Pediatric Bronchitis

Updated: Jun 22, 2023
Author: Patrick L Carolan, MD; Chief Editor: Girish D Sharma, MD, FCCP, FAAP 


Practice Essentials

Acute bronchitis is a clinical syndrome produced by inflammation of the trachea, bronchi, and bronchioles. In children, acute bronchitis usually occurs in association with viral lower respiratory tract infection. Acute bronchitis is rarely a primary bacterial infection in otherwise healthy children. (See Pathophysiology, as well as Etiology.)

Examples of normal airway color and architecture and an airway in a patient with chronic bronchitis are shown below.

Normal airway color and architecture (in a child w Normal airway color and architecture (in a child with mild tracheomalacia).
Airway of a child with chronic bronchitis shows er Airway of a child with chronic bronchitis shows erythema, loss of normal architecture, and swelling.

Signs and symptoms

Symptoms of acute bronchitis usually include productive cough and sometimes retrosternal pain during deep breathing or coughing. Generally, the clinical course of acute bronchitis is self-limited, with complete healing and full return to function typically seen within 10-14 days following symptom onset. (See Clinical Presentation.)

Chronic bronchitis is due to recurrent inflammation that may be associated with active infection resulting in degenerative changes within the bronchial tubes. Patients with chronic bronchitis have more mucus than normal because of either increased production or decreased clearance. Coughing is the mechanism by which excess secretions are cleared.

Chronic bronchitis is often associated with asthma, cystic fibrosis, dyskinetic cilia syndrome, foreign body aspiration, or exposure to an airway irritant. Recurrent tracheobronchitis may occur with tracheostomies or immunodeficiency states.

Defining chronic bronchitis and its prevalence in childhood has been complicated by the significant clinical overlap with asthma and reactive airway disease states. In adults, chronic bronchitis is defined as daily production of sputum for at least 3 months in 2 consecutive years. Some have applied this definition to childhood chronic bronchitis. Others limit the definition to a productive cough that lasts more than 3-4 weeks despite medical therapy.

Chronic bronchitis has also been defined as a complex of symptoms that includes cough that lasts more than 1 month or recurrent productive cough that may be associated with wheezing or crackles on auscultation. Elements of these descriptors are present in the working definitions of asthma, as well.[1]


Treatment of chronic bronchitis in pediatric patients includes rest, use of antipyretics, adequate hydration, and avoidance of smoke. (See Treatment.)

Analgesics and antipyretics target the symptoms of pediatric bronchitis. In chronic cases, bronchodilator therapy should be considered. Oral corticosteroids should be added if cough continues and the history and physical examination findings suggest a wheezy form of bronchitis. (See Medication.)


Acute bronchitis leads to the hacking cough and phlegm production that often follows upper respiratory tract infection. This occurs because of the inflammatory response of the mucous membranes within the lungs' bronchial passages. Viruses, acting alone or together, account for most of these infections.[2, 3]

In children, chronic bronchitis follows either an endogenous response (eg, excessive viral-induced inflammation) to acute airway injury or continuous exposure to certain noxious environmental agents (eg, allergens or irritants). An airway that undergoes such an insult responds quickly with bronchospasm and cough, followed by inflammation, edema, and mucus production. This helps explain the fact that apparent chronic bronchitis in children is often actually asthma.

Mucociliary clearance is an important primary innate defense mechanism that protects the lungs from the harmful effects of inhaled pollutants, allergens, and pathogens.[4] Mucociliary dysfunction is a common feature of chronic airway diseases.

The mucociliary apparatus consists of 3 functional compartments: the cilia, a protective mucus layer, and an airway surface liquid (ASL) layer, which work together to remove inhaled particles from the lung. Animal study data have identified a critical role for ASL dehydration in the pathogenesis of mucociliary dysfunction and chronic airway disease.[5] ASL depletion resulted in reduced mucus clearance and histologic signs of chronic airway disease, including mucous obstruction, goblet cell hyperplasia, and chronic inflammatory cell infiltration. Study animals experienced reduced bacterial clearance and high pulmonary mortality as a result.

