0% found this document useful (0 votes)

94 views35 pages

Resp Emer in Children

excellent resource in managing resp emergencies in children

Uploaded by

vgmanjunath

We take content rights seriously. If you suspect this is your content, claim it here.

Available Formats

Download as PDF, TXT or read online on Scribd

0% found this document useful (0 votes)

94 views35 pages

Resp Emer in Children

excellent resource in managing resp emergencies in children

Uploaded by

vgmanjunath

We take content rights seriously. If you suspect this is your content, claim it here.

Available Formats

Download as PDF, TXT or read online on Scribd

You are on page 1/ 35

C o m m o n Pe d i a t r i c

Respiratory
Emergencies
a, b
Joseph Choi, MD *, Gary L. Lee, MD, CCFP-EM, FRCPC

KEYWORDS
Pediatric Asthma Bronchiolitis Croup Pneumonia

Acute respiratory distress is one of the most common reasons why parents bring their
children to the emergency department (ED). Severity can range from mild, self-limiting
illness to life-threatening disease. This article reviews the 4 most common of these
conditions, namely asthma, croup, bronchiolitis, and pneumonia, to update the reader
on the current state of evidence in the assessment and treatment of these conditions.

ASTHMA IN CHILDREN

Asthma is a chronic inflammatory condition of the airways leading to episodic

wheezing, coughing, chest tightness, and shortness of breath. It is a common condi-
tion, with the highest prevalence occurring between the ages of 5 and 17 years.
Asthma afflicted 7.0 million children in this age group in the United States in 2008.1
It led to 1.7 million ED visits in 2006, and children younger than 15 years accounted
for 33% of those with a discharge diagnosis of asthma while this age group only repre-
sents 20% of the general population.1
Asthma is the most activity-limiting condition in children and accounts for 14.4
million lost school days. It is an expensive disease, with an annual burden of $15.6
billion in direct health care costs and $5.1 billion in indirect health care costs and
lost productivity, for a total annual sum of $20.7 billion.1

Pathophysiology
Asthma is a chronic disease of the lower airways punctuated with episodic acute
exacerbations. The clinical manifestations are caused by airway hyperresponsiveness
to stimuli that are generally innocuous, leading to constriction of bronchial smooth

The authors have nothing to disclose.

a
McGill University FRCP Emergency Medicine Residency Program, Royal Victoria Hospital, 687
Pine Avenue West, Room A4.62, Montreal, Quebec, Canada H3A 1A1
b
Department of Emergency Medicine, Montreal Children’s Hospital, Montreal General
Hospital, McGill University, 1650 Cedar Avenue, Montreal, Quebec, Canada H3G 1A4
* Corresponding author.
E-mail address: [email protected]

Emerg Med Clin N Am 30 (2012) 529–563

doi:10.1016/j.emc.2011.10.009 emed.theclinics.com
0733-8627/12/$ – see front matter Ó 2012 Elsevier Inc. All rights reserved.

Downloaded for manjunath hunsur ([email protected]) at JSS University from ClinicalKey.com by Elsevier on October 14, 2019.
For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved.
530 Choi & Lee

muscle (bronchospasm), the major cause of wheezing during an asthma exacerbation.

Airway inflammation and edema in response to these stimuli further narrows the
airway and restricts ventilation.2,3
These physiologic changes on the cellular level can occur through IgE-mediated
pathways (allergen-triggered asthma)4 and non–IgE-mediated pathways (asthma in
response to nonsteroidal anti-inflammatory drugs,5 certain other drugs, exercise, and
cold temperatures).3 Both pathways lead to a release of various cytokines and chemo-
kines from inflammatory cells, which promote further migration and activation of inflam-
matory cells in the lower airways, thus perpetuating the cycle.3

Diagnosis
The diagnosis of asthma is particularly challenging in the pediatric population. Young
children usually cannot be cooperative enough to undergo formal pulmonary function
testing, which is the gold standard in the diagnosis of asthma. Thus they often must be
diagnosed clinically.
Many first-time wheezers also present to the ED. Most instances of wheezing in
young children presenting to the ED are solely related to upper respiratory infections
(URI) causing inflammation of the lower airways rather than true asthma.6 The majority
of early wheezers do not go on to develop asthma in later childhood or adulthood.6,7
This distinction is an important one, as it can affect the efficacy of certain therapeutic
options.8 Clues that increase the likelihood that the wheezing is due to asthma include
the frequency of episodes (more than once a month), triggers (exercise, allergens,
tobacco smoke), prolonged respiratory symptoms in the setting of URI (symptoms
lasting more than 10 days suggest a viral trigger of asthma), personal or family history
of atopy or asthma, and a history of a good and rapid response to bronchodilator
therapy.3,6,9
Other historical features of the patient that may aid in predicting the severity of the
asthma exacerbation include the frequency and compliance in using asthma medica-
tions at home, previous hospital visits for asthma exacerbations (requiring admission
to the ward or intensive care unit [ICU]), and severity of asthma exacerbations
(requiring intubation). Social attributes of the patient and caregivers, such as the ability
to purchase medications and comply to their use, a household environment free of
known or suspected asthma triggers, and ability to obtain follow-up and access
medical services in the event of another exacerbation, have important discharge plan-
ning implications and should be elicited early.2,3,7,9
The physical examination may reveal any combination of the classic constellation of
symptoms in the acute asthma exacerbation, which includes wheezing, cough, chest
tightness, tachypnea, respiratory distress, intercostal indrawing, and accessory
muscle use.3,7,9 Of interest, the use of the scalene muscles and suprasternal
retractions have the highest interrater reliability and correlation with asthma severity.10
Clinical asthma assessment tools, such as the Pediatric Respiratory Assessment
Measure (PRAM; Table 1)10,11 and the Pediatric Asthma Severity Score (PASS),12
have been independently shown to be predictive in discriminating a patient’s length
of stay in the hospital and admission.10,12 The strength of these two scales is that
they include preschool-aged children, in comparison with older severity scales such
as the Pulmonary Index and the Pulmonary Score, which are only validated in older,
school-aged children.10–12 A recent head-to-head comparison of the two scores
showed very similar performance in their ability to predict a prolonged stay (>6 hours)
and/or admission when taken at triage.13 However, a repeat score taken 90 minutes
after treatment showed that the PRAM score was more responsive and predictive

Table 1
The Pediatric Respiratory Assessment Measure (PRAM) score

Signs 0 1 2 3
Suprasternal Absent Present
indrawing
Scalene use Absent Present
Wheezing Absent Expiratory Inspiratory and Audible without stethoscope or
only expiratory minimal air entry/silent chest
Air entry Normal Decreased Widespread Minimal air entry/silent chest
at bases decrease
Pulse oximetry >95% 92%–94% <91%
on room air

Data from Ducharme F, Chalut D, Plotnick L, et al. The Pediatric Respiratory Assessment Measure:
a valid clinical score for assessing acute asthma severity from toddlers to teenagers. J Pediatr
2008;152(4):476–80, 480.e471.

(area under the receiver-operator characteristic curve 0.82 vs 0.72).13 These tools can
be particularly useful when integrated into protocolized treatment regimens.2,9,14
Investigations should include measurement of oxygen saturation, with more severe
exacerbations deserving continuous monitoring. A blood gas sample may be useful
in severe exacerbations in addition to clinical signs to determine respiratory function
and responsiveness to therapy. In particular, normocarbia or hypercarbia in a patient
after a round of standard treatment is a worrisome sign.3,9
Peak expiratory flow (PEF) is an objective method of assessing the degree of airway
obstruction. However, it is often exceedingly difficult (if not impossible) to obtain these
measurements in children younger than 6 years, and even with a cooperative child the
measurements may not be reliable in an acute exacerbation.15,16 If PEF values are
obtained, suggested categories include mild (PEF >80% predicted), moderate (PEF
60%–80% predicted), or severe (PEF <60%),2 though different governing bodies
have varying values.3,9
Additional blood work and imaging only aid in excluding complications or other
diagnoses based on clinical suspicion,3,9 and are not routinely recommended.

First-Line Treatment
Children with acute exacerbations should be rapidly assessed and triaged to a location
in the ED where observation and frequent reassessment can be performed by medical
and nursing staff. Reassessment of patients after each round of treatment is by far the
most important aspect in the management of acute asthma exacerbations. Children,
and especially infants, are particularly at risk for respiratory failure. Hypoxemia
develops more rapidly in children than in adults; therefore monitoring of oxygen satu-
ration is necessary.3,9 Oxygen should be administered only to maintain a saturation
of greater than 92%–94%,3,9 as indiscriminate high-flow oxygen despite good satura-
tions can lead to poorer outcomes.17
Short-acting b-agonist (SABA) treatment is the most effective method of relieving
bronchospasm, and should be given to all patients with asthma exacerbations.3,9
SABA can be administered as either intermittent therapy spaced 15 to 20 minutes apart
via wet nebulizer or metered-dose inhaler (MDI) with a holding chamber, or as contin-
uous therapy via a nebulizer.18,19 In mild to moderate asthma, an MDI has been shown
to be at least equivalent if not better in efficacy than a nebulizer in infants, children, and
adults,20–23 and is more cost effective.24 Factors that influence the choice of MDI

versus nebulizer include patient cooperation, response to treatment via MDI, and
severity of the exacerbation. Salbutamol (albuterol, Ventolin) 2 to 4 puffs, can be given
every 15 minutes via MDI with chamber, waiting 5 tidal volume breaths between
puffs.3,9 More puffs can be administered (up to 10) in more resistant exacerbations.
Salbutamol can also be given at 0.15 to 0.3 mg/kg via nebulizer, with a minimum of
2.5 mg and maximum of 5 mg per nebulized mask. This volume is then diluted with
normal saline for a total of 5 mL of fluid per nebulized mask. The most severe exacer-
bations may benefit from continuous therapy19 with a nebulizer driven by oxygen if
hypoxia is also present.3,9,17 With continuous nebulization, salbutamol is recommen-
ded to be given at 0.5 mg/kg/h with the hourly dose not exceeding 10 to 15 mg/h.3
Levosalbutamol ((R)-salbutamol, also known as levalbuterol) is the pure (R)-enan-
tiomer of the salbutamol molecule. In a typical salbutamol preparation, there is
a 50:50 mixture of the (S)- and (R)-enantiomers, and it is the (R)-enantiomer that
provides the vast majority of the bronchodilating effects, due to its 100-fold higher
affinity for the b2-adrenergic receptor. The selectivity of levosalbutamol theoretically
maximizes the bronchodilating effects while minimizing systemic side effects such
as tachycardia25 and hypokalemia.26 Small trials have shown mixed results, with
some trials showing benefit in pulmonary function,27,28 reduction in hospital admission
rates,29 and reduced side effects26,30; whereas other studies have shown no differ-
ence.30,31 Levosalbutamol is considerably more expensive than the conventional
racemic mixture, and current guidelines do not recommend using one over the other.
The dose of levosalbutamol is half that of salbutamol.
Ipratropium bromide (Atrovent) has been shown to be an effective adjunct in
moderate to severe asthma in addition to inhaled b-agonists.32,33 It is a muscarinic
acetylcholine receptor blocker, which produces bronchodilation via smooth muscle
relaxation. Ipratropium bromide can be given via MDI (4–8 puffs every 15–20 minutes)
or nebulizer (0.25–0.5 mg, combined in the same nebulizer as the b-agonist).3,9 Treat-
ment can be tapered as the patient improves clinically.
Systemic corticosteroids (SCS) have been shown to decrease the need for hospital
admission from the ED when given early34,35 and to decrease the length of stay.36 SCS
should be considered in all but the mildest exacerbations.3,9,34 However, there is
evidence that shows administration of steroids to children with wheezing triggered
by a URI and with no other history suggesting asthma provides no benefit in time to
discharge, admission rate, morbidity, or mortality.8 The efficacy of oral versus intrave-
nous (IV) SCS has been shown to be equivalent in pediatric asthma exacerbations.37,38
Parenteral SCS should be reserved for those who cannot tolerate oral steroids or have
intestinal issues that would affect its absorption.3,9 Oral prednisone or prednisolone, 1
to 2 mg/kg, should be given once daily, with a maximum dose of 60 mg/d
for 3 to 5 days.2,3 Studies suggest that a 2-day course of oral dexamethasone (dosed
at 0.6 mg/kg daily, maximum of 16 mg) is as effective (measured by symptoms scores,
admission rates, and 10-day relapse rate) and well tolerated (rates of nausea and vom-
iting) as a 5-day course of oral prednisone in adults39 and children.40,41 Another study
even suggests that a single dose is non-inferior to a 5-day course of prednisone.42
Intramuscular (IM) injection of depot steroids, such as dexamethasone acetate, has
also been shown in small studies to be as effective as a 5-day course of predni-
sone.43,44 IV steroids can be given as methylprednisolone, 2 mg/kg/d in two divided
doses.3 Inhaled corticosteroids (ICS) are not currently recommended as a replacement
for SCS for the treatment of acute asthma exacerbations presenting to the ED,3,9
because of the lack of efficacy when used alone.34,35,45–48 Recent evidence suggests
that the addition of inhaled budesonide to standard therapy including SCS does not
improve outcomes.49

Second-Line Treatments
In children with severe or life-threatening asthma, the aforementioned therapies may
not be sufficient. It is crucial to recognize refractory asthma and to treat it aggressively.
Magnesium sulfate is a safe drug with few side effects, which has been shown to
have bronchodilating effects.50–52 Its use has not been shown to be beneficial in
mild to moderate asthma, but has demonstrated a reduction in admission rates for
severe asthma, with minimal side effects.53,54 A single IV dose of 25 to 75 mg/kg
(not exceeding 2 g) can be given over 2 hours.3,9 Inhaled magnesium sulfate has
been shown in small studies to improve expiratory flow measures when used in addi-
tion to inhaled b-agonists in severe asthma exacerbations,55,56 but confers no benefit
in mild to moderate episodes.57 A Cochrane review showed that nebulized magne-
sium sulfate provided significant improvement in pulmonary function tests and
a nonsignificant trend to decreased hospital admission rates in severe asthma exac-
erbations, but no statistically significant difference when included in all severities of
asthma attacks.58 Inhaled magnesium sulfate is given as the diluent in place of normal
saline (usually 2.5 mL of a 250 mmol/L solution) combined with salbutamol and ipra-
tropium bromide in the same nebulized mask.
Oral leukotriene receptor antagonists (LTRA) such as montelukast (Singulair) have
been shown to decrease symptoms of mild to moderate asthma exacerbations,59,60
but their role in severe asthma is unknown because of their slow onset of action.61
In moderate to severe asthma there is some evidence in the adult literature that IV
administration may be effective,62 but there are no corresponding studies done in chil-
dren. The oral dosage of montelukast in children is 4 to 10 mg orally once per day.
Heliox is a blend of helium and oxygen, the use of which is based on the principle of
increased ventilation into the lower airspaces in asthma, due to its low viscosity.63
Some studies have shown modest benefit63–65 whereas others show no benefit.66 It
has a level D recommendation as the driver of nebulized salbutamol in severe
asthma,3 mainly because of its lack of side effects.
Routine antibiotics are not recommended unless there is a suspicion of pneumonia
(fever, purulent sputum) or bacterial sinusitis.2,3,9 Mucolytics and sedation are not
recommended.2,3,9

