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02 Lower Respiratory Tract Infections 2014 Feb
02 Lower Respiratory Tract Infections 2014 Feb
EPIDEMIOLOGY
Annual incidence is 11.4% in children younger than 1 year
and 6% in those aged 1-2 years.
Incidence peaks in those aged 2-8 months
95% have serologic evidence of past (RSV).; presence of
antibodies to RSV does not confer immunity.
Incidence of bronchiolitis winter months in temperate
climates and during the rainy season in tropical climates.
Hospitalization -2% of cases under 6 months
Mortality rate is 1-2% of all hospitalized patients and 3-4%
for patients with underlying cardiac or pulmonary disease.
EPIDEMIOLOGY
Prognosis is excellent.
Most children recover in 3 to 5 days without sequelae,
although wheezing and cough may continue for 2 to 4
wk.
Mortality is < 1% when medical care is adequate.
Bronchiolitis has been identified as a risk factor for
asthma, but the association is controversial and the
incidence seems to decrease as children age.
Treatment
Supportive therapy
O2 supplementation as needed
IV hydration as needed
Indications for hospitalization include
accelerating respiratory distress,
ill appearance (eg, cyanosis, lethargy, fatigue),
apnea by history, hypoxemia
inadequate oral intake.
children with underlying disorders such as cardiac disease,
immunodeficiency, or bronchopulmonary dysplasia, which
put them at high risk of severe or complicated disease, also
should be considered candidates for hospitalization
In hospitalized children, 30 to 40% O2 by tent or face mask
is usually sufficient to maintain O2 saturation > 90%.
Endotracheal intubation is indicated for severe recurrent
apnea, hypoxemia unresponsive to O2 therapy, or CO2
retention or if the child cannot clear bronchial secretions.
Hydration maintained with frequent small feedings of clear
liquids. For sicker children, fluids should be given IV
initially, and the level of hydration should be monitored by
urine output and specific gravity and by serum electrolyte
determinations.
There is little evidence that systemic corticosteroids are
beneficial
Antibiotics should be withheld unless a secondary bacterial
infection (a rare sequela) occurs.
Bronchodilators are not uniformly effective some children
may respond with short-term improvement. This is
particularly true of infants who have wheezed previously.
RIBAVIRIN
active in vitro against RSV, influenza, and measles, is toxic
RSV immune globulin has been tried
Prevention of RSV infection by passive immunoprophylaxis
with monoclonal antibody to RSV ( palivizumab )
SYNAGIS decreases the frequency of hospitalization but is
costly and is indicated primarily in high-risk infants
RESPIRATORY PHYSIOTHERAPY
NEBULISATIONS WITH: Epinephrine: 0.01 mL
(ie, 0.01 mL/kg of 1:1000 solution [1 mg/mL]) SC
q15-20min, not to exceed 0.3 mL/dose
Racemic epinephrine:
<2 years: 0.25 mL of 2.25% solution via nebulizer
diluted in 3 mL NS
>2 years: 0.5 mL of 2.25% solution via nebulizer
diluted in 3 mL NS
ALBUTEROL, VENTOLINE 90 mcg; 4-8
inhalations q 20min up to 4 h, then q 1-4h prn;
use with a spacer device
NONSTANDARD THERAPIES
Heliox
Mixture of helium and oxygen that creates less
turbulent flow in airways to decrease work of breathing
Only small benefit in limited patients
Anti-RSV preparations RSV-IGIV or Palivizumab
No improvement in outcomes
Surfactant
May decrease duration of mechanical ventilation or
ICU stay
COMPLICATIONS
Highest in high-risk children
Apnea
Most in youngest children or those with previous apnea
Respiratory failure
Around 15% overall
Secondary bacterial infection
Uncommon, about 1%, most in children requiring
intubation
PNEUMONIA
•The WHO Child Health Epidemiology Reference Group estimated
an annual incidence of 150.7 million new cases, of which 11-20
million (7-13%) are severe enough to require hospital
admission.
95% of all episodes of clinical pneumonia in
young children worldwide occur in developing
countries
PATHOPHISIOLOGY
Inflammation of the alveolar space and may
compromise air exchange.
Often complicating other lower respiratory infections
such as bronchiolitis or laryngotracheobronchitis,
pneumonia may also occur via hematogenous spread
or aspiration.
Most commonly, this inflammation is the result of
invasion by bacteria, viruses, or fungi, but it can occur
as a result of chemical injury or may follow direct
lung injury
PATHOLOGY
Bronchopneumonia is a patchy consolidation involving
one or more lobes. The neutrophilic exudate is centered
in bronchi and bronchioles, with centrifugal spread to
the adjacent alveoli.
In interstitial pneumonia, patchy or diffuse inflammation
involving the interstitium is characterized by infiltration
of lymphocytes and macrophages. The alveoli do not
contain a significant exudate
Bacterial superinfection of viral pneumonia can also
produce a mixed pattern of interstitial and alveolar
airspace inflammation.
Four stages of lobar pneumonia
1. In the first stage, within 24 hours of infection,
microscopically by vascular congestion and alveolar
edema. Many bacteria and few neutrophils are present.
2. The stage of red hepatization (2-3 d) similar to the
consistency of liver: presence of many erythrocytes,
neutrophils, desquamated epithelial cells, and fibrin
within the alveoli.
