Transcript Asthma

 Asthma is a common chronic inflammatory disease of the airways
characterized by variable and recurring symptoms, reversible airflow
obstruction and bronchospasm.[2] Common symptoms include wheezing,
coughing, chest tightness, and shortness of breath.[3]
 Asthma is thought to be caused by a combination of genetic and
environmental factors.[4] Its diagnosis is usually based on the pattern of
symptoms, response to therapy over time and spirometry.[5] It is clinically
classified according to the frequency of symptoms, forced expiratory
volume in one second (FEV1), and peak expiratory flow rate.[6] Asthma may
also be classified as atopic (extrinsic) or non-atopic (intrinsic)[7] where
atopy refers to a predisposition toward developing type 1 hypersensitivity
reactions.[8]
 13][14] The occurrence of asthma has increased significantly since the 1970s.
In 2011, 235–300 million people globally were diagnosed with
asthma,[15][16] and it caused 250,000 deaths.

 Signs and symptoms
 Asthma is characterized by recurrent episodes of
wheezing, shortness of breath, chest tightness, and
coughing.[17] Sputum may be produced from the lung by
coughing but is often hard to bring up.[18] During
recovery from an attack, it may appear pus-like due to
high levels of white blood cells called eosinophils.[19]
Symptoms are usually worse at night and in the early
morning or in response to exercise or cold air.[20] Some
people with asthma rarely experience symptoms, usually
in response to triggers, whereas others may have marked
and persistent symptoms.[21]
 Associated conditions
 A number of other health conditions occur more
frequently in those with asthma, including gastroesophageal reflux disease (GERD), rhinosinusitis,
and obstructive sleep apnea.[22] Psychological
disorders are also more common,[23] with anxiety
disorders occurring in between 16–52% and mood
disorders in 14–41%.[24] However, it is not known if
asthma causes psychological problems or if
psychological problems lead to asthma.[25]
 Causes
 Asthma is caused by a combination of complex and
incompletely understood environmental and genetic
interactions.[4][26] These factors influence both its
severity and its responsiveness to treatment.[27] It is
believed that the recent increased rates of asthma are
due to changing epigenetics (heritable factors other
than those related to the DNA sequence) and a
changing living environment.[28]
Environmental
See also: Asthma-related microbes
Many environmental factors have been associated with asthma's development and exacerbation
including allergens, air pollution, and other environmental chemicals.[29] Smoking during
pregnancy and after delivery is associated with a greater risk of asthma-like symptoms.[30] Low
air quality from factors such as traffic pollution or high ozone levels,[31] has been associated with
both asthma development and increased asthma severity.[32] Exposure to indoor volatile
organic compounds may be a trigger for asthma; formaldehyde exposure, for example, has a
positive association.[33] Also, phthalates in certain types of PVC are associated with asthma in
children and adults.[34][35] There is an association between acetaminophen (paracetamol) use
and asthma.[36] The majority of the evidence does not; however, support a causal role.[37] A 2014
review found that the association disappeared when respiratory infections were taken into
account.[38] Use by a mother during pregnancy is also associated with an increased risk.[39]
 Asthma is associated with exposure to indoor allergens.[40] Common indoor allergens include:
dust mites, cockroaches, animal dander, and mold.[41][42] Efforts to decrease dust mites have
been found to be ineffective.[43] Certain viral respiratory infections, such as respiratory syncytial
virus and rhinovirus,[44] may increase the risk of developing asthma when acquired as young
children.[45] Certain other infections, however, may decrease the risk.[44]



 Family history is a risk factor for asthma, with many different genes being
implicated.[55] If one identical twin is affected, the probability of the other
having the disease is approximately 25%.[55] By the end of 2005, 25 genes
had been associated with asthma in six or more separate populations,
including GSTM1, IL10, CTLA-4, SPINK5, LTC4S, IL4R and ADAM33,
among others.[56] Many of these genes are related to the immune system or
modulating inflammation. Even among this list of genes supported by
highly replicated studies, results have not been consistent among all
populations tested.[56] In 2006 over 100 genes were associated with asthma
in one genetic association study alone;[56] more continue to be found.[57]
 Some genetic variants may only cause asthma when they are combined
with specific environmental exposures.[4] An example is a specific single
nucleotide polymorphism in the CD14 region and exposure to endotoxin (a
bacterial product). Endotoxin exposure can come from several
environmental sources including tobacco smoke, dogs, and farms. Risk for
asthma, then, is determined by both a person's genetics and the level of
endotoxin exposure.[54]
 Medical conditions
 A triad of atopic eczema, allergic rhinitis and asthma is called atopy.[58] The
strongest risk factor for developing asthma is a history of atopic disease;[45]
with asthma occurring at a much greater rate in those who have either
eczema or hay fever.[59] Asthma has been associated with Churg–Strauss
syndrome, an autoimmune disease and vasculitis. Individuals with certain
types of urticaria may also experience symptoms of asthma.[58]
 There is a correlation between obesity and the risk of asthma with both
having increased in recent years.[60][61] Several factors may be at play
including decreased respiratory function due to a buildup of fat and the fact
that adipose tissue leads to a pro-inflammatory state.[62]
 Beta blocker medications such as propranolol can trigger asthma in those
who are susceptible.[63] Cardioselective beta-blockers, however, appear safe
in those with mild or moderate disease.[64][65] Other medications that can
cause problems in same are ASA, NSAIDs, and angiotensin-converting
enzyme inhibitors.[66] COX-2 inhibitors do not appear to be a concern.[67]
 Exacerbation
 Some individuals will have stable asthma for weeks or months
and then suddenly develop an episode of acute asthma.
Different individuals react to various factors in different
ways.[68] Most individuals can develop severe exacerbation
from a number of triggering agents.[68]
 Home factors that can lead to exacerbation of asthma include
dust, animal dander (especially cat and dog hair), cockroach
allergens and mold.[68] Perfumes are a common cause of acute
attacks in women and children. Both viral and bacterial
infections of the upper respiratory tract can worsen the
disease.[68] Psychological stress may worsen symptoms—it is
thought that stress alters the immune system and thus
increases the airway inflammatory response to allergens and
irritants.[32]
 Pathophysiology.
 Obstruction of the lumen of a bronchiole by mucoid exudate, goblet
cell metaplasia, and epithelial basement membrane thickening in a
person with asthma.
 Asthma is the result of chronic inflammation of the airways which
subsequently results in increased contractability of the surrounding
smooth muscles. This among other factors leads to bouts of
narrowing of the airway and the classic symptoms of wheezing. The
narrowing is typically reversible with or without treatment.
Occasionally the airways themselves change.[17] Typical changes in
the airways include an increase in eosinophils and thickening of the
lamina reticularis. Chronically the airways' smooth muscle may
increase in size along with an increase in the numbers of mucous
glands. Other cell types involved include: T lymphocytes,
macrophages, and neutrophils. There may also be involvement of
other components of the immune system including: cytokines,
chemokines, histamine, and leukotrienes among others.
 Diagnosis
 While asthma is a well recognized condition, there is not one universal
agreed upon definition.[44] It is defined by the Global Initiative for Asthma
as "a chronic inflammatory disorder of the airways in which many cells and
cellular elements play a role. The chronic inflammation is associated with
airway hyper-responsiveness that leads to recurrent episodes of wheezing,
breathlessness, chest tightness and coughing particularly at night or in the
early morning. These episodes are usually associated with widespread but
variable airflow obstruction within the lung that is often reversible either
spontaneously or with treatment".[17]
 There is currently no precise test with the diagnosis typically based on the
pattern of symptoms and response to therapy over time.[5][44] A diagnosis of
asthma should be suspected if there is a history of: recurrent wheezing,
coughing or difficulty breathing and these symptoms occur or worsen due
to exercise, viral infections, allergens or air pollution.[70] Spirometry is then
used to confirm the diagnosis.[70] In children under the age of six the
diagnosis is more difficult as they are too young for spirometry
 Spirometry
 Spirometry is recommended to aid in diagnosis and
management.[72][73] It is the single best test for asthma. If
the FEV1 measured by this technique improves more
than 12% following administration of a bronchodilator
such as salbutamol, this is supportive of the diagnosis. It
however may be normal in those with a history of mild
asthma, not currently acting up.[44] As caffeine is a
bronchodilator in people with asthma, the use of caffeine
before a lung function test may interfere with the
results.[74] Single-breath diffusing capacity can help
differentiate asthma from COPD.[44] It is reasonable to
perform spirometry every one or two years to follow how
well a person's asthma is controlled.[75]
 Others
 The methacholine challenge involves the inhalation of increasing
concentrations of a substance that causes airway narrowing in those
predisposed. If negative it means that a person does not have
asthma; if positive, however, it is not specific for the disease.[44]
 Other supportive evidence includes: a ≥20% difference in peak
expiratory flow rate on at least three days in a week for at least two
weeks, a ≥20% improvement of peak flow following treatment with
either salbutamol, inhaled corticosteroids or prednisone, or a ≥20%
decrease in peak flow following exposure to a trigger.[76] Testing
peak expiratory flow is more variable than spirometry, however, and
thus not recommended for routine diagnosis. It may be useful for
daily self-monitoring in those with moderate to severe disease and
for checking the effectiveness of new medications. It may also be
helpful in guiding treatment in those with acute exacerbations.[77]
 Asthma is clinically classified according to the frequency of symptoms,
forced expiratory volume in one second (FEV1), and peak expiratory flow
rate.[6] Asthma may also be classified as atopic (extrinsic) or non-atopic
(intrinsic), based on whether symptoms are precipitated by allergens
(atopic) or not (non-atopic).[7] While asthma is classified based on severity,
at the moment there is no clear method for classifying different subgroups
of asthma beyond this system.[78] Finding ways to identify subgroups that
respond well to different types of treatments is a current critical goal of
asthma research.[78]
 Although asthma is a chronic obstructive condition, it is not considered as a
part of chronic obstructive pulmonary disease as this term refers
specifically to combinations of disease that are irreversible such as
bronchiectasis, chronic bronchitis, and emphysema.[79] Unlike these
diseases, the airway obstruction in asthma is usually reversible; however, if
left untreated, the chronic inflammation from asthma can lead the lungs to
become irreversibly obstructed due to airway remodeling.[80] In contrast to
emphysema, asthma affects the bronchi, not the alveoli.[81]
 Acute severe