Status Asthmaticus and Imminent Respiratory Failure

One of the most terrifying prospects for an emergency physician is the sight of a child
with asthma not responding to treatment and heading toward respiratory failure. Signs
include increasing somnolence, tiring of breathing muscles, cyanosis, and a silent
chest. Heralds of impending cardiac arrest are bradycardia, severe hypoxia, and
hypercapnia.
If not already performed, IV access should be obtained and any hypovolemia should
be corrected. This action is also taken to prevent hypotension that the induction drugs
may cause during rapid sequence intubation and positive ventilation.
IV b-agonists have not been shown to be beneficial in severe exacerbations, and
carry significant side effects.3,67 Likewise, aminophylline has not been recommended,
due to its considerable toxicity and lack of clear benefit,68 though a study has shown
some effect in children with life-threatening asthma already receiving maximum doses
of conventional therapy.69 However, in the setting of a status asthmaticus in extremis
with no response to other therapies, guidelines still endorse consideration of their use
as a last resort.2,3,9
Temporizing measures can include a trial of noninvasive positive-pressure ventila-
tion (NPPV). There are small studies analyzing the ability of NPPV to avoid intubation

and improve outcomes in children with status asthmaticus,70–75 and a Cochrane

review showed a trend toward benefit.76 If the patient is unable to tolerate NPPV
and continues to deteriorate, endotracheal intubation with mechanical ventilation is
necessary.3,9 Once the decision has been made, the most experienced physician
should make the attempt, as asthmatic patients are often difficult to intubate and
desaturate quickly. Traditionally the induction agent of choice is ketamine (1–2 mg/
kg IV) because of its mild bronchodilating properties,77 though the clinical significance
of this bronchodilation is questionable,77,78 and several trials using ketamine infusion
as an adjunct in status asthmaticus have shown no benefit.78,79 Ketamine can also
increase oral and airway secretions80 and trigger laryngospasm, and should be
used in conjunction with a paralytic agent to counteract this possibility.81 Other
choices for induction include etomidate (0.3 mg/kg IV) and propofol (1.5–3 mg/kg
IV). The paralytic agent of choice depends on patient characteristics, the presence
of contraindications to particular agents, and physician preference and experience.
A ventilator strategy that has shown benefit is one of permissive hypercapnea.3,82–86
With this strategy, PCO2 is allowed to reach up to 70 mm Hg, providing high FiO2
concentrations to maintain saturations greater than 92%, and manipulating ventilator
settings (such as the prolonging the expiratory time to allow for complete exhalation)
to minimize pressures and avoid barotrauma and other complications. Bicarbonate
can be given to correct severe acidosis.87

Disposition
The decision to hospitalize children with severe asthma depends on the severity of
the exacerbation and its response to ED therapy. Those who present with PEF
less than 25%, or have a PEF less than 40% or significant symptoms after therapy,
should be admitted for continued treatment and observation.2,3 Unstable home
situations or predicted poor compliance and follow-up are also indications for
admission.2,3,9
Children receiving treatment in the ED should be monitored for at least 1 hour after
their last round of treatment to ensure resolution of symptoms.2,3,9 In those able to
provide PEF measures, a general value of greater than 70% to 80% of expected value
is acceptable for discharge. Those with a PEF of 40% to 69% with minimal symptoms
can also be discharged if they have good follow-up and demonstrate good compli-
ance, and if medical attention is readily accessible.2,3
Follow-up with a primary care provider or asthma specialist should be arranged
within a month of discharge from the ED to reassess medications and treatment
plans,2,3 as this has been shown to improve outcomes and decrease ED visits.88,89
The appointment should be scheduled before discharge from the ED, as this has
been shown to increase compliance.90,91
Medications to be continued after discharge include inhaled salbutamol and oral
steroids as already described, with no need for a tapering dose.2,3,9 Current guidelines
state that the initiation of ICS should be considered in those with moderate to severe
exacerbations who were not previously on ICS.2,3,9 Patients should be given a 1- to 2-
month supply, as this has been shown to reduce the number of exacerbations and ED
visits.46,92,93 ICS should be continued if previously prescribed. Ipratropium bromide
has not been shown to be of benefit after discharge from the ED.
Discharge home with a peak flow meter is also recommended for children older than
5 years,3 especially in those who do not perceive mild symptoms well or have recur-
rent severe exacerbations.94
Children to be discharged should be provided a written action plan (WAP) that delin-
eates clearly discharge medications, instructions in proper inhaler and peak flow

meter technique, follow-up appointments, and warning signs that indicate a need to
return to the ED.2,3

CROUP

Croup is a common cause of stridor in the young child. Croup is characterized by

a harsh inspiratory stridor and a hoarse cough that is often described as barky or
resembling a seal, secondary to upper airway inflammation and edema. Although
usually benign and self-limiting, it can cause significant respiratory distress requiring
intubation.
Croup is the most common cause of stridor in young children older than 6 months. It
peaks between 6 and 36 months of life. At 2 years of age, 5% of all children will have
had croup.95 In a 14-year observational study in Ontario, Canada, its incidence seems
to have a biennial mid-autumn peak and an annual summer trough, with boys being
affected 1.5 times as often as girls.96

Pathophysiology
There has been much confusion in the use of the term croup. It has been used to
describe different disease entities in which stridor and hoarse cough are the predom-
inant symptoms,95 such as spasmodic croup, laryngotracheobronchitis (LTB), laryng-
otracheobronchopneumonia (LTBP), bacterial tracheitis, and diphtheria. In this review
croup specifically refers to laryngotracheitis, as the other entities have different
presentations, treatment options, and prognoses.
Croup is commonly caused by parainfluenza virus (PIV)-1.97 PIV-2 and PIV-3 are
also implicated in croup, with type 2 causing a milder form and type 3 causing
a more severe form. Other viruses that can lead to croup include influenza, respiratory
syncytial virus (RSV), rhinoviruses, enteroviruses, and measles, among others.95
Viral infection often starts via inoculation of the nares and pharynx, which leads
to typical URI symptoms of low-grade fever, coryza, and rhinorrhea. The infection
then spreads down to the larynx and subglottic area, causing cough and inflammation
and edema of the upper airway and leading to varying degrees of obstruction. Accord-
ing to Poiseuille’s equation, resistance to flow is inversely proportional to radius to the
fourth power. Therefore even slight decreases in diameter can cause significant resis-
tance, especially in the already tiny airways of the young child. The lower airways are
usually not affected in PIV-associated croup, though RSV and influenza can cause
lower respiratory symptoms.

Diagnosis
The constellation of a barky cough, hoarseness, and stridor is common in many
diseases, and differentiation between them is of utmost importance, as treatment
and potential complications vary widely.
The onset and progression of symptoms leading to the ED visit should be explored.
The history of a preceding URI in the last day or two is often elicited. In addition to
cough and stridor, the child is often febrile. Combined with other features of the
history, a suddenly stridorous child without fever or URI should raise a suspicion of
foreign body aspiration or angioneurotic edema. An immunization and travel history
should be elicited, since an unimmunized child is at higher risk of developing laryngeal
diphtheria from Corynebacterium diphtheriae infection. Pharyngitis and dysphagia are
features that are uncommon with croup, and may suggest retropharyngeal abscess,
peritonsillar abscess, epiglottitis, or diphtheria. Finally, caution is required when diag-
nosing croup in a stridorous child younger than 6 months, due to the important

differential diagnosis in this age group. The differential includes laryngomalacia (the
most common cause, and a self-limited condition that 90% grow out of by 12–18
months),98 vocal cord paralysis,99 papillomatosis,100 congenital causes (such as
hemangiomas,101 laryngeal webs,100 and neurofibromas102), and iatrogenic causes
(such as subglottic stenosis following intubation for prematurity,103 or vocal cord
paralysis caused by laryngeal nerve damage from thoracic or cardiac procedures104).
The child should otherwise appear well; a toxic-looking child should be investigated
for alternative diagnoses such as bacterial tracheitis (which can be a complication
of croup), LTB, LTBP, or epiglottitis. There should be no signs of lower airway involve-
ment such as wheezing or crackles, which may suggest an alternative diagnosis. If
hemangiomas are noted on the child, especially above the clavicles, a subglottic
hemangioma should be considered along with historical features such as a lack of
URI symptoms. A throat examination should identify pharyngeal causes of stridor
easily, though caution should be exercised if the presentation is suspicious for epiglot-
titis. The epiglottis, if visualized, should be normal.
The diagnosis of croup remains a clinical one, with additional testing being useful in
ruling out other differential diagnoses. Complete blood cell counts (CBC) may show
a mildly elevated white cell count in croup, whereas it is usually markedly elevated
or depressed in bacterial infections of the upper airway with increased neutrophils
and band forms. Posterior-anterior neck radiographs in croup may show subglottic
narrowing (steeple sign) with a smooth tracheal contour. Irregularity of this contour
suggests bacterial tracheitis and other diagnoses.95 Lower respiratory symptoms
should be investigated with a chest radiograph (CXR) to assess for a possible pneu-
monia. A lateral neck radiograph showing a thickened mass at the level of the
epiglottis (thumbprint sign) suggests epiglottitis.105 Foreign bodies may appear on
plain films, depending on the object.

Classification
Different classification scales based on physical examination findings have been
devised. The Westley Croup Score106 is the most widely known and used, although
it is used more commonly in research protocols and less frequently in clinical prac-
tice.107 Key criteria used in this score include level of consciousness, stridor, air entry,
cyanosis, and chest wall retractions.95,106,107
A simplified classification, based from the original Westley Croup Score, has been
suggested by several investigators.95,107 Mild croup is defined by an absence
of stridor at rest, minimal respiratory distress, and occasional cough. Moderate croup
has stridor at rest and increased amount of respiratory distress, but behavior and
mental status are normal. Severe croup has significant respiratory distress and mental
status changes, with increasing somnolence and decreasing air entry signifying
impending respiratory failure.

Treatment
As with all patients, the ABCs (Airway, Breathing, Circulation) must be prioritized.
Patients with signs of impending respiratory failure should be intubated with an
endotracheal tube 0.5 to 1 mm smaller than the expected size. Oxygen should
be delivered to maintain oxygen saturation greater than 92% to 94%. Where
possible, the child should be kept calm to decrease respiratory distress and
improve airway dynamics.
The mainstays of pharmacotherapy in the ED management of croup are corticoste-
roids and nebulized epinephrine. Dexamethasone remains the corticosteroid of choice
over prednisolone through its ability to decrease return visits and admissions.108 In

a recent Cochrane review, dexamethasone was shown to reduce symptoms in the ED,
decrease length of stay, and result in fewer return visits.109 Dexamethasone is given as
a single dose of 0.6 mg/kg by mouth/IM/IV (oral is preferred, though parenteral routes
have been shown to be equally effective110) to a maximum of 10 mg. There are several
studies that show lower doses of dexamethasone (0.15–0.3 mg/kg) may be equally
effective.111–113 Inhaled budesonide can be used if available (2 mg via nebulizer) and
has been shown to be similar in efficacy to dexamethasone,109,114,115 though avail-
ability, cost, and convenience makes dexamethasone a more attractive option. There
does not appear to be any additional benefit from combining oral and inhaled steroids
in the setting of croup.116 Corticosteroids should be considered in all severities of
croup.
Nebulized epinephrine is used in moderate to severe croup, and has been shown to
be highly efficacious in reducing symptom scores at 30 minutes after treatment and
time spent in the ED.117 However, the natural history of the disease is unchanged,
and thus it is important to monitor children after epinephrine treatment for rebound
reactions.106,118 Despite the theoretical benefits of L-epinephrine over racemic
epinephrine, studies did not show a benefit of choosing one over the other.117
L-Epinephrine is given as 5 mL of a 1:1000 solution (racemic epinephrine is given as
0.5 mL of a 2.25% solution in 2.5 mL of normal saline) delivered via nebulizer every
15 minutes to effect. Although serious cardiac complications from epinephrine treat-
ment are exceedingly rare, it is prudent to put children requiring multiple treatments on
continuous cardiac monitoring.
Although cold, humid air anecdotally has been thought to improve croup symptoms,
recent trials did not show this benefit in the ED setting.119–121 A study evaluating the
use of Heliox showed that it may be as effective as nebulized racemic epinephrine
in moderate to severe croup.122 Heliox also demonstrated a nonstatistically significant
trend toward improvement in croup scores when combined with epinephrine and
steroids.123 However, a Cochrane review showed no significant difference in croup
scores when Heliox was added to conventional therapy, and therefore did not
routinely recommend its use at this time.124 Antibiotics should be saved for suspected
bacterial complications such as bacterial tracheitis or LTBP. Sedatives and antitus-
sives are not indicated.95,107
Disposition
Most cases of croup are mild to moderate and respond well to steroid with or
without nebulized epinephrine therapy, and the vast majority of patients are dis-
charged home. Children with mild symptoms (ie, no stridor at rest) can be safely
sent home. Patients receiving epinephrine should be observed for 4 hours to watch
for any rebound phenomenon. Children who require multiple epinephrine doses
should be admitted for observation. ICU admission may be required in cases of
severe croup that fail to respond to treatment. On discharge, it is prudent to inform
the parents that symptoms of croup usually peak between days 2 to 3.

BRONCHIOLITIS

Bronchiolitis is the most common lower respiratory tract condition in children younger
than 2 years, and is the leading cause of hospitalization of infants. Its most common
cause, RSV, is ubiquitous worldwide, affecting nearly all children by the age of 2, often
causing dyspnea in its tiniest of victims with the potential to cause respiratory failure
and death. Significant literature and practice guidelines have been published to guide
practitioners. Active research in the field is ongoing, and even small improvements in
therapy or resource use can make a major impact given the burden of disease.

Definition and Epidemiology

Bronchiolitis is typically caused by viral infection, characterized by bronchiolar
inflammation in children usually younger than 2 years. Children from age 2 to 5
years with similar symptoms rarely have bronchiolitis, as asthma, recurrent viral
wheeze, or pneumonia are more likely diagnoses. Wheezing is the hallmark of the
American definition of bronchiolitis, where British and Australian definitions include
inspiratory crackles as part of the diagnosis.125,126 Most studies and guidelines
define bronchiolitis as the first episode of wheezing or crackles. As the presenta-
tions of bronchiolitis, viral-associated wheeze, and asthma may appear similar,
attention to the features of patients becomes very important given differing patho-
physiology and responses to treatment.125
RSV continues to be the most common cause, responsible for approximately 50%
to 80% of cases. The epidemiology of bronchiolitis follows closely that of RSV. A
strongly seasonal virus, RSV causes outbreaks most commonly between November
and March in the northern hemisphere and between May and September in the
southern hemisphere. Up to half of infected children younger than 2 years will have
lower respiratory tract symptoms, whereas older children and adults are more likely
to have upper tract disease only. Peak age for bronchiolitis is 2 to 6 months old,
with most cases occurring before age 9 months. Reinfection with RSV is common,
given poor postinfection immunity.
Recent studies demonstrate an increasing role and frequency of other viruses
causing bronchiolitis, including human metapneumovirus (10%–20%), human bocavi-
rus, rhinovirus, parainfluenza, adenovirus, influenza, and coronavirus.127–129 Although
rhinovirus and human metapneumovirus infection has been shown to be generally less
severe than RSV (Group A strains causing more severe disease than Group B strains),
etiologic diagnosis is often not known in the ED and does not currently affect ED
management.127,130
Bronchiolitis-associated hospitalizations have more than doubled over recent
decades, likely attributable to several factors including increased spread of viral
illnesses from daycare exposures, greater awareness of hospitalization criteria,
routine oximetry use, and marginally larger numbers of higher-risk children
afflicted because of higher survival rates of at-risk populations.131 Associated
mortalities for the condition fortunately have fallen from an alarming 4500 annually
in the United States in 1985 to 390 in 1999.132 Although a significant portion of
the decrease in mortality is likely attributable to proper recognition and admission
of high-risk infants and improvements in supportive care, a continuing challenge
for emergency room providers remains predicting those children in true need of
hospitalization as opposed to those requiring appropriate supportive outpatient
care.