The role of irritant exposure, particularly cigarette smoke and airborne particulates, in recurrent (wheezy) bronchitis and asthma is becoming clearer. Kreindler et al demonstrated that the ion transport phenotype of normal human bronchial epithelial cells exposed to cigarette smoke extract is similar to that of cystic fibrosis epithelia, in which sodium is absorbed out of proportion to chloride secretion in the setting of increased mucus production.[6] These findings suggest that the negative effects of cigarette smoke on mucociliary clearance may be mediated through alterations in ion transport.

McConnell et al noted that organic carbon and nitrogen dioxide airborne particulates were associated with the chronic symptoms of bronchitis among children with asthma in southern California.[7]

A chronic or recurrent insult to the airway epithelium, such as recurrent aspiration or repeated viral infection, may contribute to chronic bronchitis in childhood. Following damage to the airway lining, chronic infection with commonly isolated airway organisms may occur. The most common bacterial pathogen that causes lower respiratory tract infections in children of all age groups is Streptococcus pneumoniae. Nontypeable Haemophilus influenzae and Moraxella catarrhalis may be significant pathogens in preschoolers (age < 5 y), whereas Mycoplasma pneumoniae may be significant in school-aged children (ages 6-18 y).

Children with tracheostomies are often colonized with an array of flora, including alpha-hemolytic streptococci and gamma-hemolytic streptococci. With acute exacerbations of tracheobronchitis in these patients, pathogenic flora may include Pseudomonas aeruginosa and Staphylococcus aureus (including methicillin-resistant strains), among other pathogens. Children predisposed to oropharyngeal aspiration, particularly those with compromised protective airway mechanisms, may become infected with oral anaerobic strains of streptococci.


Acute bronchitis is generally caused by respiratory infections; approximately 90% are viral in origin, and 10% are bacterial. Chronic bronchitis may be caused by repeated attacks of acute bronchitis, which can weaken and irritate bronchial airways over time, eventually resulting in chronic bronchitis. Industrial pollution is also a common cause; however, the chief culprit is heavy long-term cigarette smoke exposure.

Viral infections include the following:

  • Adenovirus

  • Influenza

  • Parainfluenza

  • Respiratory syncytial virus

  • Rhinovirus

  • Human bocavirus[8, 9, 10]

  • Coxsackievirus

  • Herpes simplex virus

Secondary bacterial infection as part of an acute upper respiratory tract infection is extremely rare in non–smoke-exposed patients without cystic fibrosis or immunodeficiency but may include the following:

  • S pneumoniae

  • M catarrhalis

  • H influenzae (nontypeable)

  • Chlamydia pneumoniae (Taiwan acute respiratory [TWAR] agent)

  • Mycoplasma species

Air pollutants, such as those that occur with smoking and from second-hand smoke, also cause incident bronchiolitis.[11] Tsai et al demonstrated that in utero and postnatal household cigarette smoke exposure is strongly linked to asthma and recurrent bronchitis in children.[12]  A study by Ghosh et al suggested that two single-nucleotide polymorphisms (rs2228001 and rs2733532) on the DNA repair gene XPC are linked to induction of the pathogenesis of bronchitis by air pollution in children aged 2 years or younger, with the two polymorphisms specifically interacting with particulate matter of less than 2.5 μm.[13]

Other causes include the following:

  • Allergies

  • Chronic aspiration or gastroesophageal reflux

  • Fungal infection

Protracted bacterial bronchitis (chronic wet cough)

A subset of children with a chronic productive cough have a significant bacterial cause underlying their symptoms. Various terms have been used for these conditions, including protracted bacterial bronchitis or chronic wet cough. While the clinical criteria for establishing this diagnosis are somewhat nonspecific, it is characterized by cough that persists for at least 4 weeks, lacking features suggesting an alternative explanation, and resolves following 2-4 weeks of antimicrobial therapy.[14] Protracted bacterial bronchitis (PBB) is common among pediatric populations, affecting up to 40% of children newly referred for specialist management of persistent wet cough.[15]  It is speculated that an initial viral infection disrupts respiratory epithelial and ciliary function, leading to chronic inflammation supporting the formation of bacterial biofilms. If untreated, protracted bacterial bronchitis may lead to chronic suppurative lung disease or bronchiectasis.[16]

