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 symptomsAsthma 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 conditionsA number of other health conditions occur

more frequently in those with asthma, including gastro-esophageal 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]

CausesAsthma 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]

ExacerbationSome 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

SpirometrySpirometry 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 minuteHeart rate ≥ 110 beats per minuteUnable to complete sentences in one breathModerateWorsening symptomsPeak flow 50–80% best or predictedNo 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 sulfite-containing 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 non-preferred 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]

PrognosisThe 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 1st-time 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 InfantsFamily historyRecent 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 ONSETThe 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

PATTERNThe 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 causesDid the wheezing start suddenly?Foreign body aspirationIs there a pattern to the wheezing?Episodic: asthmaPersistent: congenital or genetic causeIs the wheezing associated with a cough?GERD, sleep apnea, asthma, allergies

Is the wheezing associated with feeding?GERDIs the wheezing associated with multiple respiratory illnesses?Cystic fibrosis, immunodeficiencyIs the wheezing associated with a specific season?Allergies: fall and springCroup: fall to winterRSV: fall to springDoes the wheezing get better or worse when the patient

changes position?Tracheomalacia, anomalies of the great vesselsIs there a family history of wheezing?Infections, allergic triad

WHEEZING AFTER FEEDINGAlthough 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 ONSETForeign 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

COUGHA 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 ILLNESSESMultiple 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 CHANGESTracheomalacia 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

AsthmaAllergy testingPulmonary function testingTrial of albuterol (Proventil)

Exacerbated by neck flexion; relieved by neck hyperextension

Vascular ringAngiographyBarium swallowBronchoscopyChest radiographyCT or MRI

Heart murmurs or cardiomegaly, cyanosis without respiratory distress

Cardiac diseaseAngiographyChest radiographyEchocardiographyHistory of multiple respiratory illnesses; failure to

thriveCystic fibrosis or immunodeficiencyCiliary function testingImmunoglobulin levelsSweat chloride testing

Seasonal pattern, nasal flaring, intercostal retractions

Bronchiolitis (RSV), croup, allergiesChest radiographyStridor with droolingEpiglottitisNeck radiographySudden onset of wheezing and chokingForeign body aspirationBronchoscopy

DR.HOMMFICMS

stridor

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. Give special attention to the heart and respiratory rates, cyanosis, use of accessory muscles of respiration, nasal flaring, level of consciousness, and responsiveness.

If distress is moderate to severe, further physical examination should be deferred until the patient reaches a facility equipped for emergent management of the pediatric airway.

Physical examination of a patient with suspected acute epiglottitis is contraindicated.

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,

and cutaneous hemangiomas. Growth parameters are very helpful, especially in evaluation 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 DiagnosesAirway Foreign BodyBacterial TracheitisDiphtheriaEpiglottitisInhalation InjuryLaryngeal FracturesLaryngomalaciaMeaslesMononucleosis and Epstein-Barr Virus InfectionPeritonsillar Abscess

Differential DiagnosesCongenital Arterial and Venous Anomalies: S

urgical PerspectiveCongenital StridorGastroesophageal RefluxLaryngomalaciaSubglottic StenosisTracheomalacia

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

CROUPBackground 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 life-threatening 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] .

 

EtiologyViruses 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 cost-effectiveness.[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