Clinical Presentation and Course

Nasopharyngeal viral invasion usually causes rhinorrhea and coryza. As infection
spreads via inhalation and direct spread of the virus toward the lower respiratory
tract, a dry wheezy cough develops. Low-grade fever (<39 C) may often occur. A
high (>40 C) or prolonged fever is unusual, and should prompt consideration for
coexistent infection. Lower respiratory symptoms typically start on the second to
third day of symptoms and peak within the third to fifth day. Viral invasion proceeds
distally, leading to the classic changes of bronchiolar inflammation, edema,
increased mucus production, bronchospasm, and necrosis and sloughing of epithe-
lial cells.125,126 This process leads to bronchiolar airway obstruction, atelectasis,

and hyperinflation. Tachypnea, increased respiratory effort, and wheezing become

common reasons for ED presentation. Patients may or may not have audible
crackles on examination.
The peak in symptom severity may be an important consideration with respect to ED
disposition decisions and parental education. Although symptoms may improve
substantially after 7 days, it is not uncommon for postbronchiolitic symptoms such
as dry cough and wheeze to continue on to the second and third week for almost
half of children, with up to 9% extending beyond 4 weeks.133,134 This aspect is impor-
tant to address with respect to parental anticipatory guidance and management of
parental expectations. Education on duration may potentially affect the frequency of
otherwise unwarranted return ED visits.133,134
The differential diagnosis of wheeze in the infant and young child must be consid-
ered, which includes asthma, episodic viral wheeze, bronchitis, pneumonia, conges-
tive heart failure, gastroesophageal reflux, and foreign body aspiration. Patients not
matching the traditional features of acute viral bronchiolitis may require diagnostic
testing and management appropriate for the presumptive diagnosis.
For most patients, bronchiolitis will be a mild self-limited disease and will resolve
without notable sequelae. Significant complications may occur in up to 10% to 20%
of patients and may include dehydration, hypoxemia, coinfection, apneic periods,
and respiratory failure. Rates of admission for bronchiolitis cases assessed in the
ED range between 19% and 45% in some studies.127 The duration of hospitalization
is usually between 2 and 4 days for the average patient. Children more severely
afflicted manifest with markedly increased respiratory effort, and rarely with altered
mental status, sepsis syndrome, and cyanosis. Feeding difficulties and sleeping
disturbances may occur secondary to the respiratory symptoms or occult hypoxemia,
and are thus important additional markers of severity that should be inquired about in
the ED.130 It is crucial to recognize significant feeding difficulties, which may be harbin-
gers of early respiratory failure. Approximately 3% of hospital admissions will require
ICU admission135 and as many as 1.5% may require assisted ventilation.136 Although
the mortality rate has recently remained stable, the potential lethality of the illness will
always remain a key concern.
A common question of both parents and clinicians concerns future risk of asthma in
children and infants presenting with bronchiolitis. Literature and expert opinion
suggest that viral lower respiratory tract infections do not cause asthma, but that chil-
dren affected remain at higher risk of future episodes of non-atopic wheezing as well
as asthma exacerbations.137–139

Assessment and Management

The diagnosis of bronchiolitis can be made clinically in most children with classic
signs and symptoms. Given that a very significant proportion of bronchiolitis cases
are mild, they resolve with supportive care alone. Routine diagnostic tests such as
CXR, viral cultures, and blood tests have rarely been shown to have an impact on
the clinical course, and often add unnecessary and unjustified expense.
Multiple studies and guidelines have illustrated the low yield of CXR in the setting of
bronchiolitis, particularly in the mildly ill child without risk factors. Moreover, routine
CXR has been shown to increase the rate of unnecessary antibiotic prescription
without improving outcomes.140 Schuh and colleagues141 reported on 265 cases of
children with a clinical diagnosis of likely bronchiolitis who underwent CXR. Of these,
92.8% showed airway disease and another 6.9% showed airway and airspace
disease, both patterns consistent with viral bronchiolitis. In only 0.75% of cases did
CXR reveal lobar consolidation warranting antibiotics. This study concluded that the

risk of airspace disease was particularly low in patients with O2 saturation greater than
92% and only mild to moderate respiratory distress, and that CXR was unwarranted in
this patient subgroup. Another study of 270 children found that the subset of patients
with focal findings on CXR were more likely to present with fever, have temperature
higher than 38.4 C in the ED, and were 4 times more likely to present with focal
crackles on examination.142 Settings whereby CXR has been shown to be more likely
of value include prolonged or unusually high fevers, significant hypoxemia (<90%),
previous cardiopulmonary disease, need for ICU admission or mechanical ventilation,
and atypical cases.
Although rapid RSV identification is available in many centers and offers sensitivities
up to of 90%, the added value over clinical diagnosis for patients well enough for
discharge remains questionable, and therefore should not be routinely ordered. For
those patients requiring admission, nasopharyngeal fluid testing may be of value. In
some situations, testing of febrile young infants for RSV may decrease the extent of
septic workup that would otherwise be undertaken. Rapid influenza testing may be
warranted if treatment of a positive result would be indicated.
A CBC is not routinely recommended in the setting of bronchiolitis. Although often
taken in patients being admitted, the use of an elevated white blood cell count
(WBC) to predict bacterial superinfection in this setting has been shown to be unreli-
able. A study of 1920 patients with confirmed RSV infection showed that the WBC
was unable to distinguish between those with and without serious bacterial
infection.143 WBC can also be significantly elevated in the setting of adenovirus
infections.144
Coinfection should be considered in cases with unexpectedly high or prolonged
fevers. Otitis media has been reported to be the most common coinfection with
RSV, in the range of 53% to 62%.130 Although the possibility of RSV etiology is
possible in individual cases, bacterial isolation has been shown to be extremely
common in this scenario and should be treated as such. The literature has also
addressed the issue of the extent of workup necessary in infants 1 to 90 days old
with a clinical diagnosis of bronchiolitis. It has been shown that the incidence of
serious bacterial illness (SBI) is lower compared with controls without the diagnosis
of bronchiolitis,145 though a full septic workup is still recommended for patients
younger than 1 month. In two case series of 42 and 187 children having blood, urine,
and cerebrospinal fluid cultures sent despite the diagnosis of bronchiolitis, no cases of
septicemia or meningitis were found and the incidence of urinary tract infection (UTI) in
the latter study was 2%. One study of 282 infants younger than 60 days with bronchio-
litis showed a 1.5% incidence of SBI including 3 UTI, 1 pneumococcal bacteremia,
and 1 meningitis; however, the clinical presentations included shock, apnea/cyanosis,
hypothermia, and resolving pneumonia.146 These studies together suggest that the
yield of a full septic workup in this scenario is very low, including the yield of urine
culture, and that antibiotics should be used sparingly and with clear indications.147
One notable caveat to this is that several studies have documented significantly higher
rates of bacterial coinfection (mainly bacterial pneumonia) in bronchiolitic patients ill
enough to require admission to the ICU,148,149 so further testing in this population is
likely warranted.

Treatment
Despite several studies and Cochrane reviews on the possible interventions to treat
bronchiolitis, there has been little impact on the overall course and outcome in patients
presenting to the ED.150–156 Supportive care measures such as suctioning, supple-
mental oxygen, hydration, and respiratory monitoring remain the current cornerstones

of treatment. Nasal suctioning is an easy, useful adjunctive treatment that may

improve respiratory status, given the significant secretions in many younger infants
who are obligate nose breathers; it is recommended before feeds.157 No evidence
currently exists to support deeper airway suctioning. Oxygen should be administered
for saturation less than 90% according to American Academy of Pediatrics Guide-
lines,130 and is an option in those with saturations of 90% to 94% and moderate signs
of respiratory distress.157,158 Non-invasive positive-pressure ventilation or intubation
is indicated for those rare cases presenting with respiratory failure. IV hydration is
necessary for those with dehydration and feeding difficulty. Attention to the risk of
syndrome of inappropriate antidiuretic hormone secretion (SIADH) is necessary. Chest
physiotherapy has been well studied in the inpatient setting and has not been shown
to improve short-term clinical scores or hospital course, and is therefore
discouraged.130,157–159
The benefit of bronchodilators such as epinephrine and salbutamol is controversial.
A recent Cochrane review of more than 1912 infants showed no significant effect of
bronchodilators on O2 saturation, hospital admission rate, length of stay, and disease
duration.160 There was a small improvement in clinical scores in the outpatient studies;
however, the clinical significance of this is questionable. Another systematic review
included 48 trials using bronchodilators (and/or steroids).151 Only epinephrine use
was found to decrease hospital admissions on day 1 by 33% compared with placebo
(relative risk [RR] of 0.67 with 95% confidence interval [CI] of 0.50–0.89). This figure
translates into a number needed to treat of 15 for epinephrine to avoid 1 hospitalization
(95% CI 10–45). However, a 2004 Cochrane review found the benefit of nebulized
epinephrine in inpatients to be unproven.150 Future studies will likely clarify the role
of nebulized epinephrine ED treatments.
One cost estimate of bronchodilator use in 2003 in the United States for admitted
patients was $37.5 million,160 suggesting overutilization of these often temporizing
treatments. Side effects such as tachycardia, agitation, hyperactivity, flushing, pro-
longed cough and tremor, and decreased oxygen saturation160 are reported, although
significant morbidity from their use is rare. As a result, routine use of bronchodilators in
the setting of clear bronchiolitis is discouraged in all guidelines.130,157–159
However, because of the challenges in distinguishing bronchiolitis from asthma and
episodic viral wheeze, an initial trial of bronchodilators remains an option.130,158,159 Up
to 25% of patients may respond to bronchodilators,130 although the positive placebo
response has been estimated at up to 43%.161 Clinical scores such as the Respiratory
Distress Assessment Index or Respiratory Assessment Change Score130,162 before
and after bronchodilator treatment is recommended.
Anticholinergics such as ipratropium bromide have been studied, often in conjunc-
tion with b-agonists, and have been shown not to add any benefit in the setting of
bronchiolitis.153
In examining the role of steroids in the management of bronchiolitis, a 2010
Cochrane systematic review154 of 17 controlled studies concluded no effect of
systemic or inhaled glucocorticoids on the rate of admissions or length of hospital-
ization. Furthermore, a large, multicenter, randomized controlled trial of 600 patients
in the United States showed no benefit from steroid treatment, including subgroup
analysis of those with a personal or family history of atopy or asthma.163 This
finding refutes the theory proposed by some that a small asthmatic subgroup
may benefit.
In a much debated study, the Pediatric Emergency Research Canada (PERC) group
published a multicenter ED study of a series of 800 patients who were treated with
nebulized epinephrine, dexamethasone, neither, or both, and outcome measures

such as risk of hospitalization at 1 week were documented.164 Unexpectedly, the

combined treatment of inhaled epinephrine and dexamethasone demonstrated
a significantly reduced admission rate versus placebo at day 7 (RR 0.65, 95% CI
0.44–0.95). Improvements in breathing and feeding were noted on subsequent
days, without harmful outcomes. However, given the high doses of dexamethasone
used (1 mg/kg day 1, 0.6 mg/kg days 2–6) and its potential side effects, lack of efficacy
of dexamethasone alone, and the lack of other supporting studies, this treatment
option needs further validation. Evidence for treatment synergy as well as rationale
for potential efficacy via targeting various aspects of the pathophysiology of the
disease exists.126
Nebulized hypertonic (3%) saline has emerged over the last decade as a potentially
promising inpatient therapy for bronchiolitis. Given its proposed actions on improving
clearance of mucus and cellular debris, initial studies in the setting of cystic fibrosis
showed some benefit.165 Multiple studies and a 2010 Cochrane review155 have
revealed that nebulized hypertonic saline consistently improves post-inhalation clin-
ical scores and decreases length of stay in hospital by approximately 25% or 0.94
days.166 In contrast to the inpatient data whereby nebulized hypertonic saline is given
at intervals of every 8 hours or less over several days, ED studies using 1 to 3 consec-
utive doses with a bronchodilator have not to date shown statistically significant
improvement in short-term clinical scores, nor decreased hospitalization rates
(although trends to these outcomes are suggested and decreased severity is found
at 24–72 hours).135,151,155,162,166,167 Nebulized hypertonic saline may need to be given
at adequate intervals, dose, and duration for a significant treatment benefit to be seen.
It may also be possible that ED initiation followed by continuation of treatment may
lead to later benefits in hospital. Further research is currently under way to better
establish and clarify the roles of nebulized hypertonic saline in both the outpatient
and inpatient settings.
Small studies looking at the effect of Heliox have demonstrated some benefits in
improving short-term respiratory distress scores, but without clear reductions in the
need for intubation or length of ICU stay.156,168 The use of ventilatory support with
positive-pressure ventilation has also been examined in small studies showing
improved carbon dioxide clearance and clinical scores, but without a clear decrease
in the need for intubation.135,161
Given that bacterial superinfection is rare in bronchiolitis, antibiotics should only be
administered in the setting of proven or highly likely bacterial illness or in suspected
sepsis in the unusual toxic child with bronchiolitis. Although pertussis and atypical
pneumonias such as Mycoplasma and Chlamydophila may mimic bronchiolitis, signif-
icant suspicion for these entities should exist before empiric treatment is considered.
Use of ribavirin should be restricted to immunodeficient children with severe illness,
given the lack of evidence in other scenarios.130,158,159 Surfactant treatment may play
a role in young infants requiring ICU care or intubation, although its current role in the
ED is not clearly defined.135
Given the highly contagious nature of RSV through direct contact and contact with
fomites, the importance of hand washing with soap or alcohol-based solutions must
be observed by ED personnel and must be stressed to parents. Exposure to
second-hand smoke has been found to be a risk factor RSV infection, whereas breast-
feeding has been shown to be protective. Palivizumab (Synagis), a monoclonal anti-
body against RSV given preventatively in 5 monthly doses at the start of the RSV
season, may be prescribed for infants at high risk. However, cost effectiveness
compared with isolation strategies for those infants at high risk of severe disease
has not been well studied, and calls its routine use into question.

Disposition
Admission ideally should be reserved for those at high risk of morbidity and mortality
or in whom admission allows for (1) necessary physical observation in the likelihood of
serious deterioration requiring immediate medical interventions, and (2) provision of
medical interventions and treatment that are not available or practical in the outpatient
setting.
Many attempts to define admission criteria are present in the literature. Because
bronchiolitis typically worsens and peaks after 3 to 5 days, the natural history of the
disease should be taken into account in determining disposition.
Mansbach and colleagues169 published in 2008 a multicenter cohort study to iden-
tify factors associated with safe discharge from the ED in order to create a low-risk
model. These factors include:
1. Age 2 months
2. No history of intubation
3. Eczema
4. Respiratory rate less than normal for age
5. Mild retractions
6. Initial O2 saturation 94%
7. Few treatments with b-agonists or epinephrine in the first hour
8. Adequate fluid intake.

Infants at high risk of apnea are currently considered a high-risk group and require
admission for monitoring. Willwerth and colleagues170 reviewed admitted bronchiolitis
infants over a 5-year period and retrospectively identified a set of risk criteria that pre-
dicted the occurrence of apnea in all of the 19 of 691 (2.7%) infants who developed
apnea in hospital. These criteria were: (1) born at full term but chronologic age less
than 1 month; (2) born preterm at less than 37 weeks but chronologic age less than
48 weeks post conception; or (3) witnessed prior apnea event by parents or a clinician
before admission.
In an attempt to identify predictors of bounce-back visits for worsening bronchiolitis
within 2 weeks of ED discharge, Norwood and colleagues171 reviewed 121 of 717
patients with unscheduled return visits, and identified age younger than 2 months,
male sex, and history of previous hospitalization as risk factors. Identifying patients
at higher risk of return visits or deterioration may be useful to stratify those patients
and families in need of the highest level of discharge counseling and instruction,
and follow-up with a primary care provider in the following days.
Assessment of physical signs is required to determine need for admission.
However, it must be noted that no single physical examination parameter (except
perhaps oxygen saturation) has been found to be strongly predictive of severe
disease. Studies have instead emphasized constellations of signs and symptoms.
A study in 2011 identified 5 predictors of admission. These factors were then assim-
ilated into a clinical scoring system in which each was equally weighted with 1 point172:
1. Duration of symptoms less than 5 days
2. Respiratory rate 50 breaths/min or more
3. Heart rate 155 beats/min or more
4. Oxygen saturation less than 97%
5. Age less than 18 weeks.

The study suggests that patients with scores of 3 or more may require admission
or careful monitoring, and scores could be used in conjunction with assessment

of other high-risk factors. This study, while providing promising conclusions, has yet to
be validated.