(any one of)
Peak flow 33–50%
Respiratory rate ≥ 25 breaths per minute
Heart rate ≥ 110 beats per minute
Unable to complete sentences in one breath
Moderate
Worsening symptoms
Peak flow 50–80% best or predicted
No features of acute severe asthma





An acute asthma exacerbation is commonly referred to as an asthma attack. The classic
symptoms are shortness of breath, wheezing, and chest tightness.[44] While these are the
primary symptoms of asthma,[83] some people present primarily with coughing, and in severe
cases, air motion may be significantly impaired such that no wheezing is heard.[82]
Signs which occur during an asthma attack include the use of accessory muscles of respiration
(sternocleidomastoid and scalene muscles of the neck), there may be a paradoxical pulse (a
pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the
chest.[84] A blue color of the skin and nails may occur from lack of oxygen.[85]
In a mild exacerbation the peak expiratory flow rate (PEFR) is ≥200 L/min or ≥50% of the
predicted best.[86] Moderate is defined as between 80 and 200 L/min or 25% and 50% of the
predicted best while severe is defined as ≤ 80 L/min or ≤25% of the predicted best.[86]
Acute severe asthma, previously known as status asthmaticus, is an acute exacerbation of
asthma that does not respond to standard treatments of bronchodilators and corticosteroids.[87]
Half of cases are due to infections with others caused by allergen, air pollution, or insufficient or
inappropriate medication use.[87]
Brittle asthma is a kind of asthma distinguishable by recurrent, severe attacks.[82] Type 1 brittle
asthma is a disease with wide peak flow variability, despite intense medication. Type 2 brittle
asthma is background well-controlled asthma with sudden severe exacerbations.[82]
Exercise-induced
Main article: Exercise-induced bronchoconstriction
Exercise can trigger bronchoconstriction in both people with and without asthma.[88] It occurs
in most people with asthma and up to 20% of people without asthma.[88] In athletes is
diagnosed more commonly in elite athletes, with rates varying from 3% for bobsled racers to
50% for cycling and 60% for cross-country skiing.[88] While it may occur with any weather
conditions it is more common when it is dry and cold.[89] Inhaled beta2-agonists do not appear
to improve athletic performance among those without asthma[90] however oral doses may
improve endurance and strength.[91][92]
 Occupational
 Main article: Occupational asthma
 Asthma as a result of (or worsened by) workplace exposures, is a commonly reported
occupational disease.[93] Many cases however are not reported or recognized as such.[94][95] It is
estimated that 5–25% of asthma cases in adults are work–related. A few hundred different
agents have been implicated with the most common being: isocyanates, grain and wood dust,
colophony, soldering flux, latex, animals, and aldehydes. The employment associated with the
highest risk of problems include: those who spray paint, bakers and those who process food,
nurses, chemical workers, those who work with animals, welders, hairdressers and timber
workers.[93]



