CASE

PRESENTATIO
N
BY
DR AISHA IKRAM
PG TRAINEE
PAEDS UNIT 2

CASE
8 yrs old female child Alishba d/o hamid,,, wt 20kg ,resident of surjani
town admitted with complains of
fever-

1mnths

cough-

12days

chest pain-12 days

generalized weakness
loss of appetite
According to the pts attendant she was in her usual state of health
1mnth back when she developed fever of gradual onset,low
grade,,undocumented,more at night time,not associated with rigors or
chills,relieved temporarily on taking antipyretics.she also developed
cough non productive,occur in bouts,associated with chest pain more
at lower chest,not associated with blood.she became genralized weak
day by day and also complaining of loss of appetite.

No previous history oh hospitalization or blood transfusion.

SVD at home.no history of delayed cry

Nonimmunized child

All milestones achieved on time normally

2nd issue of consangious marriage.father alive and

healthy.mother is a known case of tuberclosis diagnosed 3yrs
back and incompletly treated.4 siblings all alive and healthy

Socioeconomic status:poor

Live in 1room rented house inhabited by 7 members.not well

ventilated,hygenic condition not satisfactory.use unboiled water

GENERAL PHYSICAL EXAMINATION:

Anthropometric parameters:

Wt:20kg(<5th percentile)

Ht: 122cm (<25th percentile)

FOC:53cm

GENERAL PHYSICAL EXAMINATION:

Anemia +ve,jaundice-ve,edema-ve,clubbing-ve,cyanosisve,lymph nodes-ve

H/R:94B/m

R/R:32 Br/min

Temp:99`F

CHEST EXAMINATION:

Inspection: normal,no s/c or I/C recessions

Palpation: mild tenderness+inc vocal fremitus on left side.

Percussion:dull note on left lower lobe

Auscultation: B/L HVB+Decreased air entry on left lower lobe.

ABDOMINAL,CVS,CNS EXAMINATION:

Normal

LABORATORY INVESTIGATIONS
CBC:
Hb:10.3
Plt:169000
Tlc:8100
ESR:60
U/S Chest:
Mild amount of left sided pleural effusion seen which was
not aspirable.
Echogenic foci in lung parenchyma representing air
bronchogram suggestive of consolidation.

X RAY CHEST

DIAGNOSIS
PULMONARY KOCH`S(TUBERCULOSIS)
PNEUMONIA

TUBERCULOSIS
DEFINITION
By World Health Organization (WHO) :

Tuberculosis, or TB, is an infectious bacterial disease

caused by Mycobacterium tuberculosis, which most
commonly affects the lungs. It is transmitted from person to
person via droplets from the throat and lungs of people with
the active respiratory disease.
The World Health Organization (WHO) estimates that more
than 8 million new cases of tuberculosis occur and
approximately 2 million people die of tuberculosis worldwide
each year.
Almost 1.3 million cases and 450,000 deaths occur in
children each year. More than 30 % of the world's population
is infected with Mycobacterium tuberculosis.

ETIOLOGY
There are five closely related mycobacteria in the Mycobacterium
tuberculosis complex: M. tuberculosis, M. bovis, M. africanum, M.
microti, and M. canetti.
M. tuberculosis is the most important cause of tuberculosis disease in
humans. The tubercle bacilli are non-spore-forming, nonmotile,
pleomorphic, weakly Gram-positive curved rods 2-4 m long. They may
appear beaded or clumped in stained clinical specimens or culture
media.

LATENT TUBERCULOUS
INFECTION
Latent tuberculosis infection (LTBI) occurs after the
inhalation of infective droplet nuclei containing M.
tuberculosis.
A reactive tuberculin skin test and the absence of clinical and
radiographic manifestations are the hallmark of this stage.
Tuberculosis disease occurs when signs and symptoms or
radiographic changes become apparent.
Untreated infants with LTBI have upto 40% likelihood of
developing tuberculosis.

