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Dr Meenal Kapoor
Indraprastha Apollo Hospital
New Delhi

www.dnbpediatrics.com

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Acute inflammation, edema and necrosis of
epithelial cells lining small airways, increased
mucus production, and bronchospasm (AAP
2006)
First episode of wheezing in a child < 12-24
months with physical findings of a viral
respiratory infection and has no other
explanation for the wheezing, such as
pneumonia or atopy


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Viral infection
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Respiratory syncytial virus (RSV)- MC (50-80%)
Rhinovirus – 2nd mc
Parainfluenza viruses
Influenza virus
Adenovirus
Coronavirus
Newer respiratory viruses - human metapneumovirus (hMPV),
human bocavirus (HBoV)


Viral inoculation
viral replication in the epithelial cells of the
airway
Cell lysis
Necrotic cells slough off and release inflammatory
mediators
Airway inflammation and edema
Increased mucus production

Narrowing and obstruction of the bronchioles
Increased resistance to air flow, decreased
ventilation and air trapping

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Most common lower respiratory tract
infection in infants
Age - < 2 years, peak incidence btw 2-6 months
Winter months
In India - September to March


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Acute onset
Prodrome - rhinorrhea, cough, low grade fever
SYMPTOMS ◦ Rapid respiration
◦ Irritability, poor feeding
SIGNS –
◦ Tachycardia and tachypnea
◦ Wheeze, Crackles , grunting
◦ Retractions
◦ Cyanosis, impaired perfusion
◦ Hyper-resonant chest on percussion

Pulse oximetry
Other associated problems - conjunctivitis, otitis media, pharyngitis

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Self-limited disease
Symptoms may persist for several weeks
In previously healthy infants - the average length of
hospitalization is 3 - 4 days
Prolonged course –
◦ Younger infants
◦ Comorbid conditions (e.g., chronic lung disease)


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Host Related Risk Factors
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Environmental Risk Factors
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Prematurity, LBW
Age < 6 to 12 weeks
Chronic pulmonary disease
Hemodynamically significant congenital heart disease
Immunodeficiency
Having older siblings, Passive smoke, Household crowding

Clinical Predictors
◦ Toxic look, SpO2 <95% on room air, RR – 70/min,
Moderate/Severe chest retractions, Atelectasis on CXR

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Diagnosis - clinical
Based on history and physical examination
Laboratory tests and CXR – not required, do
not alter treatment decisions
CXR
◦ If the diagnosis is in doubt
◦ co-morbidity like chronic lung disease or heart disease is
suspected
◦ there is no improvement
◦ child severely ill


 Hyperinflation

 Peribronchial

thickening

 Patchy

atelectasis (from airway
narrowing and mucus plugging)

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Not routinely indicated
Abnormalities in TLC and DLC do not predict serious
bacterial infection in infants and young children
hospitalized with lower respiratory tract infection due
to RSV
Measurement of lactate dehydrogenase (LDH)
concentration in the nasal-wash fluid
◦ proposed as an objective indicator of bronchiolitis severity
◦ increased values (suggestive of a robust antiviral response)
have been shown to be associated with decreased risk of
hospitalization
◦ Needs further validation

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Identification of viral agents does not affect
management
In the hospital setting, determining the responsible
virus may help to avoid unnecessary antibiotic use
Available tools - Antigen detection,
Immunofluorescence, PCR, and culture of respiratory
secretions obtained by nasal wash or nasal aspirate.
New techniques - real-time polymerase chain
reaction(PCR), nested PCR, and multiplex PCR
PCR – most sensitive

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SUPPORTIVE CARE

Mainstay of treatment

(A) FLUIDS :–
 Increased risk of dehydration because of their increased
needs (related to fever and tachypnea) and reduced oral
acceptance
 Intravenous fluids
 Children who can tolerate enteral feedings - small frequent
feedings or orogastric or nasogastric feedings
 Children with bronchiolitis are also at an increased risk of
fluid retention (and subsequent pulmonary congestion)