 Differential diagnosis
 Many other conditions can cause symptoms similar to those of asthma. In children,
other upper airway diseases such as allergic rhinitis and sinusitis should be
considered as well as other causes of airway obstruction including: foreign body
aspiration, tracheal stenosis or laryngotracheomalacia, vascular rings, enlarged
lymph nodes or neck masses. In adults, COPD, congestive heart failure, airway
masses, as well as drug-induced coughing due to ACE inhibitors should be
considered. In both populations vocal cord dysfunction may present similarly.[96]
 Chronic obstructive pulmonary disease can coexist with asthma and can occur as a
complication of chronic asthma. After the age of 65 most people with obstructive
airway disease will have asthma and COPD. In this setting, COPD can be
differentiated by increased airway neutrophils, abnormally increased wall thickness,
and increased smooth muscle in the bronchi. However, this level of investigation is
not performed due to COPD and asthma sharing similar principles of management:
corticosteroids, long acting beta agonists, and smoking cessation.[97] It closely
resembles asthma in symptoms, is correlated with more exposure to cigarette
smoke, an older age, less symptom reversibility after bronchodilator administration,
and decreased likelihood of family history of atopy.[98][99]
 Prevention
 The evidence for the effectiveness of measures to prevent the development
of asthma is weak.[100] Some show promise including: limiting smoke
exposure both in utero and after delivery, breastfeeding, and increased
exposure to daycare or large families but none are well supported enough
to be recommended for this indication.[100] Early pet exposure may be
useful.[101] Results from exposure to pets at other times are inconclusive[102]
and it is only recommended that pets be removed from the home if a
person has allergic symptoms to said pet.[103] Dietary restrictions during
pregnancy or when breast feeding have not been found to be effective and
thus are not recommended.[103] Reducing or eliminating compounds known
to sensitive people from the work place may be effective.[93] It is not clear if
annual influenza vaccinations effects the risk of exacerbations.[104]
Immunization; however, is recommended by the World Health
Organization.[105] Smoking bans are effective in decreasing exacerbations of
asthma.[106]
 Management
 While there is no cure for asthma, symptoms can typically be improved.[107] A
specific, customized plan for proactively monitoring and managing symptoms
should be created. This plan should include the reduction of exposure to allergens,
testing to assess the severity of symptoms, and the usage of medications. The
treatment plan should be written down and advise adjustments to treatment
according to changes in symptoms.[108]
 The most effective treatment for asthma is identifying triggers, such as cigarette
smoke, pets, or aspirin, and eliminating exposure to them. If trigger avoidance is
insufficient, the use of medication is recommended. Pharmaceutical drugs are
selected based on, among other things, the severity of illness and the frequency of
symptoms. Specific medications for asthma are broadly classified into fast-acting
and long-acting categories.[109][110]
 Bronchodilators are recommended for short-term relief of symptoms. In those with
occasional attacks, no other medication is needed. If mild persistent disease is
present (more than two attacks a week), low-dose inhaled corticosteroids or
alternatively, an oral leukotriene antagonist or a mast cell stabilizer is
recommended. For those who have daily attacks, a higher dose of inhaled
corticosteroids is used. In a moderate or severe exacerbation, oral corticosteroids
are added to these treatments.[9]
 Lifestyle modification
 Avoidance of triggers is a key component of improving control and
preventing attacks. The most common triggers include allergens, smoke
(tobacco and other), air pollution, non selective beta-blockers, and sulfitecontaining foods.[111][112] Cigarette smoking and second-hand smoke
(passive smoke) may reduce the effectiveness of medications such as
corticosteroids.[113] Laws that limit smoking decrease the number of people
hospitalized for asthma.[114] Dust mite control measures, including air
filtration, chemicals to kill mites, vacuuming, mattress covers and others
methods had no effect on asthma symptoms.[43] Overall, exercise is
beneficial in people with stable asthma.[115]
 Medications
 Medications used to treat asthma are divided into two general classes:
quick-relief medications used to treat acute symptoms; and long-term
control medications used to prevent further exacerbation.[109]
 Fast–acting
 Salbutamol metered dose inhaler commonly used to treat asthma attacks.
 Short-acting beta2-adrenoceptor agonists (SABA), such as salbutamol
(albuterol USAN) are the first line treatment for asthma symptoms.[9] They
are recommended before exercise in those with exercise induced
symptoms.[116]
 Anticholinergic medications, such as ipratropium bromide, provide
additional benefit when used in combination with SABA in those with
moderate or severe symptoms.[9] Anticholinergic bronchodilators can also
be used if a person cannot tolerate a SABA.[79] If a child requires admission
to hospital additional ipratropium does not appear to help over a SABA.[117]
 Older, less selective adrenergic agonists, such as inhaled epinephrine, have
similar efficacy to SABAs.[118] They are however not recommended due to
concerns regarding excessive cardiac stimulation.[119]
 Long–term control
 Fluticasone propionate metered dose inhaler commonly used for
long-term control.
 Corticosteroids are generally considered the most effective
treatment available for long-term control.[109] Inhaled forms such as
beclomethasone are usually used except in the case of severe
persistent disease, in which oral corticosteroids may be needed.[109]
It is usually recommended that inhaled formulations be used once
or twice daily, depending on the severity of symptoms.[120]
 Long-acting beta-adrenoceptor agonists (LABA) such as salmeterol
and formoterol can improve asthma control, at least in adults, when
given in combination with inhaled corticosteroids.[121] In children
this benefit is uncertain.[121][122] When used without steroids they
increase the risk of severe side-effects[123] and even with
corticosteroids they may slightly increase the risk.[124][125]
 Leukotriene receptor antagonists (such as montelukast and
zafirlukast) may be used in addition to inhaled corticosteroids,
typically also in conjunction with LABA.[14][109] Evidence is
insufficient to support use in acute exacerbations.[126][127] In children
they appear to be of little benefit when added to inhaled
steroids.[128] In those under five years of age, they were the preferred
add-on therapy after inhaled corticosteroids by the British Thoracic
Society in 2009.[129]
 Arachidonate 5-lipoxygenase (5-LOX) enzyme inhibitors, such as
zileuton and St John's wort,[130][134] slow down or stop the
production of asthma-related leukotrienes which promote
inflammation, microvascular permeability, bronchoconstriction and
mucus secretion.[14][130][134] 5-LOX inhibitors possess efficacy for
treating asthma both as a monotherapy and combination therapy
with leukotriene receptor antagonists.[14]
 Mast cell stabilizers (such as cromolyn sodium) are another nonpreferred alternative to corticosteroids.[109]









Delivery methods
Medications are typically provided as metered-dose inhalers (MDIs) in combination with an
asthma spacer or as a dry powder inhaler. The spacer is a plastic cylinder that mixes the
medication with air, making it easier to receive a full dose of the drug. A nebulizer may also be
used. Nebulizers and spacers are equally effective in those with mild to moderate symptoms.
However, insufficient evidence is available to determine whether a difference exists in those
with severe disease.[135]
Adverse effects
Long-term use of inhaled corticosteroids at conventional doses carries a minor risk of adverse
effects.[136] Risks include the development of cataracts and a mild regression in stature.[136][137]
Others
When asthma is unresponsive to usual medications, other options are available for both
emergency management and prevention of flareups. For emergency management other options
include:
Oxygen to alleviate hypoxia if saturations fall below 92%.[138]
Oral corticosteroid are recommended with five days of prednisone being the same 2 days of
dexamethasone.[139]
Magnesium sulfate intravenous treatment has been shown to provide a bronchodilating effect
when used in addition to other treatment in severe acute asthma attacks.[10][140]
 Prognosis
 The prognosis for asthma is generally good, especially for
children with mild disease.[156] Mortality has decreased
over the last few decades due to better recognition and
improvement in care.[157] Globally it causes moderate or
severe disability in 19.4 million people as of 2004
(16 million of which are in low and middle income
countries).[158] Of asthma diagnosed during childhood,
half of cases will no longer carry the diagnosis after a
decade.[55] Airway remodeling is observed, but it is
unknown whether these represent harmful or beneficial
changes.[159] Early treatment with corticosteroids seems
to prevent or ameliorates a decline in lung function.[160]
 Heliox, a mixture of helium and oxygen, may also be considered in severe