The diagnosis is established by flexible bronchoscopy of the lower airways demonstrating edema, increased bronchial secretions, and positive bacterial culture following bronchoalveolar lavage. Marsh et al (2019) demonstrated that bacterial biomass, neutrophil percentage, interleukin (IL)–8, and IL-1-beta levels were significantly higher in children with protracted bacterial bronchitis undergoing bronchoalveolar lavage when compared with controls.[17] A multicenter study of patients undergoing bronchoalveolar lavage demonstrated that Streptococcus pneumoniae, nontypable Haemophilus influenzae, and Moraxella catarrhalis were the predominant infecting flora.[18] Most children with PBB will experience the resolution of cough following initial antibiotic treatment; however, up to 44% will have more than three episodes in the year following diagnosis and 16% will progress to bronchiectasis within 2 years.[19]  Both the American College of Chest Physicians[20] and the European Respiratory Society[21] statements on protracted bacterial bronchitis recommend treatment with an appropriate antibiotic for 3-4 weeks. Further investigation (chest CT, immunologic testing) is advised for those patients who do not experience improvement in symptoms.

Plastic bronchitis

Plastic bronchitis is an unusual but potentially devastating form of obstructive bronchial disease. The disease is characterized by the development of arborizing, thick, tenacious casts of the tracheobronchial tree that produce airway obstruction.[22, 23]  In one study of 34 patients with plastic bronchitis, 24 had single-ventricle congenital heart disease, 9 had primary pulmonary disease, and one had no underlying disease.[24]

Patients with congenital heart disease with single-ventricle physiology who have undergone a Fontan operation are a group at higher risk for development of this condition, for unknown reasons. In some cases, plastic bronchitis appears many years after the Fontan procedure is performed.[25] Zahorec et al describe cases occurring in the immediate postoperative period following a Fontan procedure. These patients were successfully managed with short periods of high-frequency jet ventilation and vigorous pulmonary toilet.[26]

Therapies include endoscopic debridement of the airway, vigorous pulmonary toilet, and aerosolized heparin or tissue plasminogen activator. For some, nebulized anticholinergic medication and compression vest chest physiotherapy have been helpful.[27] Shah et al performed thoracic duct ligation, resulting in complete resolution of the formation of casts in 2 patients with plastic bronchitis refractory to medical management.[28] DePopas et al (2017) describe 3 cases in which percutaneous thoracic duct intervention resulted in significant to complete resolution of symptoms associated with recurrent cast formation.[29]  Lymphatic embolization and stent grafting represent additional treatment options.[30]  These results suggest that high intrathoracic lymphatic pressures are related to the development of the recurrent bronchial casts seen in this disorder.


Data collected from the National Ambulatory Care Survey 1991 Summary showed that 2,774,000 office visits by children younger than 15 years resulted in a diagnosis of bronchitis.[31] Although the report did not separate diagnoses into acute and chronic bronchitis, the frequency of visits made bronchitis just slightly less common than otitis media and slightly more common than asthma. However, in children, asthma is often underdiagnosed and is frequently misdiagnosed as chronic or recurrent bronchitis. Since 1996, 9-14 million Americans have been diagnosed with chronic bronchitis annually.

Bronchitis, both acute and chronic, is prevalent throughout the world and is one of the top 5 reasons for childhood physician visits in countries that track such data. The incidence of bronchitis in British schoolchildren is reported to be 20.7%.

Weigl et al noted an overall increase in hospitalization for lower respiratory tract infection (laryngotracheobronchitis, bronchitis, wheezing bronchitis, bronchiolitis, bronchopneumonia, pneumonia) among German children from 1996 to 2000; this is consistent with observations among children from the United States, United Kingdom, and Sweden.[32] The incidence rate of bronchitis in children in this German cohort was 28%.

