting lesions or appearance of
new lesions is more commonly seen than in HIV
sero negative individuals due to a marked
improvement in immunity. This is called
“paradoxical response” or “immune reconstitution
phenomenon”.
111. TB with HIV co-infection
Effect of TB on HIV
TB causes release of TNF and stimulates
multiplication of virus inside T cells.
TB helps in destruction of CD4 cells
Helps release of new virions from HIV infected cells
Effect of HIV on TB
Decrease macrophage activating lymphokines.
Increase in number of CD8 cells.
Increase tissue destruction.
T4 lymphopenia.
HIV promotes T4 destruction and CD4 cells
impairment.
112. TB with HIV co-infection
Multidrug resistant TB can occur due to poor
compliance to ATT due to behavioural pattern
and increased incidence of side effects.
Malabsorption of drugs is common due to
associated diarrhoea, which can contribute to the
selection of drug resistant mutants.
ART for HIV, containing protease inhibitors (PI)
and Non nucleoside reverse transcriptase
inhibitors (NNRTI) cannot be used along with R,
as R induces metabolism of PI and reduces the
efficacy.
113. TB with HIV co-infection
The various options are :
To postpone anti retroviral therapy.
To use no PI or NNRTI containing anti
retroviral combinations (NRTI based regimens).
To use certain PI/ and/or NNRTIs with
modification in doses Efavirenz or Saquinavir with
Ritonavir, without the need to adjust the doses.
To use non R regimens ( 2SHEZ+10HE )
Regimens which are compatible with simultaneous use of
rifampicin are
2NRTI+ Abacavir (ABC)
2 NRTI+ Efavirenz (EFZ)
2 NRTI + Saquinavir (SQV)/Ritonavir (RTV)
The NRTIs can be either
Zidovudine (ZDV)+ Lamivudine (3TC) or
Stavudine (d4T) + Lamivudine (3TC)
114. TB and pregnancy
Tuberculosis during pregnancy is rarely, if ever, an indication
for a therapeutic abortion. An exception might be if a pregnant
woman has multidrug-resistant tuberculosis. A pregnant
woman with culture-proven MDRTB, should be offered
abortion counseling, because almost all of the medications
used to treat MDRTB are known to cause fetal abnormalities.
No increase in morbidity or mortality from TB has been noted
during pregnancy if treatment is adequate.
All drugs, that is, rifampicin, isoniazid, ethambutol, and
pyrazinamide can be used during pregnancy. Streptomycin is
not given due to ototoxicity to the fetus. Prophylactic
pyridoxine in the dose of 10mg/day is recommended along
with ATT.
Breast-feeding is safe during anti-TB therapy.
115. Breast feeding and Maternal
Tuberculosis
( Summary Management )
According to the time of diagnosis and bacteriological status of the mother.
Active pulmonary TB before delivery Active pulmonary TB after
delivery
> 2 months before < 2 months
before
< 2 months
after
> 2 months after
Smear negative
just before
delivery
Smear posative
just before
delivery
- - -
Treat mother
Breastfeed
No preventive
chemotherapy
for infant
BCG at birth
Treat mother
Breastfeed
Give isoniazid
to infant for 6
months
BCG after
stopping
isoniazid
Treat mother
Breastfeed
Give isoniazid to
infant for 6
months
BCG after
stopping
isoniazid
Treat mother
Breastfeed
Give isoniazid
to infant for 6
months
BCG after
stopping
isoniazid
Treat mother
Breastfeed
Give isoniazid to
infant for 6
months
BCG after
stopping
isoniazid
Monitor all infants for weight gain and health
Do not give BCG to infants who are symptomatic for yellow fever or HIV infection.
Division of Child Health and Development Update Feb. 1998
116. Liver disorders.
Isoniazid, rifampicin, pyrazinamide are all associated
with hepatitis. Of these 3 agents, pyrazinamide is the
most hepatotoxic.
Patients with liver disease should not receive
pyrazinamide. Isoniazid plus rifampicin plus one or two
non-hepatoxic drug such as streptomycin and
ethambutol can be used for a total treatment duration
of 9 months. ( 2 SHRE / 7 HR )
Alternative regimens are SHE in the initial phase
followed by HE in the continuation phase, with a total
treatment duration of 12 months. ( 2 SHE/10 HE ).
117. Renal failure
Isoniazid, rifampicin, pyrazinamide can be
given in normal dose to patients with renal
failure.
Streptomycin and ethambutol may be given
in reduced doses as both drugs are
excreted by the kidney.
