BY DR AISHA IKRAMPG TRAINEE PAEDS UNIT 2

CASE

PRESENTATION

CASE8 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,cyanosis-ve,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 INVESTIGATIONSCBC:

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

TUBERCULOSISDEFINITION

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 μm 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 μm in diameter that contain M. tuberculosis.

The chance of transmission increases when the patient has an acid-fast 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 host’s 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.

DIAGNOSIS1. 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 .

DIAGNOSISOther 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.

TREATMENTDRUGS DOSAGE

FORMSDAILY

DOSAGEmg/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 mgTab: 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)

PREVENTIONPrimary 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)