TRANSMISSION
Transmission of M. tuberculosis is person to person, usually by
airborne mucus droplet nuclei, particles 1-5 m in diameter that
contain M. tuberculosis.
The chance of transmission increases when the patient has an acidfast smear of sputum, an extensive upper lobe infiltrate or cavity,
copious production of thin sputum, and severe and forceful cough.
Environmental factors, especially poor air circulation, enhance
transmission.
Most adults no longer transmit the organism within several days to 2
wk after beginning adequate chemotherapy, but some patients remain
infectious for many weeks.
Young children with tuberculosis rarely infect other children or adults.
Children and adolescents with adult-type pulmonary tuberculosis can
transmit the organism.

PATHOGENESIS
The primary complex of tuberculosis includes local infection at the
portal of entry and the regional lymph nodes that drain the area.
The lung is the portal of entry in >98%of cases.The tubercle bacilli
multiply initially within alveoli and alveolar ducts.
When the primary infection is in the lung, the hilar lymph nodes
usually are involved, although an upper lobe focus can drain into
paratracheal nodes.
The tissue reaction in the lung parenchyma and lymph nodes
intensifies over the next 2-12 wk as the organisms grow in number and
tissue hypersensitivity develops.
The parenchymal portion of the primary complex often heals
completely by fibrosis or calcification after undergoing caseous
necrosis and encapsulation.
From 25-35% of children with tuberculosis develop extrapulmonary
manifestations compared with about 10% of immunocompetent adults.

PATHOGENESIS(CONT.)
During the development of the primary complex ( Ghon
Complex ), which is the combination of a parenchymal
pulmonary lesion and a corresponding lymph node site,
tubercle bacilli are often carried to most tissues of the
body through the blood and lymphatic vessels.
Disseminated tuberculosis occurs if the number of
circulating bacilli is large and the hosts cellular immune
response is inadequate.
These remote foci usually become encapsulated, but they
may be the origin of both extrapulmonary tuberculosis and
reactivation tuberculosis in some individuals.

PULMONARY KOCH`S:

The primary pulmonary complex includes the parenchymal

focus and the regional lymph nodes. About 70% of lung foci are
subpleural, and localized pleurisy is common.

Two or more primary foci are present in 25%of cases.

The hallmark of pri.tuberculosis in the lung is relatively large
size of regional lymphadenitis compared with the relatively
small size of initial lung focus
The usual sequence is hilar lymphadenopathy, focal
hyperinflation, and then atelectasis. The resulting radiographic
shadows have been called collapse-consolidation or segmental
tuberculosis .
The caseum causes complete obstruction of bronchus,resulting
in extensive infiltrate and collapse.most cases of tuberculous
bronchial obstructionin children resolve full with appropriate
treatment.

 Children can have lobar pneumonia without impressive hilar

lymphadenopathy.
If the primary is progressivly destructive,liquifaction of the lung
parenchyma can lead to formation of athin walled primary tuberculous
cavity.
Erosion of a parenchymal focus of tuerculosis into blood or alymphatic
vessel can result into dissemination of bacilli and a milliary pattern,with
small nodules evenly distributed on chest radiograph.
SYMPTOMS
Upto 50%of infants and children with radiographically moderate to
severe pulmonary tb have no physical findings.
Infants are more likely to experience signs and symptoms.
Nonproductive cough and mild dyspnea are the most common
symptoms.
Systemic complaints such as fever, night sweats, anorexia, and
decreased activity occur less often. Some infants have difficulty gaining
weight or develop a true failure-to-thrive syndrome that often does not
improve significantly until several months of effective treatment have
been taken.

 Some infants and young children with bronchial

obstruction have localized wheezing or decreased breath
sounds that may b accompanied by tachypnea.

PROGRESSIVE PRIMARY PULMONARY DISEASE:

A rare but serious complication of tuberculosis in a child
occurs when the primary focus enlarges steadily and
develops a large caseous center.
Significant signs or symptoms are frequent in locally
progressive disease in children.
High fever, severe cough with sputum production, weight
loss, and night sweats are common. Physical signs
include diminished breath sounds, rales, and dullness or
egophony over the cavity.