The safest regimenfor the patient with renal
failure is 2HRZ / 4RH
In post renal transplant patients:
Rifampicin-containing regimens are avoided
as rifampicin causes increased clearance of
cyclosporin.
119. TBin Children
A child usually gets TB infection from being
exposed to a sputum-positive adult.
Young children below ten years of age are at
risk of becoming infected with TB bacilli
because the immune system of young
children is less developed.
In HIV infected children the risk of
developing TB meningitis is very high and
often result in deafness, blindness, paralysis
and mental retardation.
120. TBin Children
o The diagnosis is thus largely based on the
clinical features of cough, weight loss, with a
history of close contact with an infectious
adult TB patient.
o With increasing coverage of BCG
vaccination, the tuberculin skin test is no
longer considered a confirmatory test.
o Chest X-rays of children are difficult to
interpret as the typical shadow is rarely
seen.
121. TBin Children
WHO guidelines for diagnosis
Suspect TB in a child -
Who is ill, with a history of contact with a suspect
or confirmed case of pulmonary TB;
Who does not return to normal health after
measles or whooping cough;
With loss of weight, cough, fever who does not
respond to antibiotic therapy for acute respiratory
disease;
With abdominal swelling, hard painless mass and
free fluid;
With painless firm or soft swelling in a group of
superficial lymph nodes;
With signs suggesting meningitis or disease in
the central nervous system.
122. TBin Children
•
Preventing TB disease in children
Early diagnosis and successful treatment of an infectious adult patient
is the best way to protect children from becoming infected with TB.
BCG immunization of babies soon after birth up to 2 years of age will
protect them mainly against the development of TB meningitis.
Treating TB in children
The management of TB in children is similar to those in adults.
Some important differences are:
Dosages in children per kilogram body weight should be higher as
they have a higher metabolism. They can tolerate higher doses with
fewer side-effects.
Children usually have fewer microorganisms and are less likely to
develop secondary resistance
Extra-pulmonary TB is more common in children and therefore the
drugs used should be able to penetrate and achieve the required
concentration in specific body fluids and tissues.
123. PROPHYLACTIC TREATMENT
Def : Treatment to prevent acquisition of
infection with MTB in a person
exposed to tubercle bacilli.
WHO ?
Children under the age of 5 years at risk of
being infected from a person with sputum
smear-positive TB living in the same household.
124. MANAGEMENTOFRESISTANTTB
Definitions :
a) Drug-resistant tuberculosis :
This is a case of tuberculosis
(usually pulmonary ) excreting bacilli
resistant to one or more anti-tuberculosis drugs.
b) Multidrug-resistant tuberculosis :
This is a case of tuberculosis which is resistant to
Isoniazid and Rifampicin.
125. MANAGEMENTOFRESISTANTTB
Prevention
Adequate treatment
Full supervision
High suspicion on high risk group.
Previously treated patients
Immigrants from high resistant areas
Contacts of patients
Immuno-suppressed patients
PRINCIPLE OF THERAPY
126. TREATMENT OF MDR TB
• DEF : Resistant to both H & R
• Overall response 56%
• BASIC PRINCIPLES:
- - At least 3 drugs ( preferably four or five ) if
possible one injectable aminoglycoside.
- continued for 18 - 24 mths after culture -ve
- if fail, 2 new drugs must be added
simultaneously.
- Advisable to manage patient with MDR TB
as in-patient until sputum conversion is
achieved.
- must be DOT
128. MONITORING MDR TB
• At least once a month
• Complete physical and
laboratory evaluation
• Monthly monitoring of sputum
direct smear and culture
• Discontinued isolation once
sputum negative three times
• Surgical intervention if possible.
129. Surgical Intervention
• As adjunct to medical treatment, cure
with medical therapy 56%.
• With surgery, cure rate may increase
to 85-90 %.
• May be hazardous but may be life
saving.
• After surgery, the same drug regimen
should be continued for at least 18
mths.
130. “ EVERYONE WHO BREATHES
AIR, FROM WALL STREET TO
THE GREAT WALL OF CHINA,
NEEDS TO WORRY ABOUT THE
RISK OF TUBERCULOSIS”
(World Health Organization)
131.
132. Role of PPD
• A purified protein derivative (PPD)-
tuberculin skin test may be done at
the time of initial evaluation, but a
negative PPD-tuberculin skin test
does not exclude the diagnosis of
active tuberculosis.
• However, a positive PPD-tuberculin
skin test supports the diagnosis of
1) culture-negative pulmonary
tuberculosis, 2) latent tuberculosis
infection in persons with stable
abnormal chest radiographs
consistent with inactive tuberculosis.