3. In the stage of gray hepatization (2-3 d), the lung is gray-
brown to yellow because of fibrinopurulent exudate,
disintegration of red cells, and hemosiderin.
4. The final stage of resolution :resorption and restoration
of the pulmonary architecture. Fibrinous
inflammation may extend into the pleural space, causing a
rub heard by auscultation, (resolution or to organization
and pleural adhesions)
ETIOLOGY
Bacteria accounted for 60%, of which 73% were due to
Streptococcus pneumoniae; Mycoplasma pneumoniae and
Chlamydia pneumoniae were detected in 14% and 9%,
respectively.
S pneumoniae, S aureus H influenzae are by far the most
common bacterial pathogen in 1-3 years age group
Enterococci
Newborns: group B Streptococcus, gram-negative rods
(E.coli, Klebsiella pneumoniae), Lysteria monocytogenes
Chlamydia trachomatis, U urealyticum, Mycoplasma hominis,
Treponema pallidum Toxoplasma gondi
Viruses that cause acute pneumonia
adenovirus
coronavirus
influenza A and B viruses
parainfluenza virus
respiratory syncytial virus
coxsackievirus A21
rhinovirus
BACTERIA THAT CAUSE PNEUMONIA
GRAM POSITIVE COCCI
1.Streptococcus Pneumoniae
the most common
2. Streptococcus Pyogenes
3. Streptococcus Agalactiae
ETIOLOGY OF BACTERIAL PNEUMONIA
S- Pneumoniae generally resides in the nasopharynx
and is carried asymptomatic in approximately 50% of
healthy individuals. A strong association exists with
viral illnesses, such as influenza. Viral infections
increase Pneumococcal attachment to the receptors
on activated respiratory epithelium. Once aerosolized
SP go from the nasopharynx to the alveolus,
Pneumococci infect type II alveolar cells,multiply in
the alveolus and invade alveolar epithelium.
Pneumococci spread from alveolus to alveolus
through the pores of Kohn, thereby producing
inflammation and consolidation along lobar
compartments
Patients with pneumococcal pneumonia may produce
bloody or rust-colored sputum
Streptococcus agalactiae is a commensal organism in the
genital tract and it can cause pneumonia in newborns which
inhale fluid containing the bacteria during its journey down
the birth canal and develops pneumonia soon after birth.
Staphylococcus aureus is gram positive organism,affecting
children and old people. as well as extreme ages.it can
produce thin walled air filled cavities ("pneumatoceles ")
Staphylococcal pneumonia is diagnosed by finding typical
clusters of Gram-positive cocci by microscopy and
subsequently a growth of Staphylococcus aureus in a
purulent sputum that often appears creamy and
bloodstained.
Staphylococcal pneumonia and
bronchopneumonia ( cont’)
Louse-borne
flea-borne through rats and mouse fleas
Rickettsial Pneumonia
Q fever ranging from multiple segmental opacities to
pleural effusion, lobar consolidation, or linear
atelectasis.
Hepatosplenomegaly is a common finding; it usually
is accompanied with elevation of liver enzymes
Rickettsia pneumonia cannot be distinguished
clinically, radiologically, or histologically from
atypical pneumonia.
ATYPICAL BACTERIA
These are the bacteria's that will be called as atypical bacteria and
causing also atypical pneumonias like other viral agents etc.and
constitute following organisms
Legionella
Mycoplasma pneumoniae
Chlamydia trachomatis an afebrile pneumonia,
usually seen in 2 wk to 6 months of age
Chlamydia psittaci
Chlamydia pneumoniae , Chlamydia trachomatis
This is a sexually transmitted disease that may also cause pneumonia
and bronchitis. It usually is a subacute infection of early infancy
producing a sudden cough and eosinophilia without fever that lasts
from 1-3 weeks, but it may occur in adults too.
Etiology of Pneumonia in
Hospitalized Children
• Course is mild and self limiting and resolves by 7-10 days time
hilar adenopathy
History of Empiric Therapy
carbapenems,
fluoroquinolones,
aminoglycosides,
vancomycin
Methicillin-resistant Staphylococcus aureus, known
as MRSA, is a type of Staphylococcus aureus that is
resistant to the antibiotic methicillin and other drugs
in the same class, including penicillin, amoxicillin,
and oxacillin
Therapeutic choice: vancomycin, targocid
( teicoplanin), linezolid ( zyvoxid)
Empiric Therapy of Children with Pneumonia (I)
Pentamidine isethionate
Trimethoprim-Sulfamethoxazole
atovaquone
trimetrevate
Trimethoprim-sulfamethoxazole is
preferred because of its low toxicity and
greater efficacy.
BACTRIM-DS
Bactrim DS tablet contains. 160 mg of trimethoprim
and 800 mg of Sulfamethoxazole.
21 days course
Prednisolone 40 mg bid x 5 days, then 40 mg/day x
5 days, then 20 mg/day to completion of treatment
Alternative Treatments:
TMP 15 mg/kg/day PO + dapsone 100 mg/day
x 21 days
Pentamidine 4 mg/kg/day IV x 21 days
-Atovaquone 750 mg PO bid with meal x 21 days
PCP is the most frequently identified serious in
HIV disease