REACTIVATION TUBERCULOSIS:
Pulmonary tuberculosis in adults usually represents
endogenous reactivation of a site of tuberculosis infection
established previously in the body. This form of tuberculosis
is rare in childhood but may occur in adolescence.
Children with a healed tuberculosis infection acquired before
2 yr of age rarely develop chronic reactivation pulmonary
disease, which is more common in those who acquire the
initial infection after 7 yr of age.
The most common pulmonary sites are the original
parenchymal focus,lymph nodes,or the apical
seedings(SIMON FOCI)established during hematogenous
phase
Older children and adolescents with reactivation tuberculosis
are more likely to experience fever, anorexia, malaise,
weightloss, night sweats, productive cough, hemoptysis, and
chest pain than children with primary pulmonary
tuberculosis.

 The most common radiographic presentation of this typ of

tb are extensive infiltrates or thick walled cavities in the
upper lobe

PLEURAL EFFUSION:
Tuberculous pleural effusions, which can be local or
general, originate in the discharge of bacilli into the
pleural space from a subpleural pulmonary focus or
caseated lymph node.
Asymptomatic local pleural effusion is so common that it
is basically a component of primary complex.large and
clinically significant effusions occur months or years after
primary infection
Tuberculous pleural effusion is infrequent in children <6 yr
of age and rare in children <2 yr of age.

 EXAMINATION OF PLEURAL FLUID

Examination of pleural fluid and pleural membrane is
important to establish the dignosis of tuberculous
pleurisy.
Pleural fluid is yellow in colour and only occasionaly
tinged with blood.
Specific gravity is usualy 1.012-1.025.
Protein level is 2-4g/dl
Glucose conc. May b low,although it is usually inn low
normal range (20-40mg/dl)
Acid fast smears of pleural fluid are rarely +ve.

EXTRA PULMONARY
TUBERCULOSIS IN CHILDREN

COMPLICATIONS OF
T.B
TBM:
Hydrocephalus,cranial nerve
palsies,paresis,developmental delay and seizures
Bone/joint T.B:
Deformity and contractures
GI TB:
Obstruction,strictures and fistula formation
Pulmonary T.B:
Haemoptysis,pneumothorax,bronchiectasis or fibrosis is
rare

TUBERCULIN SKIN TESTING

The development of delayed-type hypersensitivity (DTH) in most individuals infected with
the tubercle bacillus makes the tuberculin skin test a useful diagnostic tool.
The Mantoux tuberculin skin test is the intradermal injection of 0.1 mL containing 5
tuberculin units (TU) of purified protein derivative (PPD).
T cells sensitized by prior infection are recruited to the skin where they release lymphokines
that induce induration through local vasodilatation, edema, fibrin deposition, and
recruitment of other inflammatory cells to the area.
Occasional patients will have the onset of induration >72 hr after placement; this is a
positive result. Immediate hypersensitivity reactions to tuberculin or other constituents of
the preparation are short lived (<24 hr) and not considered a positive result.
Tuberculin sensitivity develops 3 wk to 3 mo-most often in 4-8 wk-after inhalation of
organisms.

DIAGNOSIS
1. History and examination (h/O TB contact):

Any person who had ATT within last 2 years from a recognize institute. This contact may be in family,
in neighborhood who handle the child frequently.
2. Tuberculin Skin Test:
A TST should be regarded as positive: . in children who are immunosuppressed (including HIV-positive children and severely
malnourished children, i.e. those with clinical evidence of marasmus or kwashiorkor): >5 mm
diameter of induration; . in all other children (whether they have received a BCG vaccination or not): >10 mm diameter of
induration
3. Radiological Diagnosis:
Lung is the most common and the first site of involvement of TB.
.
Primary complex in the lungs can be diagnosed by primary focus ( round coin shadow),
draining lymph vessels and the hilar nodes.
.
Tuberculous bronchopneumonia or consolidation due to aspiration of caseous material into
the lung.
4. AFB Smear and Culture:
. M. Tuberculosis is isolated from most of the body fluids and tissues.
. It is usually very difficult to get sputum in children less than 6 years of age as they swallow but not
cough out the sputum.
. Sputum specimens for culture should be collected from adolescents and older children who are
capable to expectorate. The best culture specimen in young children is the early morning gastric
acid obtained before the child has arisen and peristalsis has emptied the stomach of the pooled
secretions that have been swallowed overnight
5. Biopsy:
In case of tuberculous adenitis, requires excisional biopsy.