PNEUMONIA IN CHILDREN

Pediatric pneumonia is the number one cause of mortality in children worldwide, with
an annual incidence of more than 150 million cases per year. More children die of
pneumonia than of diarrheal illnesses, malaria, and AIDS,173 making it a significant
global health care concern. In developed countries pneumonia in children, although
significantly less likely to cause mortality, remains a common ED presentation.
Assessment
The assessment of a child for pneumonia can be challenging for numerous reasons:

1. Significant overlap in presentation may occur with other common respiratory

conditions such as bronchiolitis, asthma, and bronchitis, among others
2. Significant overlap in the presentation between viral, bacterial, and atypical patho-
gens makes definitive diagnosis challenging given lack of readily available, precise,
rapid, noninvasive etiologic testing in the ED setting
3. The extent to which diagnostic testing may truly aid and change the clinical course
is often not known
4. An important minority of cases may be caused by atypical pathogens requiring
specific testing and treatment beyond standard empiric treatments.
Clinical Presentation
Although the classic presenting symptoms of fever, productive cough, dyspnea and
chest pain can assist the ED practitioner in recognizing pneumonia, children may
have less typical presentations that require a higher level of suspicion and discernment.
Neonates and infants may simply present with lethargy, poor feeding, or irritability.
Atypical pneumonias may present with predominantly upper respiratory tract or
systemic symptoms such as malaise, headache, vomiting, or rash. Neck pain and,
rarely, meningismus may be a manifestation of an upper lobe consolidative process.
Abdominal pain is a not uncommon presenting symptom of pneumonia in children,
although usually cough, fever, or other symptoms of a URI are present.174 Fever
without a localizable source may be a less common presentation, but is well described.
The World Health Organization guidelines advocate measurement of respiratory
rate as an important initial guide to suspecting pneumonia. These guidelines suggest
thresholds of RR greater than 60 in infants younger than 2 months, RR greater than 50
in infants 2 to 12 months old, RR greater than 40 in children 1 to 5 years old, and RR
greater than 30 in children older than 5 years175,176 as a simple tool that may help
detect as many as 50% to 80% of pneumonias. Respiratory rates should be counted
for a full minute when the child is calm. However, studies show the specificity of
tachypnea in developed countries is reportedly low in infants under 6 months (39%)
compared with older children up to age 5 years (67%).177 Tachypnea beyond age-
specific limits was found in 61% of children under 2 years old and in 26% of those
patients older than 2 years in another study of radiographically confirmed pneu-
monia,178 underscoring the limits of using tachypnea alone to predict pneumonia.
Other physical findings associated with pneumonia in infants and younger children
include nasal flaring, grunting, and retractions, although their specificity for pneumonia
is low in infants and younger children, who are more likely to have bronchiolitis. The
prevalence of classic pneumonia signs such as crackles (49%), decreased breath
sounds (58%), and fever (88%) were documented in a 2008 study of 101 cases of

community-acquired pneumonia (CAP).178 Wheeze may occasionally occur in typical

bacterial pneumonia (reported in the literature at 4.9%), but is more likely associated
with viral lower respiratory tract infection and Mycoplasma (atypical) pneumonia (up to
30%).179 Absence of all respiratory findings, especially without fever or cough, makes
pneumonia highly unlikely, though occult pneumonia (defined as pneumonia in the
absence of any noted respiratory and auscultatory findings on examination) has an
incidence of 5% to 6%,176 with absence of auscultatory findings in up to 30%.180
For the emergency physician, a careful assessment of presenting signs is crucial to
determine the likelihood of diagnosis as well as appropriate treatment and disposition.
These signs include hypoxemia, abnormal respiratory rates (respiratory rate >70 or
apnea in infants under 2 months, or respiratory rate >50 in children ages 1–4), signs
of significantly increased work of breathing, inability to maintain oral hydration, clinical
signs of dehydration, signs of sepsis/shock/toxicity, and high fever.181 Significantly
decreased breath sounds or dullness at a lung base may suggest a dense consolida-
tion or effusion/empyema. Features associated with empyema described in a Finnish
study included pain on abdominal palpation and tachypnea with greater duration of
fever before admission.182 In contrast to the adult literature, severity scores and
indices (eg, CURB-65 score, Pneumonia Severity Index, and so forth) have not to
date been validated for use in pediatric pneumonia.

Etiology
Most pediatric pneumonia seen in the ED is caused by respiratory viruses, typical
bacterial agents (primarily Streptococcus pneumoniae), or atypical bacterial agents
(Mycoplasma and Chlamydophila). Awareness and knowledge of rare but “critically
causal” agents is important to properly diagnose and treat these unusual causes,
which include tuberculosis, pertussis, Legionella, coronavirus/severe acute respira-
tory syndrome (SARS), H1N1 influenza, hantavirus, varicella, measles, fungi, and
potential bioterrorist agents such as anthrax and plague. Workup and treatment
beyond the standard empiric approach would be required and is beyond the scope
of this review.
The single most important predictor of the causative agent for pneumonia is age.
Neonatal pneumonia (<1 month) is unique, as it has a significant incidence of maternally
transmitted organisms such as group B Streptococcus, gram-negative organisms
(Escherichia coli, Haemophilus influenzae), Listeria monocytogenes, anaerobes, and
occasionally herpes simplex virus and cytomegalovirus. In the age group between 2
and 12 weeks an organism unique to this age range is Chlamydophila trachomatis,
which causes an afebrile pneumonitis syndrome characterized by a well-appearing
child presenting with cough, tachypnea, and interstitial infiltrates on CXR. The inci-
dence of this disease has declined significantly with prenatal screening for this verti-
cally transmitted organism from mothers. Other bacteria commonly seen in the first
3 to 4 months include H influenzae (nontypable or Type B), Moraxella catarrhalis, Strep-
tococcus pyogenes, Staphylococcus aureus and, rarely, Bordetella pertussis.
In younger children, especially under the age of 2 years, viral causes predominate.
RSV is the most common, followed by parainfluenza, adenovirus, rhinovirus, human
metapneumovirus, and influenza viruses. Bacterial causes, mainly S pneumoniae, is
common, especially in children who require hospitalization. Between the age of 2
and 5 years, the incidence of pneumococcal and atypical organisms rises. In
school-aged children, there is a greater increase in the incidence of Mycoplasma
and Chlamydophila pneumonia, while S pneumoniae remains the most common
bacterial cause. Viral agents remain an important cause in this age group. Tubercu-
losis accounts for a very small percentage of pediatric CAP.

Classic pneumococcal pneumonia presents with sudden onset of high fever and
rigors with a productive cough, focal pleuritic chest pain, mild to moderate systemic
toxicity (lethargy, malaise, nausea, vomiting), and focal chest findings on examination.
Unfortunately, only a small minority of patients who have a confirmed pneumococcal
pneumonia present with these findings. Initial ED presentations may be subtle or atyp-
ical. WBC and C-reactive protein (CRP) may be helpful in more severe disease but are
nonspecific for milder cases.144 CXR is significantly limited given that pneumococcus
may present as a bronchopneumonia instead of lobar infiltrate.
Features that may be more common in pneumonia caused by Mycoplasma or Chla-
mydophila include a more insidious onset with constitutional symptoms of malaise,
myalgias, pharyngitis, headache, low-grade fever, and a dry cough that progressively
worsens. Bullous myringitis and rashes such as erythema nodosum or a generalized
maculopapular eruption occasionally occur with Mycoplasma infection.
Viral pneumonias are most common in those younger than 5 years, often presenting
in the fall or winter, and usually associated with a viral prodrome such as coryza, phar-
yngitis, low-grade fever, and dry cough. Viral pneumonias account for the majority of
pneumonias in children younger than 2 years in North America. Radiographically, peri-
hilar predominance with peribronchial thickening, hyperinflation, and interstitial
involvement is most often seen; however, lobar infiltrates can also be seen.183 Coin-
fection with viral and bacterial agents is fairly common, especially in those under
the age of 5 years, often ranging from 20% to 35% in many studies.178,184
Staphylococcal pneumonia is rare but is associated with more severe illness, espe-
cially in the setting of viral coinfection. Reports suggest a rising incidence with the
increased prevalence of methicillin-resistant Staphylococcus aureus (MRSA) in the
community and in hospital settings.185 Risk factors for staphylococcal pneumonia
include younger age (<1 year old), complicated CXR appearance (effusion/empyema,
cavitating or necrotizing infiltrate, lung abscess), toxic appearance, known MRSA
contacts or history of community-acquired MRSA, and viral coinfection (notably influ-
enza A).186,187 Presentation in the ED with hemoptysis, hypotension, and leukopenia
should also heighten suspicion for the organism.186

Investigations and Workup

Well-appearing children with a clinical diagnosis of pneumonia require no specific
workup, as outcome with empiric therapy is very favorable. Circumstances that
warrant more rigorous efforts to identify a specific etiologic agent include:

1. The ill child requiring intensive care (ie, those with evidence of hypotension, sepsis,
shock, hypoxemia <92%, hypovolemia, respiratory distress, altered mental status)
or age <3 months (at higher risk of hypoxemia, apnea, and mortality than older
children)175,188
2. Significant comorbidities including immunocompromise, underlying cardiopulmo-
nary disease (eg, cystic fibrosis) or neuromuscular/neurologic impairment
3. Evidence of complicated pneumonia on CXR (significant effusion/empyema, pneu-
matocele, lung abscess)
4. Patients failing treatment, having persistent fever or prolonged clinical courses, or
showing clinical deterioration189
5. Suspected resistant microbes or rare etiologies (eg, varicella, SARS, fungi,
tuberculosis)189
6. Unexplained community outbreaks caused by an unclear organism.

Knowledge of local epidemiologic data is important to recognize the possibility of

community outbreaks or rising antibiotic resistance patterns. The recent outbreaks
of SARS in 2002 to 2003 and of H1N1 in 2008 to 2009 serve as poignant reminders
that vigilance is key, and stringent infection control precautions are crucial to mini-
mizing the spread of disease. Appropriate contact, droplet, and airborne precautions
must be used. Household contact counseling, testing and treatment may be indicated
in outbreaks of serious respiratory infections.
Clinical diagnosis of pneumonia in children is challenging, and physician judgment
based on physical findings alone has been shown to have limited predictive power. In
a study of 2071 children undergoing CXR in a pediatric ED for suspicion of pneumonia,
7% showed definite pneumonia while 15% showed definite or probable pneu-
monia.190 Among the group judged by clinicians to have a high likelihood of pneu-
monia (>75%), CXR revealed definite consolidation in 30.6% and definite or
probable consolidation in 52.8%. In the low-likelihood (<5% clinician suspicion) cate-
gory, 4.3% showed definite and 10.0% showed definite or probable pneumonia.
Another study in 2007 showed a prevalence rate of only 41.2% of positive or equivocal
pneumonia in patients with clinical signs of pneumonia.176 Although not addressing
the issue of sensitivity of CXR to the diagnosis, these studies highlight the potential
limitations of diagnosis and treatment decisions based on purely clinical grounds.
Many studies use radiographic criteria as the gold standard in the diagnosis of
pneumonia, but evidence suggests that CXR lacks sensitivity in making the diagnosis,
and lacks specificity in differentiating potential causes.191 CXR has been shown to
have limited specificity in differentiating typical bacterial from atypical bacterial and
viral pneumonias. Although lobar consolidation and effusion are more commonly
seen with typical bacterial causes, atypical agents such as Mycoplasma may present
with lobar infiltrates as well as the more classic interstitial pattern and hilar adenop-
athy.181 In 2002, Virkki and colleagues183 evaluated 254 cases of CAP in which
etiology was determined in 85%, and compared with CXR findings. Although the
classic alveolar/lobar pattern was significantly correlated with a bacterial cause in
78% (P<.001), the interstitial pattern traditionally associated with atypical bacteria
and viral infections was less specific, with 50% caused by bacteria (typical and atyp-
ical) and 50% caused by viruses. Variability among guidelines regarding the necessity
of CXR exists. It has been shown that antimicrobial choice as well as overall outcome
is not affected with the use of CXR in children 2 months to 5 years of age with mild
disease.140 As a result, they should not be considered mandatory in these cases.
Although CXR is often ordered in the large number of children with wheezing seen in
EDs, the incidence of radiographic pneumonia is very low (3.7%–4.9%) unless fever
(>38 C), abdominal pain, or significant hypoxemia (<92%) is present.179 Moreover,
atelectasis may often mimic early consolidation. In those under the age of 2 years
with wheezing and crackles, viral bronchiolitis is the most likely diagnosis, with bacte-
rial superinfection being very rare in mild cases.
Ultrasonography has recently emerged as a valuable tool in the diagnosis of pneu-
monia. Most studies in the adult literature on lung ultrasonography suggest higher
sensitivity than CXR, better delineation of complications (such as loculated effusion,
empyema, abscess, necrosis, and pneumatocele), and rapid performance times
(usually less than 5 minutes).192,193 Ultrasonography in children has compared very
favorably with computed tomography (CT) scanning with respect to diagnosis, compli-
cations, and guidance of thoracocentesis, without radiation exposure and risk.194
Furthermore, ultrasonography is less likely to require patient sedation in comparison
with CT scanning. Given these advantages, ED clinicians should be aware of its
evolving role.

CBC and differential can sometimes be helpful in suggesting a bacterial cause of

pneumonia. A European study reported that S pneumoniae pneumonia was more
commonly associated with WBC of greater than 15,000 to 20,000/mm3, and
a mean of 25,000/mm3 if there was also a concomitant bacteremia.144 However, inva-
sive viral disease such as adenovirus or even influenza may cause similar WBC eleva-
tions, so interpretation should be done with caution in consideration of the overall
clinical picture. Acute phase reactants such as erythrocyte sedimentation rate and
CRP have shown suboptimal utility as sole determinants to distinguish bacterial
from viral causes, due to limited specificities.181,194 Although a procalcitonin level
greater than 1.0 ng/mL was helpful in distinguishing bacterial from viral CAP in a recent
study,178 it was unable to distinguish pneumococcal from atypical bacterial
pneumonia.
Blood cultures can be highly specific for the etiologic organism and can identify
antimicrobial sensitivity patterns important to later care, but play little to no role in
initial ED management. Two ED-based studies have shown that bacteremia occurs
in only 2% to 3% of patients with radiographic CAP.195,196 Shah and colleagues195
reported higher yields of up to 13% in a subset of patients with complicated
pneumonia. Due to the overall low yield, the use of blood cultures should be individ-
ualized to patients with suspected bacteremia, more ill patients, or patients with
complications.
Bacterial serology from serum or urine samples is currently neither widely available
nor practical in most EDs. Sensitivity and specificity is low, therefore testing is not rec-
ommended by most recent guidelines.175,181,189,194,197 Cold agglutinin testing,
although easy to perform, was shown to have a positive predictive value of only
70%.181 Mycoplasma IgM detection via enzyme-linked immunosorbent assay is sensi-
tive and may be considered in children older than 2 years.189 Urine for pneumococcal
antigen has been shown to lack high specificity in children. Legionella antigen testing
in the urine may be considered for more severe cases requiring admission to the ICU
or when clinical suspicion is high. Nasopharyngeal testing for pertussis and skin
testing for tuberculosis should be done when these entities are suspected. Further
testing should be based on clinical suspicion.
Rapid viral testing is now available in many settings, and can allow early diagnosis of
influenza and RSV. Early identification allows treatment decisions with antivirals (which
are rarely indicated), infectious precaution advice, and isolation as inpatients. Disad-
vantages include cost and low benefit/expense ratio in cases where clinical diagnosis
is already clear and the necessity of obtaining specific etiologic diagnosis is low. The
overall utility is generally low and should not be routine.198 Testing may be considered
in those with severe illness warranting hospitalization.
Sputum for Gram stain and culture may be feasible for older school-aged children
capable of producing more reliable sputum specimens, and may be done for those
requiring hospitalization for severe disease.194,199 Limitations include frequent poor-
quality specimens (especially in younger children) and difficulties in culturing organ-
isms such as Mycoplasma, Chlamydophila, Legionella, Moraxella, and tuberculosis.
Nasopharyngeal and throat cultures have poor reliability in predicting the etiology of
pneumonia and are not recommended.