unresponsive cases.[10]
Intravenous salbutamol is not supported by available evidence and is thus used only
in extreme cases.[138]
Methylxanthines (such as theophylline) were once widely used, but do not add
significantly to the effects of inhaled beta-agonists.[138] Their use in acute
exacerbations is controversial.[141]
The dissociative anesthetic ketamine is theoretically useful if intubation and
mechanical ventilation is needed in people who are approaching respiratory arrest;
however, there is no evidence from clinical trials to support this.[142]
For those with severe persistent asthma not controlled by inhaled corticosteroids
and LABAs, bronchial thermoplasty may be an option.[143] It involves the delivery of
controlled thermal energy to the airway wall during a series of
bronchoscopies.[143][144] While it may increase exacerbation frequency in the first few
months it appears to decrease the subsequent rate. Effects beyond one year are
unknown.[145] Evidence suggests that sublingual immunotherapy in those with both
allergic rhinitis and asthma improve outcomes.[146]
 Approach to wheezing in children
 Dr Homm
 A wheeze is a musical and continuous sound that
originates from oscillations in narrowed airways.
Wheezing is heard mostly on expiration as a result
of critical airway obstruction. Wheezing is
polyphonic when there is widespread narrowing of
the airways causing various pitches or levels of
obstruction to airflow as seen in asthma.
Monophonic wheezing refers to a single-pitch
sound that is produced in the larger airways during
expiration as in distal tracheomalacia or
bronchomalacia. When obstruction occurs in the
extrathoracic airways during inspiration, the noise
is referred to as stridor.
 Acute bronchiolitis is predominantly a viral
disease. Respiratory syncytial virus (RSV) is
responsible for >50% of cases.Other agents include
parainfluenza ,adenovirus, Mycoplasma, and,
occasionally, other viruses.. There is no evidence of a
bacterial cause for bronchiolitis, although bacterial
pneumonia is sometimes confused clinically with
bronchiolitis and bronchiolitis is rarely followed by
bacterial superinfection
 Acute bronchiolitis is usually preceded by exposure to an
older contact with a minor respiratory syndrome within the
previous wk. The infant 1st develops a mild upper respiratory
tract infection with sneezing and clear rhinorrhea. This may
be accompanied by diminished appetite and fever of 38.5–
39°C (101–102°F), although the temperature may range from
subnormal to markedly elevated. Gradually, respiratory
distress ensues, with paroxysmal wheezy cough, dyspnea, and
irritability. The infant is often tachypneic, which may interfere
with feeding. The child does not usually have other systemic
complaints, such as diarrhea or vomiting. Apnea may be more
prominent than wheezing early in the course of the disease,
particularly with very young infants (<2 mo old) or former
premature infants.
 The physical examination is characterized most
prominently by wheezing. The degree of tachypnea does
not always correlate with the degree of hypoxemia or
hypercarbia, so the use of pulse oximetry and
noninvasive carbon dioxide determination is essential.
Work of breathing may be markedly increased, with
nasal flaring and retractions. Auscultation may reveal
fine crackles or overt wheezes, with prolongation of the
expiratory phase of breathing. Barely audible breath
sounds suggest very severe disease with nearly complete
bronchiolar obstruction. Hyperinflation of the lungs may
permit palpation of the liver and spleen.
 In acute bronchiolitis, chest radiography reveals
hyperinflated lungs with patchy atelectasis. The
white blood cell and differential counts are usually
normal. Viral testing (usually rapid
immunofluorescence, polymerase chain reaction, or
viral culture) is helpful if the diagnosis is uncertain
or for epidemiologic purposes. The diagnosis is
clinical, particularly in a previously healthy infant
presenting with a first-time wheezing episode during
a community outbreak.
 Infants with acute bronchiolitis who are experiencing respiratory
distress should be hospitalized; the mainstay of treatment is
supportive. If hypoxemic, the child should receive cool humidified
oxygen. Sedatives are to be avoided because they may depress
respiratory drive. The infant is sometimes more comfortable if
sitting with head and chest elevated at a 30-degree angle with neck
extended. The risk of aspiration of oral feedings may be high in
infants with bronchiolitis, owing to tachypnea and the increased
work of breathing. The infant may be fed through a nasogastric
tube. If there is any risk for further respiratory decompensation
potentially necessitating tracheal intubation, however, the infant
should not be fed orally but be maintained with parenteral fluids.
Frequent suctioning of nasal and oral secretions often provides
relief of distress or cyanosis. Oxygen is indicated in all infants with
hypoxia
 .Treatment. Bronchodilators produce modest short-term
improvement in clinical features, included both infants with 1sttime wheezing and those with recurrent wheezing, complicating
interpretation of the data. Nebulized epinephrine may be more
effective than β-agonists. the individual patient. Corticosteroids,
whether parenteral, oral, or inhaled, have been used for
bronchiolitis despite conflicting and often negative studies.
Corticosteroids are not recommended in previously healthy infants
with RSV. Ribavirin, an antiviral agent administered by aerosol, has
been used for infants with congenital heart disease or chronic lung
disease. There is no convincing evidence of a positive impact on
clinically important outcomes such as mortality and duration of
hospitalization. Antibiotics have no value unless there is secondary
bacterial pneumonia. Likewise, there is no support for RSV
immunoglobulin administration during
 PROGNOSIS
 Infants with acute bronchiolitis are at highest risk for further
respiratory compromise in the 1st 48–72 hr after onset of cough and
dyspnea; the child may be desperately ill with air hunger, apnea, and
respiratory acidosis. The case fatality rate is <1%, with death attributable to
apnea, uncompensated respiratory acidosis, or severe dehydration. After
this critical period, symptoms may persist. The median duration of
symptoms in ambulatory patients is ≈12 days. Infants with conditions such
as congenital heart disease, bronchopulmonary dysplasia, and
immunodeficiency often have more severe disease, with higher morbidity
and mortality. There is a higher incidence of wheezing and asthma in
children with a history of bronchiolitis unexplained by family history or
other atopic syndromes. It is unclear whether bronchiolitis incites an
immune response that manifests as asthma later or whether those infants
have an inherent predilection for asthma that is merely unmasked by their
episode of RSV. Approximately 60% of infants who wheeze will stop
wheezing.
 PREVENTION
 Reduction in the severity and incidence of acute
bronchiolitis due to RSV is possible through the
administration of pooled hyperimmune RSV intravenous
immunoglobulin (RSV-IVIG, RespiGam) and
palivizumab (Synagis), an intramuscular monoclonal
antibody to the RSV F protein, before and during RSV
season. Palivizumab is recommended for infants <2 yr of
age with chronic lung disease (bronchopulmonary
dysplasia) or prematurity. Meticulous handwashing is
the best measure to prevent nosocomial transmission
 Wheezing in infants and children is a common
problem presented to primary care offices.
Approximately 25 to 30 percent of infants will have
at least one episode of wheezing.1 By three years of
age, an episode of wheezing will have occurred in 40
percent of children, and by six years of age, almost
one half of children will have had at least one episode
of wheezing.1 Most infants and children with
recurrent wheezing have asthma, but other causes
should be considered in the differential diagnosis.
 . The most common causes of wheezing in children






include
asthma,
allergies
, infections,
gastroesophageal reflux disease,
and obstructive sleep apnea.
Less common causes include congenital abnormalities,
foreign body aspiration, and cystic fibrosis.
 Asthma is the most likely cause of recurrent wheezing in
children younger than five years.
 The most common causes of wheezing in young children
are asthma, allergies, gastroesophageal reflux disease,
infections, and obstructive sleep apnea.
 Response to bronchodilators may help differentiate
asthma from other causes of wheezing.
 Chest radiography should be performed in children with
recurrent wheezing or a single episode of unexplained
wheezing that does not respond to bronchodilators.