DIAGNOSIS
Other New Techniques:
1. DNA probes:These probes use DNA sequence that is complementary to
specific RNA or DNA sequence of M. Tuberculosis.
It is 100 % sensitive and specific when used on isolated
organism, the sensitivity drops when probes are used
directly on patient samples.
2. Polymerase Chain Reaction:PCR increases the sensitivity of DNA testing.
Results are available with PCR technique within 48 hours.
It is 95 % sensitive and specific for M. Tuberculosis in
sputum +ve pulmonary tuberculosis.

TREATMENT
DRUGS

DOSAGE
FORMS

DAILY
DOSAGE
mg/kg

Route

ADVERSE
REACTIONS

INH

Syp: 50
mg/5ml
Tab: 100 mg

10 15 mg

Oral

Mild hepatic
enzymes elevation,
Hepatitis, Peripheral
Neuritis.
Hypersensitivity.

RIF

Syp:100
mg/5 ml

10 20

Oral

Orange discoloration
of secretion or urine,
Hepatitis,
Influenza like
reaction,
Thrombocytopenia.
Pruritus.

PZA

Tab: 500 mg

20-40

Oral

Hepatotoxic Effects,
Hyperuricemia.
Athralgias.

Ethambutol

Tab: 100 mg
Tab: 400 mg

20

Oral

Optic Neuritis,
Decrease red-green
color discrimation.

STM

Vial 1 g

20-40

I/M

Auditory & vestibular

toxic effects.
Nephrotoxic Effects.

 Children with suspected or confirmed pulmonary TB or

tuberculous, can be treated with

a three-drug regimen (HRZ) for 2 months .

followed by a twodrug (HR) regimen for 4 months.

Streptomycin should not be used as part of first-line treatment
regimens for children with pulmonary TB or tuberculous
peripheral lymphadenitis
Children with suspected or confirmed tuberculous meningitis
and children with suspected or confirmed osteoarticular TB
should be treated with

a four drug regimen (HRZE) for 2 months,

followed by a two-drug regimen (HR) for 10 months, the

total duration of treatment being 12 months.
(H;Isoniazid ,,,,,,,,, R;Rifampicin ,,,,,,,,,Z;Pyrazinamide
E;Ethambutol)

PREVENTION

Primary Prevention ( BCG Vaccination):

BCG vaccine activates the host cell-mediated immunity to mycobacterial

antigens and prevents infection or progression to disease if a subsequent
infection with M. Tuberculosis occurs.
Efficacy 0-80 % in preventing subsequent TB, it limit serious disseminated
tuberculosis especially miliary TB and meningitis.
In settings where TB is highly endemic or where there is high risk of
exposure to TB, a single dose of BCG vaccine should be given to all infants
In children who are known to be HIV-infected, BCG vaccine should not be
given.
Clinical evaluation of household and close contacts for active TB should be
done on the basis of their risk for having or developing active TB or for the
potential consequences of the disease if it develops. Priority should be
given to contacts who are: children with symptoms suggestive of TB
children <5yrs of age
children with known or suspected immunocompromising conditions
(especially those living with HIV)

REFERENCES
WHO guidelines for tuberculosis treatment
Nelson textbook of paediatrics.
WHO Guidance for national tuberculosis programmes on
the management of tuberculosis in children,,2014
National guidelines for diagnosis and management of
tuberculosis in children(national tb control
programme,pakistan)