Treatment
Treatment regimens in suspected bacterial CAP take into account the age of the child,
treatment setting, severity, special circumstances in each case, and local patterns of
organisms and antibiotic susceptibilities.175,181,189,194,197,199 Consideration for with-
holding antibiotics should be given for those non-ill children with clinical presentations

Table 2
Empiric antibiotic therapy for suspected bacterial community-acquired pneumonia

Age Outpatient Treatment Inpatient Treatment

Neonate Not recommended > Admit Ampicillin 50–200 mg/kg/d IV div q
6–12 h plus
Cefotaxime 150–200 mg/kg/d IV
div q 6 h–q 8 h

If ill, add gentamycin 7.5 mg/kg/d

IV div q 8 h

If HSV likely, add acyclovir 500 mg/

m2/dose IV q 8 h
1–4 months If afebrile pneumonitis If afebrile pneumonitis
Clarithromycin 15 mg/kg/d PO div Clarithromycin 15 mg/kg/d PO/IV div
BIDa or BIDa or
Erythromycin 40 mg/kg/d PO div q 6 h Erythromycin 40 mg/kg/d PO or
20 mg/kg/d IV div q 6 h
Amoxicillin 90 mg/kg/d PO div
BID–TIDb,c If febrile, cefotaxime 150–200 mg/kg/d
IV div q 8 h
If febrile or hypoxic > Admit or cefuroxime IV 150 mg/kg/d
IV div q 8 h

If ill or MRSA suspected,

add vancomycin 40–60 mg/kg/
d IV div q 6–8 h or
clindamycin 40 mg/kg/d IV div q 6–8 h

If MSSA suspected,
cloxacillin 150–200 mg/kg/d IV
div q 6 h
4 months Amoxicillin 90 mg/kg/d PO div Ceftriaxone 50–100 mg/kg/d IV
to 5 years BID–TIDb,c div q 12–24 h or
Cefotaxime 150–200 mg/kg/d IV div
If atypical suspected add q 8 h or
Macrolide PO (doses as above) Cefuroxime 150 mg/kg/d IV div
q8h
Second-line alternatives:
Amoxicillin-clavulanic acid If Streptococcus pneumoniae
90 mg/kg/d PO div BID or TIDb,c likely,
Cefuroxime axetil 30 mg/kg/d PO div Ampicillin 150–200 mg/kg/d IV
BID div q 8 h–q 6 h

If severely ill,
add vancomycin 40–60 mg/kg/d
IV div q 6–8 h or
cloxacillin 150–200 mg/kg/d IV
div q 6 h
or if pleural effusion,
clindamycin 40 mg/kg/d IV div
q 6–8 h

If atypical suspected: Macrolide IV

or PO (doses as above)a
(continued on next page )

Table 2
(continued)
Age Outpatient Treatment Inpatient Treatment
5–18 years Azithromycin 10 mg/kg/d, Day 1 1 Ceftriaxone 50 mg/kg/d IV div
5 mg/kg/d, Days 2–5 or q 12 h or q 24 h (max 2 g/d) or
Clarithromycin 15 mg/kg/d div Cefuroxime 150 mg/kg/d IV div
BID or q 8 h (max 1.5 g/d) or
Erythromycin 40 mg/kg/d div q 6 h

If S pneumoniae likely If S pneumoniae likely,

Amoxicillin 90 mg/kg/d PO div BIDb,c Ampicillin 150–200 mg/kg/d
IV div q 8 h–q 6 h
Alternatives:
Doxycyclined 2–4 mg/kg/d PO div BID If atypicals suspected
Amoxicillin-clavulanic acid 90 Macrolide IV or PO (doses as
mg/kg/d PO div BID or TIDb,c above)
Cefuroxime axetil 30 mg/kg/d PO div
BID If severely ill,
Levofloxacine 500 mg PO daily or add vancomycin 40–60 mg/kg/d
Moxifloxacine 400 mg PO daily IV div q 6–8 h or
cloxacillin 150–200 mg/kg/d
IV div q 6 h, or

If pleural effusion,
clindamycin 40 mg/kg/d IV div
q 6–8 h

Abbreviations: BID, twice daily; div, divided (for dosages based on a daily dose, which needs to be
then divided into intervals); HSV, herpes simplex virus; IV, intravenous; MRSA, methicillin-resistant
Staphylococcus aureus; MSSA, methicillin-sensitive Staphylococcus aureus; PO, by mouth; q, every;
TID, 3 times daily.
a
Azithromycin: Safety and effectiveness not fully established in infants under 6 months of age.
Not approved by US Food and Drug Administration in this age group.
b
Higher-dose amoxicillin recommended especially if in day-care attendance, recently on antibi-
otics, or hospitalized in last 3 months, age under 2 years, or area with S pneumoniae penicillin resis-
tance greater than 2.0 mg/mL.
c
Lower-dose amoxicillin 45 mg/kg/d potentially effective in absence of risk factors for resistant
S pneumoniae.
d
Avoid if younger than 8 years, because of effects on dentition.
e
Use only if growth plates are closed.
Data from Refs.175,181,189,194,199

consistent with viral illness, given the association between inappropriate antibiotic use
and increase in resistant organisms. Suggested empiric antibiotic treatments for CAP
are listed in Table 2.
Anaerobic coverage should be considered if aspiration is suspected. Antiviral
therapy for influenza-related pneumonia should be initiated in high-risk populations
within 48 hours of symptom onset. The anti-RSV treatment ribavirin should be limited
to high-risk patients as per American Academy of Pediatrics Guidelines.130
A large multicenter trial (the PIVOT trial) in 2007, of 246 cases of pediatric CAP
comparing oral amoxicillin to IV penicillin followed by oral amoxicillin demonstrated
similar outcomes, suggesting IV treatment may not always be necessary for admitted
patients with milder cases, thereby saving hospital costs and avoiding IV cannula-
tion.200 Examining the duration of antibiotic therapy, a 2008 Cochrane systematic
review concluded equal efficacy of 3-day versus 5-day treatment regimens in mild
CAP in otherwise healthy children 2 months to 5 years of age.201

Adjunctive Treatments
Standard supportive care includes oxygen for hypoxemia less than 92%, suctioning of
younger infants, and bronchodilators as necessary. IV fluids should be given when
necessary but with caution, given the association of SIADH with more severe pneumo-
nias. IV fluid regimens started in the ED may require adjustment in the presence of
hyponatremia. Chest physiotherapy has been found to be of no added value and is
not routinely recommended. Steroids have no role currently in the treatment of the
pneumonia. Noninvasive ventilator support with continuous positive airway pressure
or bilevel positive airway pressure may be necessary for those with respiratory failure.
Intubation is rarely indicated.

Complications
Complications of pneumonia may include sepsis, respiratory failure, effusion,
empyema, abscess, pneumatocele, and infectious spread such as, meningitis, septic
arthritis, or osteomyelitis.175,181 Small free-flowing parapneumonic effusions sus-
pected to be transudative may be given a trial of antibiotics and reassessed for pleuro-
centesis as necessary. Moderate and large effusions, especially if in respiratory
distress, should be considered for prompt pleurocentesis before starting antibiotics,
as this may affect culture results.175 Proven empyemas should be drained and further
treatment decisions should be made in consultation with thoracic surgery. Pulmonary

Table 3
Suggested admission criteria for pediatric community-acquired pneumonia

Definite admission Age <1 month

Oxygen saturation 92%
Signs of significant respiratory distress (tachypnea/apnea, significant
work of breathing)
Signs of sepsis or toxic appearance
Complicated pneumonia on chest radiograph (effusion/empyema,
pneumatocele, necrosis, or lung abscess)
Probable admission Age 1–3 months
Oxygen saturation 93%–94%
Significant comorbidity (chronic lung disease, congenital
heart disease, cystic fibrosis, etc)
Significant burden of disease (multilobar or complete lobar
consolidation)
Immunocompromise (sickle cell disease, human immunodeficiency
virus, post-splenectomy, malignancy/recent chemotherapy)
Unresolving or worsening illness
Significant dehydration/vomiting
Inability of parents/caregivers to ensure adequate observation or
follow-up
Consider admission Age 3–6 months
Failure of outpatient treatment, especially if any clinical deterioration
Larger infiltrate or significant atelectasis on chest radiograph
Outpatient therapy Non-ill or minimally ill child
Uncomplicated mild pneumonia
Adequate oxygenation
Tolerating feeds well
Reliable parents for observation and follow-up

Data from Refs.175,181,189,194,199

and infectious disease specialist involvement may be warranted for cases of unresolv-
ing infiltrates, abscesses, pneumatoceles, or effusions.

Admission Criteria/Predictors of Poor Outcome

Worldwide, significantly at-risk groups include neonates, human immunodeficiency
virus (HIV)-related pneumonia (3–8 times higher case fatality rates compared with
non-HIV infected), and severely malnourished children.188 Significant hypoxemia is
also associated with a 2- to 5-fold increase in risk of death.202 Predictors of antibiotic
treatment failure include young age, immunocompromised state (eg, HIV or malnutri-
tion), presence of empyema, prior antibiotic use, poor adherence to treatment, and
antibiotic resistance.188
Admission criteria based on published guidelines and literature reviews have been
proposed, though they have not been vigorously studied. Such criteria should be used
with clinical judgment while taking into account modifying factors. Suggested admis-
sion criteria are listed in Table 3.
Other options for less ill or complicated patients include admission to a short-stay or
observation unit for children in whom rapid clinical response is expected, or once-daily
IV or IM antibiotics such as ceftriaxone with daily follow-up by an intensive ambulatory
care service, as exists in some major hospitals.

Follow-Up
Forty-eight-hour follow-up is strongly recommended for all children diagnosed with
pneumonia,174 especially if any signs of deterioration occur. The World Health Orga-
nization definition of clinical improvement requires “slower breathing, less fever, eating
better.”202 In children with clinical improvement, follow-up radiography is suggested in
cases of complicated pneumonia, round pneumonia, congenital abnormalities, lobar
collapse, complicated courses, or persistent clinical abnormalities.181,189 A recent
radiographic follow-up study demonstrated that residual or new changes on CXR
could be seen in 30% of cases after 3 to 7 weeks but did not affect management.203

SUMMARY

Common respiratory illnesses including asthma, croup, bronchiolitis, and pneumonia

will undoubtedly continue to make up the bulk of pediatric respiratory problems pre-
senting to EDs. Given their potential to cause life-threatening illness, emergency clini-
cians will need to continue to maintain and update their knowledge on current
recommendations for these illnesses. Underuse of some key therapies and overutili-
zation of unproven therapies and low-utility diagnostic tests are several important
areas that can be improved through improved education and knowledge of published
clinical practice guidelines.

REFERENCES

1. American Lung Association, Epidemiology and Statistics Unit. Trends in asthma

morbidity and mortality. Washington, DC. Available at: http://www.lungusa.org/
finding-cures/our-research/trend-reports/asthma-trend-report.pdf. Accessed
April 13, 2011.
2. Global Initiative for Asthma. Global strategy for asthma management and
prevention. Bethesda (MD): Global Initiative for Asthma; 2010.
3. National Heart, Lung, and Blood Institute (US). Expert panel report 3: guidelines
for the diagnosis and management of asthma. Bethesda (MD): National Heart,

Lung, and Blood Institute, U.S. Department of Health and Human Services,
National Institutes of Health; 2007.
4. Busse WW, Lemanske RF. Asthma. N Engl J Med 2001;344(5):350–62.
5. Stevenson D, Szczeklik A. Clinical and pathologic perspectives on aspirin sensi-
tivity and asthma. J Allergy Clin Immunol 2006;118(4):773–86 [quiz: 787–8].
6. Global Initiative for Asthma. Global strategy for the diagnosis and management
of asthma in children 5 years and younger. Bethesda (MD): Global Initiative for
Asthma; 2009.
7. Brand PL, Baraldi E, Bisgaard H, et al. Definition, assessment and treatment of
wheezing disorders in preschool children: an evidence-based approach. Eur
Respir J 2008;32(4):1096–110.
8. Panickar J, Lakhanpaul M, Lambert P, et al. Oral prednisolone for preschool
children with acute virus-induced wheezing. N Engl J Med 2009;360(4):
329–38.
9. British Thoracic Society and the Scottish Intercollegiate Guidelines Network.
British guideline on the management of asthma. London, England: The British
Thoracic Society; 2009.
10. Ducharme F, Chalut D, Plotnick L, et al. The pediatric respiratory assessment
measure: a valid clinical score for assessing acute asthma severity from
toddlers to teenagers. J Pediatr 2008;152(4):476–80, 480.e471.
11. Chalut DS, Ducharme FM, Davis GM. The Preschool Respiratory Assessment
Measure (PRAM): a responsive index of acute asthma severity. J Pediatr
2000;137(6):762–8.
12. Gorelick M, Stevens M, Schultz T, et al. Performance of a novel clinical score,
the Pediatric Asthma Severity Score (PASS), in the evaluation of acute asthma.
Acad Emerg Med 2004;11(1):10–8.
13. Gouin S, Robidas I, Gravel J, et al. Prospective evaluation of two clinical scores
for acute asthma in children 18 months to 7 years of age. Acad Emerg Med
2010;17(6):598–603.
14. Goldberg R, Chan L, Haley P, et al. Critical pathway for the emergency depart-
ment management of acute asthma: effect on resource utilization. Ann Emerg
Med 1998;31(5):562–7.
15. Eid N, Yandell B, Howell L, et al. Can peak expiratory flow predict airflow
obstruction in children with asthma? Pediatrics 2000;105(2):354–8.
16. Gorelick M, Stevens M, Schultz T, et al. Difficulty in obtaining peak expiratory flow
measurements in children with acute asthma. Pediatr Emerg Care 2004;20(1):22–6.
17. Rodrigo G, Rodriquez Verde M, Peregalli V, et al. Effects of short-term 28% and
100% oxygen on PaCO2 and peak expiratory flow rate in acute asthma:
a randomized trial. Chest 2003;124(4):1312–7.
18. Camargo CA, Spooner CH, Rowe BH. Continuous versus intermittent beta-
agonists in the treatment of acute asthma. Cochrane Database Syst Rev
2003;4:CD001115.
19. Papo MC, Frank J, Thompson AE. A prospective, randomized study of contin-
uous versus intermittent nebulized albuterol for severe status asthmaticus in
children. Crit Care Med 1993;21(10):1479–86.
20. Cates CCJ, Bara A, Crilly JA, et al. Holding chambers versus nebulisers for
beta-agonist treatment of acute asthma. Cochrane Database Syst Rev 2003;3:
CD000052.
21. Closa RM, Ceballos JM, Gmez-Pap A, et al. Efficacy of bronchodilators admin-
istered by nebulizers versus spacer devices in infants with acute wheezing. Pe-
diatr Pulmonol 1998;26(5):344–8.

22. Wildhaber JH, Devadason SG, Hayden MJ, et al. Aerosol delivery to wheezy
infants: a comparison between a nebulizer and two small volume spacers. Pe-
diatr Pulmonol 1997;23(3):212–6.
23. Rubilar L, Castro Rodriguez JA, Girardi G. Randomized trial of salbutamol via
metered-dose inhaler with spacer versus nebulizer for acute wheezing in chil-
dren less than 2 years of age. Pediatr Pulmonol 2000;29(4):264–9.
24. Doan Q, Shefrin A, Johnson D. Cost-effectiveness of metered-dose inhalers for
asthma exacerbations in the pediatric emergency department. Pediatrics 2011;
127(5):e1105–11 peds.2010-2963.
25. Asmus MJ, Hendeles L. Levalbuterol nebulizer solution: is it worth five times the
cost of albuterol? Pharmacotherapy 2000;20(2):123–9.
26. Milgrom H, Skoner DP, Bensch G, et al. Low-dose levalbuterol in children with
asthma: safety and efficacy in comparison with placebo and racemic albuterol.
J Allergy Clin Immunol 2001;108(6):938–45.
27. Nelson HS, Bensch G, Pleskow WW, et al. Improved bronchodilation with leval-
buterol compared with racemic albuterol in patients with asthma. J Allergy Clin
Immunol 1998;102(6):943–52.
28. Gawchik SM, Saccar CL, Noonan M, et al. The safety and efficacy of nebulized
levalbuterol compared with racemic albuterol and placebo in the treatment of
asthma in pediatric patients. J Allergy Clin Immunol 1999;103(4):615–21.
29. Carl J, Myers T, Kirchner HL, et al. Comparison of racemic albuterol and leval-
buterol for treatment of acute asthma. J Pediatr 2003;143(6):731–6.
30. Tripp K, McVicar W, Nair P, et al. A cumulative dose study of levalbuterol and
racemic albuterol administered by hydrofluoroalkane-134a metered-dose
inhaler in asthmatic subjects. J Allergy Clin Immunol 2008;122(3):544–9.
31. Lam S, Chen J. Changes in heart rate associated with nebulized racemic albu-
terol and levalbuterol in intensive care patients. Am J Health Syst Pharm 2003;
60(19):1971–5.
32. Plotnick LH, Ducharme FM. Combined inhaled anticholinergics and beta2-
agonists for initial treatment of acute asthma in children. Cochrane Database
Syst Rev 2000;4:CD000060.
33. Rodrigo GJ, Castro Rodriguez JA. Anticholinergics in the treatment of children
and adults with acute asthma: a systematic review with meta-analysis. Thorax
2005;60(9):740–6.
34. Rowe BH, Edmonds ML, Spooner CH, et al. Corticosteroid therapy for acute
asthma. Respir Med 2004;98(4):275–84.
35. Fiel S, Vincken W. Systemic corticosteroid therapy for acute asthma exacerba-
tions. J Asthma 2006;43(5):321–31.
36. Smith M, Iqbal Shaikh Mohammed SI, Rowe Brian H, et al. Corticosteroids for
hospitalised children with acute asthma. Cochrane Database Syst Rev 2003;1.
Available at: http://www.mrw.interscience.wiley.com/cochrane/clsysrev/articles/
CD002886/frame.html. Accessed May 1, 2011.
37. Becker JM, Arora A, Scarfone RJ, et al. Oral versus intravenous corticosteroids
in children hospitalized with asthma. J Allergy Clin Immunol 1999;103(4):
586–90.
38. Barnett PL, Caputo GL, Baskin M, et al. Intravenous versus oral corticosteroids
in the management of acute asthma in children. Ann Emerg Med 1997;29(2):
212–7.
39. Kravitz J, Dominici P, Ufberg J, et al. Two days of dexamethasone versus 5 days
of prednisone in the treatment of acute asthma: a randomized controlled trial.
Ann Emerg Med 2011;58(2):200–4.