Causes of Wheezing in Children and Infants
Family history
Recent infectious illness in the family (e.g., viral upper
respiratory illness, pertussis, tuberculosis) suggests
probable causes of wheezing. A family history of asthma,
allergies, or eczema increases suspicion of asthma.
AGE AT ONSET
The age at onset helps to distinguish between congenital
and noncongenital causes of wheezing. In infants,
wheezing is more likely to be caused by a congenital
abnormality than in older children
 PATTERN
 The pattern of wheezing may suggest the etiology.
Episodic wheezing that is seasonal or is associated
with environmental exposures is likely to be caused
by asthma.4 Persistent wheezing from birth is likely
the result of a congenital anatomic anomaly, and
children with persistent respiratory illnesses with
wheezing should be evaluated for cystic fibrosis,
bronchopulmonary dysplasia, laryngomalacia,
agammaglobulinemia, and primary ciliary
dyskinesia.7
 SEASONALITY
 Some cases of wheezing are seasonal. Upper and lower respiratory tract
infections can cause wheezing. Respiratory syncytial virus (RSV) is a
significant cause of wheezing in young children. Most RSV infections in the
United States occur between November and May, with peak activity in
January or February.8 RSV is the most common cause of bronchiolitis in
children, with 80 percent of cases occurring in children younger than one
year.9 Other viruses known to cause wheezing in children include human
metapneumovirus, which typically affects infants from December through
April,10 and human bocavirus, which is a parvovirus found in young
children hospitalized for lower respiratory tract infections.11 Although the
prevalence of human bocavirus in the United States has not been well
studied, it is most common in the first, second, and fourth quarters of the
year in Canada.5 Wheezing associated with croup is more common in the
fall and winter. Wheezing associated with outdoor allergens is more
common in the spring and fall; indoor allergens to dust mites and house
pets can cause symptoms year-round. Wheezing from asthma can be
triggered by changes in weather.4
 Questions to Distinguish the Etiology of Wheezing in









Children
How old was the patient when the wheezing started?
Distinguishes congenital from noncongenital causes
Did the wheezing start suddenly?
Foreign body aspiration
Is there a pattern to the wheezing?
Episodic: asthma
Persistent: congenital or genetic cause
Is the wheezing associated with a cough?
GERD, sleep apnea, asthma, allergies
Is the wheezing associated with feeding?
GERD
Is the wheezing associated with multiple respiratory illnesses?
Cystic fibrosis, immunodeficiency
Is the wheezing associated with a specific season?
Allergies: fall and spring
Croup: fall to winter
RSV: fall to spring
Does the wheezing get better or worse when the patient
changes position?
 Tracheomalacia, anomalies of the great vessels
 Is there a family history of wheezing?
 Infections, allergic triad









 WHEEZING AFTER FEEDING
 Although tracheoesophageal fistulas and laryngeal
clefts are rare causes of vomiting and wheezing after
feeding, these symptoms are usually caused by
GERD.7,12 Infants with GERD typically have poor
weight gain and may have been offered numerous
formulas for “milk intolerance.” The long-assumed
association between GERD and airway
hyperresponsiveness has recently been called into
question by a small randomized controlled trial that
 SUDDEN ONSET
 Foreign body aspiration can occur anytime, but it is most
common between eight months and four years of age.14
High airway obstruction causes coughing, gagging,
choking, and wheezing. However, symptoms are not as
dramatic and are often difficult to diagnose when the
object is aspirated into the subglottic area.
Laryngotracheal foreign bodies are usually discovered
within 24 hours, and 90 percent of children with
laryngotracheal foreign bodies are diagnosed within one
week.14 Children may have recurrent symptoms or
nonresolution of pneumonia as a result of obstructive
atelectasis
 COUGH
 A cough after eating in a wheezing child suggests
GERD.12 A dry, unproductive cough that worsens at
night can be a result of GERD, allergies, or asthma.
Obstructive sleep apnea should be considered in
children whose coughing or wheezing awakens them
at night and is associated with snoring. Sleep apnea
in infants is usually a result of craniofacial
anomalies, but the main cause in older children is
adenotonsillar hypertrophy.6
 MULTIPLE RESPIRATORY ILLNESSES
 Multiple respiratory illnesses without obvious cause in
the first year of life suggest cystic fibrosis,
immunodeficiency syndromes, or primary ciliary
dyskinesia. Steatorrhea and failure to thrive further
suggest cystic fibrosis. With the widespread use of
neonatal screening, cystic fibrosis is often discovered at
birth. Continuous rhinitis from birth is consistent with
primary ciliary dyskinesia.7 Another uncommon cause of
wheezing is congenital laryngomalacia, which can
present as multiple respiratory infections and can
present later in childhood.15
 POSITIONAL CHANGES
 Tracheomalacia and anomalies of the great vessels
should be considered when wheezing occurs with
positional changes in infants.
















Differential Diagnosis of Wheezing According to Characteristic Signs and Symptoms
Signs and symptoms
Presumptive diagnosis
Further evaluation
Associated with feeding, cough, and vomiting
Gastroesophageal reflux disease
24-hour pH monitoring Barium swallow
Associated with positional changes
Tracheomalacia; anomalies of the great vessels
Angiography
Bronchoscopy
CT Chest radiographyor MRI
Echocardiography
Auscultatory crackles, fever
Pneumonia
Chest radiography
 Episodic pattern, cough; patient responds to




bronchodilators
Asthma
Allergy testing
Pulmonary function testing
Trial of albuterol (Proventil)
 Exacerbated by neck flexion; relieved by neck






hyperextension
Vascular ring
Angiography
Barium swallow
Bronchoscopy
Chest radiography
CT or MRI
 Heart murmurs or cardiomegaly, cyanosis without









respiratory distress
Cardiac disease
Angiography
Chest radiography
Echocardiography
History of multiple respiratory illnesses; failure to thrive
Cystic fibrosis or immunodeficiency
Ciliary function testing
Immunoglobulin levels
Sweat chloride testing
 Seasonal pattern, nasal flaring, intercostal








retractions
Bronchiolitis (RSV), croup, allergies
Chest radiography
Stridor with drooling
Epiglottitis
Neck radiography
Sudden onset of wheezing and choking
Foreign body aspiration
Bronchoscopy
stridor
DR.HOMM
FICMS
Definition
 Stridor is an abnormal, high-pitched sound produced by
turbulent airflow through a partially obstructed airway at
the level of the supraglottis, glottis, subglottis, and/or
trachea.The tonal characteristics of the sound are
extremely variable (ie, harsh, musical, or breathy);.
Stridor is a symptom, not a diagnosis or disease, and the
underlying cause must be determined. Inspiratory
stridor suggests a laryngeal obstruction. Biphasic stridor
suggests a subglottic or glottic anomaly. In addition to a
complete history and physical, as well as other possible
additional studies, most cases require flexible and/or
rigid endoscopy to adequately evaluate the etiology of
stridor
 References
 Children who appear chronically ill should be tested for metabolic
disorders, immunodeficiency, and cystic fibrosis. In infants, wheezing that
is audible without a stethoscope and that is not associated with respiratory
distress is usually a sign of a congenital airway lesion.16
 Children can be examined in the parent's arms, if necessary. Retractions,
nasal flaring, and grunting can signal respiratory distress. Auscultation can
identify the presence and location of wheezing, stridor, and crackles;
however, these physical findings may be absent in children who are unable
to take a deep breath. Skin; cardiac; and ear, nose, and throat examination
may also be helpful. Signs and symptoms such as allergic shiners, atopic
dermatitis, lymphadenopathy, a heart murmur, and rhinorrhea can suggest
a diagnosis. Clubbing and nail color changes suggest chronic respiratory
disease other than asthma. Table 3 lists history and physical examination
findings that suggest specific causes of wheezing.3,4,16,17