(B) NASAL DECONGESTION
 Saline nose drops and cleaning of nostrils by gentle
suction
(C) RESPIRATORY SUPPORT
 Supplemental oxygen
 CPAP ----------- inconclusive evidence
 Mechanical ventilation - clinical deterioration
(worsening respiratory distress, listlessness, and poor
peripheral perfusion), apnea/ bradycardia/ hypercarbia


BRONCHODILATORS
 Routine use of bronchodilators in the
management of bronchiolitis is debatable
 Consider a trial of bronchodilator with careful
monitoring.
 Salbutamol inhalation (personal or family
history of atopy or asthma)
 Epinephrine inhalation
 Further doses of either medications continued
only on documentation of improvement

HYPERTONIC SALINE
 Aerosolized hypertonic saline - therapeutic
modality for acute bronchiolitis.
 Acts by
◦ Decreasing epithelial edema
◦ improving elasticity and viscosity of mucus
◦ improving airway clearance
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Unanswered questions - optimal volume,
frequency of administration and effective
device


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SYSTEMIC CORTICOSTEROIDS
◦ No significant differences found in hospital admission rate, length of
stay, clinical score after 12 hours, or hospital readmission rate
◦ Hence, it is recommended not to use glucocorticoids

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CORTICOSTEROIDS + EPINEPHRINE
◦ Possible synergy
◦ Reduction in hospital admissions
◦ Still under evaluation

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INHALED CORTICOSTEROIDS
◦ No evidence for use

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CPAP
Surfactant - In severe bronchiolitis there may
be secondary surfactant insufficiency
suggesting possible role of administration of
exogenous surfactant
Current evidence - potential use in acute
severe bronchiolitis requiring mechanical
ventilation
Heliox
Aerosolized Ribavirin

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Aerosolized Ribavirin
synthetic nucleoside analogue
acts by inhibiting viral protein synthesis
delivered as a small-particle aerosol for 18
to 20 hours per day
in high risk infants (immunocompromised
and/or hemodynamically significant
cardiopulmonary disease) and
in infants requiring mechanical ventilation


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Oral bronchodilators
Montelukast
Inhaled/Systemic corticosteroids
Chest physiotherapy
Antibiotics
Steam inhalation
RSV polyclonal immunoglobulin / Palivizumab
Inhaled Furosemide/Inhaled interferon alfa2a / Inhaledrecombinant human DNase


General measures
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Barrier nursing measures to prevent
nosocomial infections

Specific measures - Immunoprophylaxis
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Polyclonal antibodies
Monoclonal antibodies


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Contain RSV IgG
Prepared from pooled plasma
I/V route
Before RSV season
Disadvantages –
◦ need for I/V access;
◦ risk of transmission of blood-borne infections,
◦ possible interference with antibody response to
routine immunization specifically live vaccines


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Produced by recombinant DNA technology
Targets the fusion protein of RSV, inhibiting
its entry into the cell and thereby preventing
infection
Reduces hospitalization rate in high risk
infants but does not reduce mortality rates
Expensive


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I/M
Dose - 15 mg/kg monthly during the RSV season
Maximum of 5 doses is generally sufficient
prophylaxis during one season
Once a child qualifies for prophylaxis,
administration should continue throughout the
RSV season and not stop at the point he or she
reaches any certain age.
Adv –
◦ Can be given with routine immunizations since it does
not interfere with the immunologic response to vaccines
◦ Minimal S/E


Infants Eligible for a
Maximum of 5 Doses

Infants Eligible for a
Maximum of 3 Doses

•Infants younger than 24
months of age with chronic lung
disease and requiring medical
therapy
•Infants younger than 24
months of age and requiring
medical therapy for congenital
heart disease
•Preterm infants born at 31
weeks, 6 days of gestation or
less
•Certain infants with
neuromuscular disease or
congenital abnormalities of the
airways

•Preterm infants with
gestational age of 32 weeks, 0
days to 34 weeks, 6 days with
at least 1 risk factor and born 3
months before or during RSV
season.


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Motavizumab ( 2nd generation mAb)
Numax-YTE ( 3rd generation)
Under clinical trials


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