40. Greenberg R, Kerby G, Roosevelt G. A comparison of oral dexamethasone with

oral prednisone in pediatric asthma exacerbations treated in the emergency
department. Clin Pediatr 2008;47(8):817–23.
41. Shefrin R. Use of dexamethasone and prednisone in acute asthma exacerba-
tions in pediatric patients. Can Fam Physician 2009;55(7):704–6.
42. Altamimi M. Single-dose oral dexamethasone in the emergency management of
children with exacerbations of mild to moderate asthma. Pediatr Emerg Care
2006;22(12):786–93.
43. Gordon S, Tompkins T, Dayan P. Randomized trial of single-dose intramuscular
dexamethasone compared with prednisolone for children with acute asthma.
Pediatr Emerg Care 2007;23(8):521–7.
44. Gries DM, Moffitt DR, Pulos E, et al. A single dose of intramuscularly adminis-
tered dexamethasone acetate is as effective as oral prednisone to treat asthma
exacerbations in young children. J Pediatr 2000;136(3):298–303.
45. FitzGerald JM, Becker A, Sears MR, et al. Doubling the dose of budesonide versus
maintenance treatment in asthma exacerbations. Thorax 2004;59(7):550–6.
46. Edmonds ML, Camargo CA, Pollack CV, et al. Early use of inhaled corticoste-
roids in the emergency department treatment of acute asthma. Cochrane Data-
base Syst Rev 2003;3:CD002308.
47. Schuh S, Dick P, Stephens D, et al. High-dose inhaled fluticasone does not
replace oral prednisolone in children with mild to moderate acute asthma. Pedi-
atrics 2006;118(2):644–50.
48. Schuh S, Reisman J, Alshehri M, et al. A comparison of inhaled fluticasone and
oral prednisone for children with severe acute asthma. N Engl J Med 2000;
343(10):689–94.
49. Upham BD, Mollen CJ, Scarfone RJ, et al. Nebulized budesonide added to
standard pediatric emergency department treatment of acute asthma:
a randomized, double-blind trial. Acad Emerg Med 2011;18(7):665–73.
50. Spivey WH, Skobeloff EM, Levin RM. Effect of magnesium chloride on rabbit
bronchial smooth muscle. Ann Emerg Med 1990;19(10):1107–12.
51. Ciarallo L, Sauer AH, Shannon MW. Intravenous magnesium therapy for
moderate to severe pediatric asthma: results of a randomized, placebo-
controlled trial. J Pediatr 1996;129(6):809–14.
52. Noppen M, Vanmaele L, Impens N, et al. Bronchodilating effect of intravenous
magnesium sulfate in acute severe bronchial asthma. Chest 1990;97(2):373–6.
53. Rowe BH, Bretzlaff JA, Bourdon C, et al. Intravenous magnesium sulfate treat-
ment for acute asthma in the emergency department: a systematic review of
the literature. Ann Emerg Med 2000;36(3):181–90.
54. Rowe BH, Bretzlaff JA, Bourdon C, et al. Magnesium sulfate for treating exacer-
bations of acute asthma in the emergency department. Cochrane Database
Syst Rev 2000;2:CD001490.
55. Gallegos-Solorzano MC, Perez-Padilla R, Hernandez-Zenteno RJ. Usefulness of
inhaled magnesium sulfate in the coadjuvant management of severe asthma
crisis in an emergency department. Pulm Pharmacol Ther 2010;23(5):432–7.
56. Hughes R, Goldkorn A, Masoli M, et al. Use of isotonic nebulised magnesium
sulphate as an adjuvant to salbutamol in treatment of severe asthma in adults:
randomised placebo-controlled trial. Lancet 2003;361(9375):2114–7.
57. Bessmertny O, DiGregorio RV, Cohen H, et al. A randomized clinical trial of
nebulized magnesium sulfate in addition to albuterol in the treatment of acute
mild-to-moderate asthma exacerbations in adults. Ann Emerg Med 2002;
39(6):585–91.

58. Blitz M, Blitz S, Beasely R, et al. Inhaled magnesium sulfate in the treatment of
acute asthma. Cochrane Database Syst Rev 2005;4. Available at: http://www.
mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD003898/frame.html.
Accessed May 1, 2011.
59. Harmanci K, Bakirtas A, Turktas I, et al. Oral montelukast treatment of preschool-
aged children with acute asthma. Ann Allergy Asthma Immunol 2006;96(5):
731–5.
60. Nelson K, Smith S, Trinkaus K, et al. Pilot study of oral montelukast added to
standard therapy for acute asthma exacerbations in children aged 6 to 14 years.
Pediatr Emerg Care 2008;24(1):21–7.
61. Dockhorn RJ, Baumgartner RA, Leff JA, et al. Comparison of the effects of intrave-
nous and oral montelukast on airway function: a double blind, placebo controlled,
three period, crossover study in asthmatic patients. Thorax 2000;55(4):260–5.
62. Camargo C, Smithline H, Malice MP, et al. A randomized controlled trial of intra-
venous montelukast in acute asthma. Am J Respir Crit Care Med 2003;167(4):
528–33.
63. Gupta VK, Cheifetz IM. Heliox administration in the pediatric intensive care unit:
an evidence-based review. Pediatr Crit Care Med 2005;6(2):204–11.
64. Kim I, Phrampus E, Venkataraman S, et al. Helium/oxygen-driven albuterol
nebulization in the treatment of children with moderate to severe asthma exac-
erbations: a randomized, controlled trial. Pediatrics 2005;116(5):1127–33.
65. Lee D, Hsu CW, Lee H, et al. Beneficial effects of albuterol therapy driven by he-
liox versus by oxygen in severe asthma exacerbation. Acad Emerg Med 2005;
12(9):820–7.
66. Rivera M, Kim T, Stewart G, et al. Albuterol nebulized in heliox in the initial ED
treatment of pediatric asthma: a blinded, randomized controlled trial. Am J
Emerg Med 2006;24(1):38–42.
67. Travers A, Jones AP, Kelly K, et al. Intravenous beta2-agonists for acute asthma
in the emergency department. Cochrane Database Syst Rev 2001;2:CD002988:
68. Mitra A, Bassler D, Goodman K, et al. Intravenous aminophylline for acute
severe asthma in children over two years receiving inhaled bronchodilators. Co-
chrane Database Syst Rev 2005;2:CD001276.
69. Ream RS, Loftis LL, Albers GM, et al. Efficacy of IV theophylline in children with
severe status asthmaticus. Chest 2001;119(5):1480–8.
70. Akingbola O, Simakajornboon N, Hadley E Jr, et al. Noninvasive positive-
pressure ventilation in pediatric status asthmaticus. Pediatr Crit Care Med
2002;3(2):181–4.
71. Bernet V, Hug M, Frey B. Predictive factors for the success of noninvasive mask
ventilation in infants and children with acute respiratory failure. Pediatr Crit Care
Med 2005;6(6):660–4.
72. Carroll C, Schramm C. Noninvasive positive pressure ventilation for the treat-
ment of status asthmaticus in children. Ann Allergy Asthma Immunol 2006;
96(3):454–9.
73. Essouri S, Chevret L, Durand P, et al. Noninvasive positive pressure ventilation:
five years of experience in a pediatric intensive care unit. Pediatr Crit Care Med
2006;7(4):329–34.
74. Padman R, Lawless ST, Kettrick RG. Noninvasive ventilation via bilevel positive
airway pressure support in pediatric practice. Crit Care Med 1998;26(1):
169–73.
75. Thill P, McGuire J, Baden H, et al. Noninvasive positive-pressure ventilation in
children with lower airway obstruction. Pediatr Crit Care Med 2004;5(4):337–42.

76. Ram FS, Wellington S, Rowe B, et al. Non-invasive positive pressure ventilation
for treatment of respiratory failure due to severe acute exacerbations of asthma.
Cochrane Database Syst Rev 2005;3:CD004360.
77. Brown RH, Wagner EM. Mechanisms of bronchoprotection by anesthetic induc-
tion agents: propofol versus ketamine. Anesthesiology 1999;90(3):822–8.
78. Allen J, Macias C. The efficacy of ketamine in pediatric emergency department
patients who present with acute severe asthma. Ann Emerg Med 2005;46(1):
43–50.
79. Howton JC, Rose J, Duffy S, et al. Randomized, double-blind, placebo-
controlled trial of intravenous ketamine in acute asthma. Ann Emerg Med
1996;27(2):170–5.
80. Green S, Roback M, Krauss B. Anticholinergics and ketamine sedation in chil-
dren: a secondary analysis of atropine versus glycopyrrolate. Acad Emerg
Med 2010;17(2):157–62.
81. Green SM, Roback MG, Kennedy RM, et al. Clinical practice guideline for emer-
gency department ketamine dissociative sedation: 2011 update. Ann Emerg
Med 2011;57(5):449–61.
82. Bellomo R, McLaughlin P, Tai E, et al. Asthma requiring mechanical ventilation. A
low morbidity approach. Chest 1994;105(3):891–6.
83. Cox RG, Barker GA, Bohn DJ. Efficacy, results, and complications of mechan-
ical ventilation in children with status asthmaticus. Pediatr Pulmonol 1991;
11(2):120–6.
84. Darioli R, Perret C. Mechanical controlled hypoventilation in status asthmaticus.
Am Rev Respir Dis 1984;129(3):385–7.
85. Dworkin G, Kattan M. Mechanical ventilation for status asthmaticus in children.
J Pediatr 1989;114(4):545–9.
86. Hickling KG, Walsh J, Henderson S, et al. Low mortality rate in adult respiratory
distress syndrome using low-volume, pressure-limited ventilation with permis-
sive hypercapnia: a prospective study. Crit Care Med 1994;22(10):1568–78.
87. Menitove SM, Goldring RM. Combined ventilator and bicarbonate strategy in the
management of status asthmaticus. Am J Med 1983;74(5):898–901.
88. Sin D, Bell N, Svenson L, et al. The impact of follow-up physician visits on emer-
gency readmissions for patients with asthma and chronic obstructive pulmonary
disease: a population-based study. Am J Med 2002;112(2):120–5.
89. Zeiger RS, Heller S, Mellon MH, et al. Facilitated referral to asthma specialist
reduces relapses in asthma emergency room visits. J Allergy Clin Immunol
1991;87(6):1160–8.
90. Zorc J, Scarfone R, Li Y, et al. Scheduled follow-up after a pediatric emergency
department visit for asthma: a randomized trial. Pediatrics 2003;111(3):495–502.
91. Baren J, Boudreaux E, Brenner B, et al. Randomized controlled trial of emer-
gency department interventions to improve primary care follow-up for patients
with acute asthma. Chest 2006;129(2):257–65.
92. Sin D, Man SF. Low-dose inhaled corticosteroid therapy and risk of emergency
department visits for asthma. Arch Intern Med 2002;162(14):1591–5.
93. Edmonds M, Brenner Barry E, Camargo Carlos A, et al. Inhaled steroids for
acute asthma following emergency department discharge. Cochrane Database
Syst Rev 2000;3. Available at: http://www.mrw.interscience.wiley.com/cochrane/
clsysrev/articles/CD002316/frame.html. Accessed May 1, 2011.
94. Cowie RL, Revitt SG, Underwood MF, et al. The effect of a peak flow-based
action plan in the prevention of exacerbations of asthma. Chest 1997;112(6):
1534–8.

95. Cherry J. Clinical practice. Croup. N Engl J Med 2008;358(4):384–91.

96. Segal A, Crighton E, Moineddin R, et al. Croup hospitalizations in Ontario: a 14-
year time-series analysis. Pediatrics 2005;116(1):51–5.
97. Peltola V, Heikkinen T, Ruuskanen O. Clinical courses of croup caused by influ-
enza and parainfluenza viruses. Pediatr Infect Dis J 2002;21(1):76–8.
98. Groblewski J, Shah R, Zalzal G. Microdebrider-assisted supraglottoplasty for
laryngomalacia. Ann Otol Rhinol Laryngol 2009;118(8):592–7.
99. Antony R, Al Rawas A, Irwin M. Stridor in a newborn. CMAJ 2005;173(6):601–2.
100. Mancuso RF. Stridor in neonates. Pediatr Clin North Am 1996;43(6):1339–56.
101. Koplewitz B, Springer C, Slasky B, et al. CT of hemangiomas of the upper
airways in children. AJR Am J Roentgenol 2005;184(2):663–70.
102. Rahbar R, Litrovnik B, Vargas S, et al. The biology and management of laryngeal
neurofibroma. Arch Otolaryngol Head Neck Surg 2004;130(12):1400–6.
103. Durden F, Sobol S. Balloon laryngoplasty as a primary treatment for subglottic
stenosis. Arch Otolaryngol Head Neck Surg 2007;133(8):772–5.
104. Spanos W, Brookes J, Smith M, et al. Unilateral vocal fold paralysis in premature
infants after ligation of patent ductus arteriosus: vascular clip versus suture liga-
ture. Ann Otol Rhinol Laryngol 2009;118(10):750–3.
105. Strife JL. Upper airway and tracheal obstruction in infants and children. Radiol
Clin North Am 1988;26(2):309–22.
106. Westley CR, Cotton EK, Brooks JG. Nebulized racemic epinephrine by IPPB for
the treatment of croup: a double-blind study. Am J Dis Child 1978;132(5):484–7.
107. Bjornson CL, Johnson DW. Croup—treatment update. Pediatr Emerg Care 2005;
21(12):863–70 [quiz: 871–3].
108. Sparrow A, Geelhoed G. Prednisolone versus dexamethasone in croup: a rand-
omised equivalence trial. Arch Dis Child 2006;91(7):580–3.
109. Russell K, Liang Y, O’Gorman K, et al. Glucocorticoids for croup. Cochrane
Database Syst Rev 2011;1:CD001955.
110. Cetinkaya F, Tfeki B, Kutluk G. A comparison of nebulized budesonide, and
intramuscular, and oral dexamethasone for treatment of croup. Int J Pediatr Oto-
rhinolaryngol 2004;68(4):453–6.
111. Geelhoed GC, Macdonald WB. Oral dexamethasone in the treatment of croup: 0.15
mg/kg versus 0.3 mg/kg versus 0.6 mg/kg. Pediatr Pulmonol 1995;20(6):362–8.
112. Dobrovoljac M, Geelhoed G. 27 years of croup: an update highlighting the
effectiveness of 0.15 mg/kg of dexamethasone. Emerg Med Australas 2009;
21(4):309–14.
113. Chub Uppakarn S, Sangsupawanich P. A randomized comparison of dexameth-
asone 0.15 mg/kg versus 0.6 mg/kg for the treatment of moderate to severe
croup. Int J Pediatr Otorhinolaryngol 2007;71(3):473–7.
114. Duman M, Ozdemir D, Atasever S. Nebulised L-epinephrine and steroid combi-
nation in the treatment of moderate to severe croup. Clin Drug Investig 2005;
25(3):183–9.
115. Klassen TP, Craig WR, Moher D, et al. Nebulized budesonide and oral dexa-
methasone for treatment of croup: a randomized controlled trial. JAMA 1998;
279(20):1629–32.
116. Geelhoed GC. Budesonide offers no advantage when added to oral dexameth-
asone in the treatment of croup. Pediatr Emerg Care 2005;21(6):359–62.
117. Bjornson C, Russell Kelly F, Vandermeer B, et al. Nebulized epinephrine for croup
in children. Cochrane Database Syst Rev 2011;2. Available at: http://www.mrw.
interscience.wiley.com/cochrane/clsysrev/articles/CD006619/frame.html. Ac-
cessed May 1, 2011.