History
The most common presenting symptom is loud, raspy, noisy breathing. The caretaker may interpret
this symptom as wheezing or even as a severe upper respiratory tract infection. Depending on the
underlying etiology, the presentation may be acute or chronic.
A thorough history may provide helpful clues to the underlying etiology of stridor.
Place particular emphasis on the age of onset, duration, severity, and progression of the stridor;
precipitating events (eg, crying, feeding); positioning (eg, prone, supine, sitting); quality and nature
of crying; presence of aphonia; and other associated symptoms (eg, paroxysms of cough, aspiration,
difficulty feeding, drooling, sleep disordered breathing).[6]
Perinatal history is especially important and should include direct questioning regarding maternal
condylomata, type of delivery (including shoulder dystocia), endotracheal intubation use and
duration, and presence of congenital anomalies.
Past surgical history, particularly neck or cardiothoracic surgeries, puts the recurrent laryngeal
nerve at risk of injury
Obtain a detailed developmental history.
In addition, elicit history of color change, cyanosis, respiratory effort, and apnea to determine the
severity of stridor.
A feeding and growth history should be evaluated because significant airway obstruction can lead to
caloric waste, resulting in lack of weight gain and growth. Additionally, regurgitation and spitting
up could be a sign of gastroesophageal reflux (GER) that can cause laryngeal and tracheal mucosal
irritation that could lead to edema and stridor.
 Physical
 On initial presentation, especially in patients with acute onset of symptoms,










immediately assess the child for severity of stridor and respiratory compromise. Gi
special attention to the heart and respiratory rates, cyanosis, use of accessory musc
of respiration, nasal flaring, level of consciousness, and responsiveness.
If distress is moderate to severe, further physical examination should be deferred u
the patient reaches a facility equipped for emergent management of the pediatric
airway.
Physical examination of a patient with suspected acute epiglottitis is contraindicate
The patient may prefer certain positions that alleviate the stridor.
Note the presence of infection in the oral cavity; crepitations or masses in the soft
tissues of the face, neck, or chest; and deviation of the trachea.
Use care when examining (especially palpating) the oral cavity or pharynx because
sudden dislodgement of a foreign body or rupture of an abscess can cause further
airway compromise.
Drooling from the mouth suggests poor handling of secretions.
Observe the character of the cough, cry, and voice.
The presence of fever and toxicity generally implies serious bacterial infections.
Careful auscultation of the nose, oropharynx, neck, and chest helps to discern the
location of the stridor.
In infants, give special attention to craniofacial morphology, patency of the nares, a
cutaneous hemangiomas. Growth parameters are very helpful, especially in evaluat
of chronic stridor


Causes
Acute stridor

Laryngotracheobronchitis, commonly known as croup, is the most common cause of acute stridor in children
aged 6 months to 2 years. The patient has a barking cough that is worse at night and may have low-grade fever.

Aspiration of foreign body is common in children aged 1-2 years. Usually, foreign bodies are food such as nuts, hot dogs,
popcorn, and hard candy that is inhaled. A history of coughing and choking that precedes development of respiratory symptoms
may be present.
 Bacterial tracheitis is relatively uncommon and mainly affects children younger than 3 years. It is a secondary infection
(most commonly due to Staphylococcus aureus) following a viral process (commonly croup or influenza).
 Retropharyngeal abscess
is a complication of bacterial pharyngitis observed in children younger than 6 years. The
patient presents with abrupt onset of high fevers, difficulty swallowing, refusal to feed, sore throat, hyperextension of the neck, and
respiratory distress.
 Peritonsillar abscess is an infection in the potential space between the superior constrictor muscles and the
tonsil. It is common in adolescents and preadolescents. The patient develops severe throat pain, trismus, and trouble swallowing
or speaking.
 Spasmodic croup, also termed acute spasmodic laryngitis, occurs most commonly in children aged 1-3 years.
Presentation may be identical to croup.
 Allergic reaction (ie, anaphylaxis) occurs within 30 minutes of an adverse exposure. Hoarseness and inspiratory
stridor may be accompanied by symptoms (eg, dysphagia, nasal congestion, itching eyes, sneezing, wheezing) that indicate the
involvement of other organs.
 Epiglottitis is a medical emergency occurring most commonly in children aged 2-7 years. Clinically, the patient
experiences an abrupt onset of high-grade fever, sore throat, dysphagia, and drooling.

Chronic stridor
 Laryngomalacia is the most common cause of inspiratory stridor in the neonatal period and early infancy and