118. Taussig LM, Castro O, Beaudry PH, et al. Treatment of laryngotracheobronchitis

(croup). Use of intermittent positive-pressure breathing and racemic epineph-
rine. Am J Dis Child 1975;129(7):790–3.
119. Scolnik D, Coates A, Stephens D, et al. Controlled delivery of high vs low
humidity vs mist therapy for croup in emergency departments: a randomized
controlled trial. JAMA 2006;295(11):1274–80.
120. Neto G, Kentab O, Klassen T, et al. A randomized controlled trial of mist in the acute
treatment of moderate croup. Acad Emerg Med 2002;9(9):873–9.
121. Moore M, Little P. Humidified air inhalation for treating croup. Cochrane
Database Syst Rev 2006;(3). Available at: http://www.mrw.interscience.wiley.
com/cochrane/clsysrev/articles/CD002870/frame.html. Accessed May 1, 2011.
122. Weber JE, Chudnofsky CR, Younger JG, et al. A randomized comparison of
helium-oxygen mixture (Heliox) and racemic epinephrine for the treatment
of moderate to severe croup. Pediatrics 2001;107(6):E96.
123. Terregino CA, Nairn SJ, Chansky ME, et al. The effect of heliox on croup: a pilot
study. Acad Emerg Med 1998;5(11):1130–3.
124. Vorwerk C, Coats T. Heliox for croup in children. Cochrane Database Syst Rev
2010;2:CD006822.
125. Everard M. Acute bronchiolitis and croup. Pediatr Clin North Am 2009;56(1):
119–33.
126. Ducharme FM. Management of acute bronchiolitis. BMJ 2011;342:d1658.
127. Mansbach JM, McAdam AJ, Clark S, et al. Prospective multicenter study of the
viral etiology of bronchiolitis in the emergency department. Acad Emerg Med
2008;15(2):111–8.
128. Midulla F, Scagnolari C, Bonci E, et al. Respiratory syncytial virus, human boca-
virus and rhinovirus bronchiolitis in infants. Arch Dis Child 2010;95(1):35–41.
129. Miron D, Srugo I, Kra-Oz Z, et al. Sole pathogen in acute bronchiolitis—is there
a role for other organisms apart from RSV? Pediatr Infect Dis J 2010;2010(29):
e7–10.
130. American Academy of Pediatrics Subcommittee on Diagnosis and Management
of Bronchiolitis. Diagnosis and management of bronchiolitis. Pediatrics 2006;
118(4):1774–93.
131. Shay DK, Holman RC, Newman RD, et al. Bronchiolitis-associated hospitaliza-
tions among US children, 1980-1996. JAMA 1999;282(15):1440–6.
132. Shay DK, Holman RC, Roosevelt GE, et al. Bronchiolitis-associated mortality
and estimates of respiratory syncytial virus-associated deaths among US chil-
dren, 1979-1997. J Infect Dis 2001;183(1):16–22.
133. Swingler GH, Hussey GD, Zwarenstein M. Duration of illness in ambulatory chil-
dren diagnosed with bronchiolitis. Arch Pediatr Adolesc Med 2000;154(10):
997–1000.
134. Petruzella FD, Gorelick MH. Duration of illness in infants with bronchiolitis eval-
uated in the emergency department. Pediatrics 2010;126(2):285–90.
135. Bialy L, Foisy M, Smith M, et al. The Cochrane library and the treatment of bronchio-
litis in children: an overview of reviews. Evid Base Child Health 2011;6(1):258–75.
136. Goutzamanis J. Bronchiolitis. In: Frank LR, Jobe KA, editors. Admission &
discharge decisions in emergency medicine. Philadelphia: Hanley & Belfus,
Inc; 2002. p. 246–50.
137. Everard M. What link between early respiratory viral infections and atopic
asthma? Lancet 1999;354(9178):527–8.
138. Gern JE. Viral respiratory infection and the link to asthma. Pediatr Infect Dis J
2008;27(10):S97–103.

139. Stein RT, Sherrill D, Morgan WJ, et al. Respiratory syncytial virus in early life
and risk of wheeze and allergy by age 13 years. Lancet 1999;354(9178):
541–5.
140. Swingler GH, Hussey GD, Zwarenstein M. Randomised controlled trial of clinical
outcome after chest radiograph in ambulatory acute lower-respiratory infection
in children. Lancet 1998;351(9100):404–8.
141. Schuh S, Lalani A, Allen U, et al. Evaluation of the utility of radiography in acute
bronchiolitis. J Pediatr 2007;150(4):429–33.
142. Mahabee-Gittens EM, Bachman DT, Shapiro ED, et al. Chest radiographs in the
pediatric emergency department for children 18 months of age with wheezing.
Clin Pediatr 1999;38(7):395–9.
143. Purcell K, Fergie J. Lack of usefulness of an abnormal white blood cell count for
predicting a concurrent serious bacterial infection in infants and young children
hospitalized with respiratory syncytial virus lower respiratory tract infection. Pe-
diatr Infect Dis J 2007;2007(26):311–5.
144. Peltola V, Mertsola J, Ruuskanen O. Comparison of total white blood cell count
and serum C-reactive protein levels in confirmed bacterial and viral infections.
J Pediatr 2006;149(5):721–4.
145. Liebelt EL, Qi K, Harvey K. Diagnostic testing for serious bacterial infections in
infants aged 90 days or younger with bronchiolitis. Arch Pediatr Adolesc Med
1999;153(5):525–30.
146. Antanow J, Hansen K, McKinstry CA. Sepsis evaluations in hospitalized infants
with bronchiolitis. Pediatr Infect Dis J 1998;17(3):231–6.
147. Thorburn K, Harigopal S, Reddy V, et al. High incidence of pulmonary bacterial
co-infection in children with severe respiratory syncytial virus (RSV) bronchioli-
tis. Thorax 2006;61(7):611–5.
148. Bilavsky E, Shouval D, Yarden-Bilavsky H. A prospective study of the risk for
serious bacterial infections in hospitalized febrile infants with or without bron-
chiolitis. Pediatr Infect Dis J 2008;27(3):269–82.
149. Duttweiler L, Nadal D, Frey B. Pulmonary and systemic bacterial co-infections in
severe RSV bronchiolitis. Arch Dis Child 2004;89(12):1155–7.
150. Hartling L, Bialy Liza M, Vandermeer B, et al. Epinephrine for bronchiolitis. Cochrane
Database Syst Rev 2011;(6). Available at: http://www.mrw.interscience.wiley.com/
cochrane/clsysrev/articles/CD003123/frame.html. Accessed April 13, 2011.
151. Hartling L, Fernandes RM, Bialy L, et al. Steroids and bronchodilators for acute
bronchiolitis in the first two years of life: systematic review and meta-analysis.
BMJ 2011;342:d1714.
152. Chavasse Richard JPG, Seddon P, Bara A, et al. Short acting beta2-agonists for
recurrent wheeze in children under two years of age. Cochrane Database Syst
Rev 2002;2. Available at: http://www.mrw.interscience.wiley.com/cochrane/
clsysrev/articles/CD002873/frame.html. Accessed April 13, 2011.
153. Everard M, Bara A, Kurian M, et al. Anticholinergic drugs for wheeze in children
under the age of two years. Cochrane Database Syst Rev 2005;3. Available at:
http://www.mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD001279/frame.
html. Accessed April 13, 2011.
154. Fernandes Ricardo M, Bialy Liza M, Vandermeer B, et al. Glucocorticoids for
acute viral bronchiolitis in infants and young children. Cochrane Database
Syst Rev 2010;10. Available at: http://www.mrw.interscience.wiley.com/cochrane/
clsysrev/articles/CD004878/frame.html. Accessed April 13, 2011.
155. Zhang L, Mendoza-Sassi Raúl A, Wainwright C, et al. Nebulized hypertonic
saline solution for acute bronchiolitis in infants. Cochrane Database Syst Rev

2008;4. Available at: http://www.mrw.interscience.wiley.com/cochrane/clsysrev/

articles/CD006458/frame.html. Accessed April 13, 2011.
156. Liet JM, Ducruet T, Gupta V, et al. Heliox inhalation therapy for bronchiolitis in infants.
Cochrane Database Syst Rev 2010;4. Available at: http://www.mrw.interscience.
wiley.com/cochrane/clsysrev/articles/CD006915/frame.html. Accessed April 13,
2011.
157. Bronchiolitis Guideline Team, Cincinatti Children’s Hospital Medical Team.
Evidenced-based care guideline for management of bronchiolitis in infants 1
year of age or less with a first time epidose. Cincinnatti (OH): Bronchiolitis Pedi-
atric Evidence-Based Care Guidelines, Cincinnatti Children’s Hospital Medical
Center. Available at: http://www.cincinnatichildrens.org/service/j/anderseon-
center/evidence-based-care/bronchiolitis/. Accessed October 27, 2011.
158. Turner T, WIlkinson F, Harris C. Evidence-based guideline for the management
of bronchiolitis. Aust Fam Physician 2008;37(6):6–13.
159. Bronchiolitis in children—a national clinical guideline. Scottish Intercollegiate
Guidelines Network; 2006. Available at: http://www.sign.ac.uk/pdf/sign91.pdf.
Accessed April 13, 2011.
160. Gadomski Anne M, Brower M. Bronchodilators for bronchiolitis. Cochrane Data-
base Syst Rev 2010;12. Available at: http://www.mrw.interscience.wiley.com/
cochrane/clsysrev/articles/CD001266/frame.html. Accessed April 13, 2011.
161. Seiden JA, Scarfone RJ. Bronchiolitis: an evidence-based approach to manage-
ment. Clin Pediatr Emerg Med 2009;10(2):75–81.
162. Grewal S, Ali S, McConnell DW, et al. A randomized trial of nebulized 3% hyper-
tonic saline with epinephrine in the treatment of acute bronchiolitis in the emer-
gency department. Arch Pediatr Adolesc Med 2009;163(11):1007–12.
163. Corneli HM, Zorc JJ, Mahajan P, et al. A multicenter, randomized, controlled trial
of dexamethasone for bronchiolitis. N Engl J Med 2007;357(4):331–9.
164. Plint AC, Johnson DW, Patel H, et al. Epinephrine and dexamethasone in chil-
dren with bronchiolitis. N Engl J Med 2009;360(20):2079–89.
165. Wark P, McDonald Vanessa M. Nebulised hypertonic saline for cystic fibrosis. Co-
chrane Database Syst Rev 2009;2. Available at: http://www.mrw.interscience.wiley.
com/cochrane/clsysrev/articles/CD001506/frame.html. Accessed April 13, 2011.
166. Chaudhry K, Sinert R. Is nebulized hypertonic saline solution an effective treat-
ment for bronchiolitis in infants? Ann Emerg Med 2010;55(1):120–2.
167. Kuzik BA, Flavin MP, Kent S, et al. Effect of inhaled hypertonic saline on hospital
admission rate in children with viral bronchiolitis: a randomized trial. CJEM 2010;
12(6):477.
168. Kim IK, Corcoran T. Recent developments in heliox therapy for asthma and
bronchiolitis. Clin Pediatr Emerg Med 2009;10(2):68–74.
169. Mansbach JM, Clark S, Christopher NC, et al. Prospective multicenter study of
bronchiolitis: predicting safe discharges from the emergency department. Pedi-
atrics 2008;121(4):680–8.
170. Willwerth BM, Harper MB, Greenes DS. Identifying hospitalized infants who have
bronchiolitis and are at high risk for apnea. Ann Emerg Med 2006;48(4):441–7.
171. Norwood A, Mansbach JM, Clark S, et al. Prospective multicenter study of bron-
chiolitis: predictors of an unscheduled visit after discharge from the emergency
department. Acad Emerg Med 2010;17(4):376–82.
172. Marlais M, Evans J, Abrahamson E. Clinical predictors of admission in infants
with acute bronchiolitis. Arch Dis Child 2011;96(7):648–52.
173. Black RE, Cousens S, Johnson HL, et al. Global, regional, and national causes of
child mortality in 2008: a systematic analysis. Lancet 2010;375(9730):1969–87.

174. Homier V, Bellevance C, Xhignesse M. Prevalence of pneumonia in children

under 12 years of age who undergo abdominal radiography in the emergency
department. CJEM 2007;9(5):347–51.
175. Evidence-Based (EB) Clinical Decision Support Team & Community-Acquired
Pneumonia Content Expert Team - Texas Children’s Hospital. Community-
acquired pneumonia (CAP) clinical guideline. Available at: http://www.bcm.
edu/web/pediatrics/documents/rp_archive_21.pdf. Accessed October 27, 2011.
176. Murphy CG, Van De Pol AC, Harper MB, et al. Clinical predictors of occult pneu-
monia in the febrile child. Acad Emerg Med 2007;14(3):243–9.
177. Shah S, Bachur R, Kim D, et al. Lack of predictive value of tachypnea in the
diagnosis of pneumonia in children. Pediatr Infect Dis J 2010;29:406–9.
178. Korppi M, Don M, Valent F, et al. The value of clinical features in differentiating
between viral, pneumococcal and atypical bacterial pneumonia in children.
Acta Paediatr 2008;97(7):943–7.
179. Mathews B, Shah S, Cleveland RH, et al. Clinical predictors of pneumonia
among children with wheezing. Pediatrics 2009;124(1):e29–36.
180. Korppi M. Antibiotic therapy for pneumonia in the pediatric population. Pediatr
Health 2007;1(1):77.
181. British Thoracic Society. BTS guidelines for the management of community-
acquired pneumonia in childhood. Thorax 2002;57(Suppl 1):i1–24.
182. Lahti E, Peltola V, Virkki R, et al. Development of parapneumonic empyema in
children. Acta Paediatr 2007;96(11):1686–92.
183. Virkki R, Juven T, Rikalainen H, et al. Differentiation of bacterial and viral pneu-
monia in children. Thorax 2002;57(5):438–41.
184. Michelow IC, Olsen K, Lozano J, et al. Epidemiology and clinical characteristics
of community-acquired pneumonia in hospitalized children. Pediatrics 2004;
113(4):701–7.
185. Carrillo-Marquez M, Hulten K, Hammerman W, et al. Staphylococcus aureus
pneumonia in children in the era of community-acquired methicillin-resistance
at Texas Children’s Hospital. Pediatr Infect Dis J 2011;30(7):545–50.
186. Wallin T, Hern H, Frazee B. Community-acquired methicillin-resistant Staphylo-
coccus aureus. Emerg Med Clin North Am 2008;26:431–55.
187. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the Infectious
Diseases Society of America for the treatment of methicillin-resistant Staphylo-
coccus aureus infections in adults and children: executive summary. Clin Infect
Dis 2011;52(3):285–92.
188. Graham S, English M, Hazir T, et al. Challenges to improving case management
of childhood pneumonia at health facilities in resource-limited settings. Bull
World Health Organ 2008;86(5):349–55.
189. Clinical Practice Guidelines Group - Toward Optimized Practice (TOP) Program.
Guideline for the diagnosis and management of community acquired pneu-
monia: pediatric - 2008 Update. Available at: http://www.topalbertadoctors.
org/cpgs.php?sid=15&cpg_cats=61. Accessed April 26, 2011.
190. Newman M, Scully K, Kim D. Physician assessment of the likelihood of pneu-
monia in pediatric emergency department. Pediatr Emerg Care 2010;26(11):
817–22.
191. Lynch T, Bialy L, Kellner J. A systematic review on the diagnosis of pediatric
bacterial pneumonia: when gold is bronze. PLoS One 2010;5(8):1–7.
192. Cortellaro F, Colombo S, Coen D, et al. Lung ultrasound is an accurate diag-
nostic tool for the diagnosis of pneumonia in the emergency department. Emerg
Med J 2010. [Epub ahead of print].

193. Kurian J, Levin TL, Han BK, et al. Comparison of ultrasound and CT in the eval-
uation of pneumonia complicated by parapneumonic effusion in children. Am J
Roentgenol 2009;193(6):1648–54.
194. Community Acquired Pneumonia Guideline Team, Cincinnati Children’s Hospital
Medical Center. Evidence-based care guideline for medical management of
community acquired pneumonia in children 60 days to 17 years of age. Avail-
able at: http://www.cincinnatichildrens.org/service/j/anderson-center/evidence-
based-care/community-acquired-pneumonia/. Accessed October 27, 2011.
195. Shah S, Dugan M, Bell L, et al. Blood cultures in the emergency department
evaluation of childhood pneumonia. Pediatr Infect Dis J 2011;30:475–9.
196. Hickey RW, Bowman MJ, Smith GA. Utility of blood cultures in pediatric patients
found to have pneumonia in the emergency department. Ann Emerg Med 1996;
27(6):721–5.
197. Jadavji T, Law B. A practical guide for the diagnosis and treatment of pediatric
pneumonia. CMAJ 1997;156(5):S703.
198. Wilde JA. Rapid diagnostic testing for the identification of respiratory agents in
the emergency department. Clin Pediatr Emerg Med 2002;3(3):181–90.
199. Bradley JS, Byington CL, Shah SS, et al. The management of community-
acquired pneumonia in infants and children older than 3 months of age: clinical
practice guidelines by the Pediatric Infectious Diseases Society and the Infec-
tious Diseases Society of America. Clin Infect Dis 2011;53(7):e25–76.
200. Atkinson M, Lakhanpaul M, Smyth A, et al. Comparison of oral amoxicillin and
intravenous benzyl penicillin for community acquired pneumonia in children
(PIVOT trial): a multicentre pragmatic randomised controlled equivalence trial.
Thorax 2007;62(12):1102–6.
201. Haider Batool A, Lassi Zohra S, Bhutta Zulfiqar A. Short-course versus long-
course antibiotic therapy for non-severe community-acquired pneumonia in
children aged 2 months to 59 months. Cochrane Database Syst Rev 2008;2.
Available at: http://www.mrw.interscience.wiley.com/cochrane/clsysrev/articles/
CD005976/frame.html. Accessed June 12, 2011.
202. Ayieko P, English M. Case management of childhood pneumonia in developing
countries. Pediatr Infect Dis J 2007;26(5):432–40.
203. Virkki R, Juven T, Mertsola J, et al. Radiographic follow-up of pneumonia in chil-
dren. Pediatr Pulmonol 2005;40(3):223–7.

BMJ Pediatric Asthma in A Nutshell
No ratings yet
BMJ Pediatric Asthma in A Nutshell
14 pages
Children Nebulizer
No ratings yet
Children Nebulizer
8 pages
Asthma Training for Health Students
No ratings yet
Asthma Training for Health Students
32 pages
Interstitial Lung Disease
No ratings yet
Interstitial Lung Disease
31 pages
Hemodynamic Monitoring Techniques
No ratings yet
Hemodynamic Monitoring Techniques
6 pages
Non-Pharmacological Modalities For Tobacco Cessation: An Overview
No ratings yet
Non-Pharmacological Modalities For Tobacco Cessation: An Overview
11 pages
COPD Patient Teaching Plan
50% (2)
COPD Patient Teaching Plan
2 pages
Childhood Asthma
No ratings yet
Childhood Asthma
9 pages
Venous Thrombosis and Embolism Prevention and Management
No ratings yet
Venous Thrombosis and Embolism Prevention and Management
39 pages
Asthma: A. Definition
No ratings yet
Asthma: A. Definition
6 pages
Neutropenia
No ratings yet
Neutropenia
12 pages
Migraine
No ratings yet
Migraine
16 pages
Acute Severe Asthma
No ratings yet
Acute Severe Asthma
5 pages
Annotated Bibliography
No ratings yet
Annotated Bibliography
20 pages
Rhinitis
No ratings yet
Rhinitis
7 pages
BTS - NICE - SIGN Joint Chronic Asthma Guideline Slide Deck
No ratings yet
BTS - NICE - SIGN Joint Chronic Asthma Guideline Slide Deck
16 pages
Acute Exacerbation of Asthma
No ratings yet
Acute Exacerbation of Asthma
31 pages
CPAP vs BiPAP for Sleep Apnea
100% (1)
CPAP vs BiPAP for Sleep Apnea
2 pages
Wheezing Child...
No ratings yet
Wheezing Child...
71 pages
Pulmonary Fibrosis
No ratings yet
Pulmonary Fibrosis
5 pages
Definition:: Between 16
No ratings yet
Definition:: Between 16
3 pages
Pediatric Nursing Unit 9
100% (1)
Pediatric Nursing Unit 9
48 pages
BRONCHIECTASIS
100% (1)
BRONCHIECTASIS
40 pages
Prognosis MG
No ratings yet
Prognosis MG
7 pages
Microcephaly: DR Yog Raj Khinchi
No ratings yet
Microcephaly: DR Yog Raj Khinchi
37 pages
Fetal Development & Growth Guide
No ratings yet
Fetal Development & Growth Guide
42 pages
Asphyxia
No ratings yet
Asphyxia
19 pages
Family Health Assessment
No ratings yet
Family Health Assessment
12 pages
Common Pediatric Procedures..Nati c2
No ratings yet
Common Pediatric Procedures..Nati c2
60 pages
CRHSP Peds Drug Dosage
No ratings yet
CRHSP Peds Drug Dosage
4 pages
Recent Trials in Neonatology - Part II
No ratings yet
Recent Trials in Neonatology - Part II
70 pages
Asthma: A. Practice Essentials
No ratings yet
Asthma: A. Practice Essentials
8 pages
Pathophysiology of Asthma
No ratings yet
Pathophysiology of Asthma
71 pages
Pediatric Hypoglycemia Review
No ratings yet
Pediatric Hypoglycemia Review
35 pages
Nursing Drug Study Guide
No ratings yet
Nursing Drug Study Guide
3 pages
CH 150 Management of Cough in Office Practice
No ratings yet
CH 150 Management of Cough in Office Practice
8 pages
Hyperthermia
No ratings yet
Hyperthermia
20 pages
Chronic Lower Respiratory Tract Infections
100% (2)
Chronic Lower Respiratory Tract Infections
32 pages
Magnesium Sulphate Regimens in Eclampsia - High Risk Calicut 21st Nov. 2010
No ratings yet
Magnesium Sulphate Regimens in Eclampsia - High Risk Calicut 21st Nov. 2010
46 pages
IBS
No ratings yet
IBS
44 pages
O&G - Abnormal Presentation
No ratings yet
O&G - Abnormal Presentation
32 pages
Hyperemesis Gravidarum: Kelompok 5 Andi Cipta Andi Salma Vadhila Nur Alia Resmi Julita Putri Rismayanti
100% (1)
Hyperemesis Gravidarum: Kelompok 5 Andi Cipta Andi Salma Vadhila Nur Alia Resmi Julita Putri Rismayanti
7 pages
Laryngeal Mask Lma
No ratings yet
Laryngeal Mask Lma
25 pages
Tonsillectomy
0% (1)
Tonsillectomy
6 pages
Bronchial Asthma Report
No ratings yet
Bronchial Asthma Report
63 pages
Intersex by AHMED ABDULWAHAB
No ratings yet
Intersex by AHMED ABDULWAHAB
16 pages
HISTORY - There Is No Substitute For A Thorough Patient History For Determining Whether Other Conditions Are
No ratings yet
HISTORY - There Is No Substitute For A Thorough Patient History For Determining Whether Other Conditions Are
9 pages
Antenatal Care
100% (2)
Antenatal Care
4 pages
Breastfeeding
No ratings yet
Breastfeeding
13 pages
Status Asthmaticus
No ratings yet
Status Asthmaticus
5 pages
Vaccination
No ratings yet
Vaccination
4 pages
Caring For Critically Ill Patients With The ABCDEF Bundle Results of The ICU Liberation Collaborative in Over 15,000 Adults Pun2018
No ratings yet
Caring For Critically Ill Patients With The ABCDEF Bundle Results of The ICU Liberation Collaborative in Over 15,000 Adults Pun2018
12 pages
Encephalopathy in Children: An Approach To Assessment and Management
No ratings yet
Encephalopathy in Children: An Approach To Assessment and Management
8 pages
Pregnancy Coagulation Disorders
100% (1)
Pregnancy Coagulation Disorders
12 pages
Permanent Family Planning
No ratings yet
Permanent Family Planning
24 pages
Pediatric Poisoning Insights
100% (1)
Pediatric Poisoning Insights
97 pages
Renal or Urinary Tract Disorder
No ratings yet
Renal or Urinary Tract Disorder
6 pages
Orchitis
No ratings yet
Orchitis
35 pages
A Child Presenting With Breathing Difficulties (Asthma)
No ratings yet
A Child Presenting With Breathing Difficulties (Asthma)
54 pages
Asthma
No ratings yet
Asthma
45 pages
Readings - Setting The Ventilator - Setting The Ventilator (25 Min) - COV19x Courseware - Edx
No ratings yet
Readings - Setting The Ventilator - Setting The Ventilator (25 Min) - COV19x Courseware - Edx
4 pages
Coronavirus: Novel Coronavirus (COVID-19) Infection: Terminology
No ratings yet
Coronavirus: Novel Coronavirus (COVID-19) Infection: Terminology
12 pages
Pediatric Pallor & Hepatosplenomegaly
No ratings yet
Pediatric Pallor & Hepatosplenomegaly
8 pages
Mechanical Ventilation for Clinicians
No ratings yet
Mechanical Ventilation for Clinicians
4 pages
Mechanical Ventilation Pediatric Volume Mode Skill Respiratory Therapy COVID 19 Toolkit - 070420
No ratings yet
Mechanical Ventilation Pediatric Volume Mode Skill Respiratory Therapy COVID 19 Toolkit - 070420
8 pages
Pul HTN
No ratings yet
Pul HTN
27 pages
Best Practices For Sample Collection, Packaging, Transportation, and Testing
No ratings yet
Best Practices For Sample Collection, Packaging, Transportation, and Testing
28 pages
Shock Presentation
No ratings yet
Shock Presentation
20 pages
Pediatrics Slo Clinical Instructors Precepting Handbook 1516
No ratings yet
Pediatrics Slo Clinical Instructors Precepting Handbook 1516
16 pages
Pediatric Gastritis, Gastropathy, and Peptic Ulcer Disease: Education Gap
No ratings yet
Pediatric Gastritis, Gastropathy, and Peptic Ulcer Disease: Education Gap
10 pages
2018-2019 Medical School Calendar
No ratings yet
2018-2019 Medical School Calendar
1 page
Teaching Toolbox Bedside
No ratings yet
Teaching Toolbox Bedside
26 pages
MCMI Grossman
100% (2)
MCMI Grossman
151 pages
Second Lesson Plan Final 1
100% (1)
Second Lesson Plan Final 1
8 pages
THE EFFECTS OF LISTENING TO RONDALLA MUSICAL ENSEMBLE ON THE MOOD AND STRESS LEVELS OF THE YOUNG ADULTS OF MAPÚA MALAYAN COLLEGES LAGUNA: BASIS FOR MUSIC THERAPY INTERVENTION STRATEGIES - Extended Abstract
No ratings yet
THE EFFECTS OF LISTENING TO RONDALLA MUSICAL ENSEMBLE ON THE MOOD AND STRESS LEVELS OF THE YOUNG ADULTS OF MAPÚA MALAYAN COLLEGES LAGUNA: BASIS FOR MUSIC THERAPY INTERVENTION STRATEGIES - Extended Abstract
5 pages
The Impact of Social Media On Society
No ratings yet
The Impact of Social Media On Society
4 pages
Dealing With Guilt When A Child Dies
No ratings yet
Dealing With Guilt When A Child Dies
3 pages
BAMS - Time Table Update - 130225
No ratings yet
BAMS - Time Table Update - 130225
33 pages
Carmencita M. Abaquin Is A Nurse With Master's Degree in Nursing Obtained
0% (1)
Carmencita M. Abaquin Is A Nurse With Master's Degree in Nursing Obtained
2 pages
Chapter Five Structured Observation
No ratings yet
Chapter Five Structured Observation
16 pages
Science Thesis Topics For High School
100% (3)
Science Thesis Topics For High School
7 pages
Child Therapy Techniques PDF
100% (2)
Child Therapy Techniques PDF
49 pages
Chapter One Sample
No ratings yet
Chapter One Sample
5 pages
DRUG USE-WPS Office
No ratings yet
DRUG USE-WPS Office
2 pages
Group Term Life Insurance Form
No ratings yet
Group Term Life Insurance Form
4 pages
Understanding The Self Chapter 9 - 11
No ratings yet
Understanding The Self Chapter 9 - 11
7 pages
Module 3 A Sustaining Natural Resources and Environmental Quality 3
No ratings yet
Module 3 A Sustaining Natural Resources and Environmental Quality 3
65 pages
Enn1504 Ass2 21805431
No ratings yet
Enn1504 Ass2 21805431
4 pages
Cleaning Validation
No ratings yet
Cleaning Validation
40 pages
Case Study Hydroflouric Acid
No ratings yet
Case Study Hydroflouric Acid
16 pages
MODULE 6 Leadership and Management
No ratings yet
MODULE 6 Leadership and Management
4 pages
AbsorbaTack IFU PDF
No ratings yet
AbsorbaTack IFU PDF
22 pages
2024 Medical Research Conference
No ratings yet
2024 Medical Research Conference
18 pages
14 Iyun TN Sertif Sinaq
No ratings yet
14 Iyun TN Sertif Sinaq
40 pages
Please Search On The Filipino Cultural Characteristics and Health Care Beliefs and Practices in Health Education
No ratings yet
Please Search On The Filipino Cultural Characteristics and Health Care Beliefs and Practices in Health Education
16 pages
Lesson 5
No ratings yet
Lesson 5
8 pages
Hamers New Medicine
No ratings yet
Hamers New Medicine
4 pages
T NG H P Writing Khóa Ôn
No ratings yet
T NG H P Writing Khóa Ôn
31 pages
MSc Public Health Nursing SOP
No ratings yet
MSc Public Health Nursing SOP
2 pages
User Manual-1
No ratings yet
User Manual-1
10 pages
CSC Treatment Advances
No ratings yet
CSC Treatment Advances
15 pages
Gender Inequality
100% (6)
Gender Inequality
11 pages

Resp Emer in Children

Uploaded by

Resp Emer in Children

Uploaded by

C o m m o n Pe d i a t r i c

Asthma is a chronic inflammatory condition of the airways leading to episodic

The authors have nothing to disclose.

Emerg Med Clin N Am 30 (2012) 529–563

muscle (bronchospasm), the major cause of wheezing during an asthma exacerbation.

Status Asthmaticus and Imminent Respiratory Failure

and improve outcomes in children with status asthmaticus,70–75 and a Cochrane

Croup is a common cause of stridor in the young child. Croup is characterized by

Definition and Epidemiology

Clinical Presentation and Course

and hyperinflation. Tachypnea, increased respiratory effort, and wheezing become

Assessment and Management

of treatment. Nasal suctioning is an easy, useful adjunctive treatment that may

such as risk of hospitalization at 1 week were documented.164 Unexpectedly, the

1. Significant overlap in presentation may occur with other common respiratory

community-acquired pneumonia (CAP).178 Wheeze may occasionally occur in typical

Investigations and Workup

Knowledge of local epidemiologic data is important to recognize the possibility of

CBC and differential can sometimes be helpful in suggesting a bacterial cause of

Age Outpatient Treatment Inpatient Treatment

If ill, add gentamycin 7.5 mg/kg/d

If HSV likely, add acyclovir 500 mg/

If ill or MRSA suspected,

If atypical suspected: Macrolide IV

If S pneumoniae likely If S pneumoniae likely,

Definite admission Age <1 month

Data from Refs.175,181,189,194,199

Admission Criteria/Predictors of Poor Outcome

Common respiratory illnesses including asthma, croup, bronchiolitis, and pneumonia

1. American Lung Association, Epidemiology and Statistics Unit. Trends in asthma

40. Greenberg R, Kerby G, Roosevelt G. A comparison of oral dexamethasone with

95. Cherry J. Clinical practice. Croup. N Engl J Med 2008;358(4):384–91.

118. Taussig LM, Castro O, Beaudry PH, et al. Treatment of laryngotracheobronchitis

2008;4. Available at: http://www.mrw.interscience.wiley.com/cochrane/clsysrev/

174. Homier V, Bellevance C, Xhignesse M. Prevalence of pneumonia in children

You might also like