accounts for up to 75% of all cases of stridor.Stridor may be exacerbated by crying or feeding. Placing the patient in a prone
position with the head up improves the stridor; supine position worsens the stridor.
Laryngomalacia is usually benign and self-limiting and improves as the child reaches age 1 year. If significant obstruction or lack of
weight gain is present, surgical correction or supraglottoplasty may be considered if there are observed tight mucosal bands
holding the epiglottis close to the true vocal cords or redundant mucosa overlying the arytenoids. ]
It should be kept in mind that the presentation of laryngomalacia in older children (late-onset laryngomalacia) can differ from that
of congenital laryngomalacia.Possible manifestations of late-onset laryngomalacia include obstructive sleep apnea syndrome,
exercise-induced stridor, and even dysphagia. Supraglottoplasty can be an effective treatment option.
Patients with subglottic stenosis can present with inspiratory or biphasic stridor. Symptoms can be evident at any time
during the first few years of life. a. Acquired stenosis is most commonly caused by prolonged intubation
 Vocal cord dysfunction is likely the second most common cause of stridor in infants. Unilateral vocal cord paralysis
can be congenital or secondary to birth or surgical trauma, such as cardiothoracic surgery. Patients with a unilateral vocal cord
paralysis present with a weak cry and biphasic stridor that is louder when awake and improves when lying with the affected side
down. Bilateral vocal cord paralysis is a more serious entity. Patients usually present with aphonia and a high-pitched biphasic
stridor that may progress to severe respiratory distress. It is usually associated with CNS abnormalities, such as Arnold-Chiari
malformation or increased intracranial pressure. Vocal cord paralysis in infants usually resolves within 24 months.
 Laryngeal dyskinesia, exercise-induced laryngomalacia, and paradoxical vocal cord motion are other
neuromuscular disorders that may be considered
.
 Laryngeal webs are caused by an incomplete recanalization of the laryngeal lumen during embryogenesis. Most (75%)
are in the glottic area. Infants with laryngeal webs have a weak cry and biphasic stridor. Intervention is recommended in the
setting of significant obstruction and includes cold knife or CO2 laser ablation.
 Laryngeal cysts are a less frequent cause of stridor. They are usually found in the supraglottic region in the epiglottic
folds. Patients may present with stridor, hoarse voice, or aphonia. Cysts may cause obstruction of the airway lumen if they are very
large.
 Laryngeal hemangiomas (glottic or subglottic) are rare, and half of them are accompanied by cutaneous
hemangiomas in the head and neck. Patients usually present with inspiratory or biphasic stridor that may worsen as the
hemangioma enlarges. Typically, hemangiomas present in the first 3-6 months of life during the proliferative phase and regress by
age 12-18 months. Medical or surgical intervention is based on the severity of symptoms. Treatment options consist of oral
steroids, intralesion steroids, laser therapy with CO2 or potassium-titanyl-phosphate (KTP) lasers, or surgical resection. Oral
propranolol has been proven to be an effective medical treatment in the appropriate population (contraindicated in children with
severe asthma, diabetes, or heart disease).
 Laryngeal papillomas occur secondary to vertical transmission of the human papilloma virus from maternal
condylomata or infected vaginal cells to the pharynx or larynx of the infant during the birth process. These are primarily treated
with surgical excision, with questionable use of cidofovir and interferon in refractory cases.[A high rate of recurrence of disease is
noted, with a need for multiple surgical debridements and a small risk of malignancy (5% malignant degeneration).
 Tracheomalacia is the most common cause of expiratory stridor. It is caused by a defect on the cartilage resulting in
the loss of rigidity necessary to maintain the tracheal lumen patent or by an extrinsic compression of the trachea.
 Tracheal stenosis can be congenital or secondary to extrinsic compression. Congenital stenosis is usually related to
complete tracheal rings, is characterized by a persistent stridor, and requires surgery based on severity of symptoms. The most
common extrinsic causes of stenosis include vascular rings, slings, and a double aortic arch that encircles the trachea and
esophagus. Pulmonary artery slings are also associated with complete tracheal rings. External compression can also result in
tracheomalacia. Patients usually present during the first year of life with noisy breathing, intercostal retractions, and a prolonged
expiratory phase.











Differential Diagnoses
Airway Foreign Body
Bacterial Tracheitis
Diphtheria
Epiglottitis
Inhalation Injury
Laryngeal Fractures
Laryngomalacia
Measles
Mononucleosis and Epstein-Barr Virus Infection
Peritonsillar Abscess
 Differential Diagnoses
 Congenital Arterial and Venous Anomalies: Surgical





Perspective
Congenital Stridor
Gastroesophageal Reflux
Laryngomalacia
Subglottic Stenosis
Tracheomalacia














Laboratory Studies
On initial evaluation, pulse oximetry may be useful to determine the extent and severity of the
stridor and respiratory compromise.
For moderate-to-severe cases, arterial blood gas may be needed.
Other laboratory evaluations may be performed as dictated by the clinical situation.
Generally, no investigations are required for mild stridor.
Imaging Studies
Anteroposterior (AP) and lateral radiographs of the neck and chest are useful to evaluate the
airway and lungs.
Barium esophagram may be performed if vascular compression, tracheoesophageal fistula,
GER, or neurological dysfunction is suspected.
Contrast-enhanced CT scanning can demonstrate mediastinal masses or aberrant vessels.
An MRI may be helpful in delineating lesions of the upper airway and vascular anomalies.
If GER is suspected, a pH probe or barium swallow may be performed to support the diagnosis.
Other Tests
Pulmonary function testing may be useful to differentiate restrictive and obstructive lung
processes and to define whether the obstruction is in the upper or lower airway.
Polysomnography may be required under certain circumstances, especially if history suggests
obstructive sleep apnea.
 Procedures
 The key to defining stridor of all phases is to look at the airway.
Direct laryngoscopy and bronchoscopy is the criterion standard for
making a diagnosis in infants and children with stridor.
 In children with stable oxygen saturations and in whom findings on
a lateral neck radiograph or the clinical picture does not indicate
acute epiglottitis, the initial procedure to evaluate stridor should be
a flexible laryngoscopy performed by an otolaryngologist in the
clinic with topical vasoconstrictor and/or topical anesthetic as
needed. The status of the larynx can be addressed, looking for
abnormalities such as laryngomalacia, true vocal cord paresis or
paralysis, laryngeal tumors or cysts, or signs and symptoms of GER.
Often, a good evaluation is possible, or, occasionally, only a glimpse
of the subglottis is observed, which may help direct further
evaluation, such as a formal direct laryngoscopy and bronchoscopy
in the operating room.
 Medical Care
 The treatment of stridor must be tailored according to the underlying or
predisposing condition. Emergent management consists of ensuring that the airway
is adequate. If not, appropriate resuscitative measures must be initiated. Some
conditions (eg, epiglottitis, bacterial tracheitis) may require antibiotics, while
steroids may be useful in other situations.
Surgical Care
 Certain conditions, such as severe laryngomalacia, laryngeal stenosis, critical
tracheal stenosis, laryngeal and tracheal tumors and lesions (eg, laryngeal
papillomas, hemangiomas, others), and foreign body aspiration, require surgical
correction. Occasionally, tracheotomy is used to protect the airway to bypass
laryngeal abnormalities and stent or bypass tracheal abnormalities. Other
conditions, such as retropharyngeal and peritonsillar abscess, may have to be dealt
with on an emergent basis. Please see relevant articles for specific management
 Diet
 Patients with moderate to severe stridor should be given nothing by mouth (NPO) in
preparation for possible intubation, laryngoscopy, bronchoscopy, and tracheotomy
CROUP
Background
 Croup is a common, primarily pediatric viral respiratory tract
illness. As its alternative names, laryngotracheitis and
laryngotracheobronchitis, indicate, croup generally affects the
larynx and trachea, although this illness may also extend to the
bronchi. It is the most common etiology for hoarseness, cough, and
onset of acute stridor in febrile children. Symptoms of coryza may
be absent, mild, or marked. The vast majority of children with croup
recover without consequences or sequelae; however, it can be lifethreatening in young infants.
 Croup manifests as hoarseness, a seal-like barking cough,
inspiratory stridor, and a variable degree of respiratory distress.
However, morbidity is secondary to narrowing of the larynx and
trachea below the level of the glottis (subglottic region)

 croup
 History
 Croup usually begins with nonspecific respiratory symptoms (ie, rhinorrhea, sore
throat, cough). Fever is generally low grade (38-39°C) but can exceed 40°C. Within
1-2 days, the characteristic signs of hoarseness, barking cough, and inspiratory
stridor develop, often suddenly, along with a variable degree of respiratory distress.
Symptoms are perceived as worsening at night, with most ED visits occurring
between 10 pm and 4 am. Symptoms typically resolve within 3-7 days but can last as
long as 2 weeks.
 Spasmodic croup (recurrent croup) typically presents at night with the sudden onset
of "croupy" cough and stridor. The child may have had mild upper respiratory
complaints prior to this, but more often has behaved and appeared completely well
prior to the onset of symptoms. Allergic factors may cause recurrent croup due to
respiratory epithelial changes from the viral infection.
 Another diagnostic consideration is gastroesophageal reflux (GER). Studies of
children presenting with recurrent croup have reported relief of their respiratory
symptoms when treated for reflux.[13] .

 Etiology
 Viruses causing acute infectious croup are spread
through either direct inhalation from a cough and/or
sneeze or by contamination of hands from contact with
fomites, with subsequent touching the mucosa of the
eyes, nose, and/or mouth. The most common viral
etiologies are parainfluenza viruses. The type of
parainfluenza (1, 2, and 3) causing outbreaks varies each
year.
 The primary ports of entry are the nose and
nasopharynx. The infection spreads and eventually
involves the larynx and trachea.
 Spasmodic croup (laryngismus stridulus) is a
noninfectious variant of the disorder, with a clinical
presentation similar to that of the acute disease but
with less coryza. This type of croup always occurs at
night and has the hallmark of reoccurring in
children; hence it has also been called “recurrent
croup.” In spasmodic croup, subglottic edema occurs
without the inflammation typical in viral disease.
Although viral illnesses may trigger this variant, the
reaction may be of allergic etiology rather than a
direct result of an infectious process
Child with croup. Note the steeple or pencil sign of the proximal trachea evident
on this anteroposterior film
 Approach Considerations
 Urgent care or emergency department treatment of croup depends on the degree of
respiratory distress. In mild croup, a child may present with only a croupy cough
and may require nothing more than parental reassurance, given alertness, baseline
minimal respiratory distress, proper oxygenation, and stable fluid status. The
caregivers may only need education regarding the course of the disease and
supportive homecare guidelines.
 However, any infant/child who presents with significant respiratory
distress/complaints with stridor at rest must have a thorough clinical evaluation to
ensure the patency of the airway and maintenance of effective oxygenation and
ventilation. Keep young children as comfortable as possible, allowing him or her to
remain in a parent's arms and avoiding unnecessary painful interventions that may
cause agitation, respiratory distress, and lead to increased oxygen requirements.
Persistent crying increases oxygen demands, and respiratory muscle fatigue can
worsen the obstruction.
 Concurrently, careful monitoring of the heart rate (for tachycardia), respiratory rate
(for tachypnea), respiratory mechanics (for sternal wall retractions), and pulse
oximetry (for hypoxia) are important. Assessment of the patient’s hydration status,
given the risk of increased insensible losses from fever and tachypnea, along with a
history of decreased oral intake, is also imperative.
 The current cornerstones of treatment in the
urgent care clinics or emergency departments
are corticosteroids and nebulized epinephrine;
steroids have proven beneficial in severe,
moderate, and even mild croup.[22] In the
straightforward cases of croup, antibiotics are
not prescribed, as the primary cause is viral.
Lack of improvement or worsening of symptoms
can be due to a secondary bacterial process,
which would require the use of antimicrobials
for treatment. Typically, these patients initially
would have had moderate-to-severe croup
scores, requiring inpatient care and observation.
 Infants and children with severe respiratory distress or
compromise may require 100% oxygenation with
ventilation support, initially with a bag-valve-mask
device. If the airway and breathing require further
stabilization due to increasing respiratory fatigue and
hence, worsening hypercarbia, (as evident by ABG) the
patient should be intubated with an endotracheal tube.
Intubation should be accomplished with an endotracheal
tube that is 0.5-1 mm smaller than predicted. Once
airway stabilization is achieved, these patients are
transferred for their ongoing care to a pediatric intensive
care unit.
Corticosteroids
Corticosteroids are beneficial due to their anti-inflammatory action, whereby laryngeal mucosal
edema is decreased. They also decrease the need for salvage nebulized epinephrine.
Corticosteroids may be warranted even in those children who present with mild symptoms.
Treatment of croup with corticosteroids has not shown significant adverse effects; however
despite the low risk, their use should be carefully evaluated for children with diabetes, an
underlying immunocompromised state, or those recently exposed to or diagnosed with varicella
or tuberculosis, due to the potential risk of exacerbating the systemic disease process.
 A single dose of dexamethasone has been shown to be effective in reducing the overall severity
of croup, if administered within the first 4-24 hours after the onset of illness. The long half-life
of dexamethasone (36-54 h) often allows for a single injection or dose to cover the usual
symptom duration. Studies have shown that dexamethasone dosed at 0.15 mg/kg is as effective
as 0.3 mg/kg or 0.6 mg/kg (with a maximum daily dose of 10 mg) in relieving the symptoms of
mild-to-moderate croup. Despite this knowledge, clinicians still tend to favor the dose of 0.6
mg/kg for initial treatment of croup. This dosage, in fact, is more effective for patients
diagnosed with severe croup and remains the optimal amount for safety, benefit and costeffectiveness.[33, 34]
 Dexamethasone has shown the same efficacy if administered intravenously, intramuscularly, or
orally.[35] The route of administration is patient-dependent as based on the patient’s age, ability
to tolerate orals, an severity of presenting illness. The use of inhaled corticosteroids
(budesonide) with systemic treatment does not provide additional benefit.[36]


 Cool mist administration
 Throughout the 19th and most of the 20th century, cool mist administration was the
mainstay of treatment. Hospitals had "croup rooms" filled with cool mist.
Theoretically, mist moistens airway secretions, decreases their viscosity, and
soothes the inflamed mucosa. Animal data show that microaerosol inhalation
activates mechanoreceptors that produce a reflex slowing of respiratory flow rate
and leads to improved airflow.
 However, despite its continued widespread use, little evidence supports the clinical
efficacy of cool mist or humidification therapy. Randomized studies of children with
moderate-to-severe croup revealed no difference in outcome between those who
received cool mist and those who did not.[23] Mist tents, used in the hospital setting,
can disperse fungus and molds if not properly cleaned.
 More importantly, the tents separate the child from the parent by creating a “plastic
barrier," causing anxiety and agitation, potentially worsening the child’s symptoms
and hindering ongoing clinical assessment.[24, 25, 26] In the home, vaporizers (heated
humidification) producing hot steam to moisten the air should not be used because
of the risk of scalding or burns.[27]
 Epinephrine
 Nebulized racemic epinephrine is a 1:1 mixture of dextro (D) isomers and levo (L)
isomers of epinephrine with the L form (L-epinephrine) as the active component. Its
use is typically reserved for patients in the hospital setting with moderate-to-severe
respiratory distress. Epinephrine works by adrenergic stimulation, which causes
constriction of the precapillary arterioles, thereby decreasing capillary hydrostatic
pressure. This leads to fluid resorption from the interstitium and improvement in
the laryngeal mucosal edema.[22] Epinephrine’s beta2-adrenergic activity leads to
bronchial smooth muscle relaxation and bronchodilation. Its effectiveness is
immediate with evidence of therapeutic benefit within the first 30 minutes and then,
lasts from 90-120 minutes (1.5-2 h).
 Patients who receive nebulized racemic epinephrine in the emergency department
should be observed for at least 3 hours post last treatment because of concerns for a
return of bronchospasm, worsening respiratory distress, and/or persistent
tachycardia. Patients can be discharged home only if they demonstrate healthy
color, good air entry, baseline consciousness, and no stridor at rest and have
received a dose of corticosteroids