A study by Berhane et al indicated that as a result of improvements in ambient air quality in Southern California, bronchitic symptoms decreased in that region’s children between 1993 and 2012.[33, 34]

Differences in population prevalences have been identified in patients with chronic bronchitis. For example, because of the association of chronic bronchitis with asthma and the concentration of asthma risk factors among inner-city populations, this population group is at higher risk.

The incidence of acute bronchitis is equal in males and females. The incidence of chronic bronchitis is difficult to state precisely because of the lack of definitive diagnostic criteria and the considerable overlap with asthma. However, in recent years, the prevalence of chronic bronchitis has been reported to be consistently higher in females than in males.

Acute (typically wheezy) bronchitis occurs most commonly in children younger than 2 years, with another peak seen in children aged 9-15 years. Chronic bronchitis affects people of all ages but is more prevalent in persons older than 45 years.


Acute bronchitis is almost always a self-limited process in the otherwise healthy child. However, it frequently results in absenteeism from school and, in older patients, work. Chronic bronchitis is manageable with proper treatment and avoidance of known triggers (eg, tobacco smoke). Proper management of any underlying disease process, such as asthma, cystic fibrosis, immunodeficiency, heart failure, bronchiectasis, or tuberculosis, is also key. These patients need careful periodic monitoring to minimize further lung damage and progression to chronic irreversible lung disease.

A long-term prospective study found that children who had bronchitis at least once before the age of 7 years were more likely to have been diagnosed with asthma and pneumonia by age 53 years. The association with asthma and pneumonia in adulthood was strongest for participants who had a history of recurrent-protracted childhood bronchitis.[35]

An analysis of data from a nationwide British cohort study showed that children who had a lower respiratory tract infection (LRTI) such as bronchitis by the age of 2 years were 93% more likely to die of respiratory disease by age 73 years than children who had not had a LRTI by age 2 years. The rate of premature adult death caused by respiratory disease was a 2.1% among those who had a LRTI during early childhood, versus 1.1% among those who did not report a LRTI before age 2 years.[36]


Complications are extremely rare and should prompt evaluation for tracheobronchial aspiration, anomalies of the respiratory tract, or immunodeficiency. Complications may include the following:

  • Bronchiectasis

  • Bronchopneumonia

  • Acute respiratory failure

Patient Education

Instruct older patients regarding the need for immunization against pertussis, diphtheria, and influenza, which reduces the risk of bronchitis due to the causative organisms. Instruct these patients to avoid passive environmental tobacco smoke; to avoid air pollutants, such as wood smoke, solvents, and cleaners; and to obtain medical attention for prolonged respiratory infections.

Instruct parents that children may attend school or daycare without restrictions except during episodes of acute bronchitis with fever. Also instruct parents that children may return to school or daycare when signs of infection have decreased, appetite returns, and alertness, strength, and a feeling of well-being allow.




Acute bronchitis begins as a respiratory tract infection that manifests as the common cold. Symptoms often include coryza, malaise, chills, slight fever, sore throat, and back and muscle pain.

The cough in these children is usually accompanied by a nasal discharge. The discharge is watery at first, then after several days becomes thicker and colored or opaque. It then becomes clear again and has a mucoid watery consistency before it spontaneously resolves within 7-10 days. Purulent nasal discharge is common with viral respiratory pathogens and, by itself, does not imply bacterial infection.

Initially, the cough is dry and may be harsh or raspy sounding. The cough then loosens and becomes productive. Children younger than 5 years rarely expectorate. In this age group, sputum is usually seen in vomitus (ie, posttussive emesis). Parents frequently note a rattling sound in the chest. Hemoptysis, a burning discomfort in the chest, and dyspnea may be present.

Studies of chronic cough in children note that postnasal drip and signs or symptoms of asthma are most common.[37]

Brunton et al noted that adult patients with chronic bronchitis have a history of persistent cough that produces yellow, white, or greenish sputum on most days for at least 3 months of the year and for more than 2 consecutive years.[38] Wheezing and reports of breathlessness are also common. Pulmonary function testing in these adult patients reveals irreversible reduction in maximal airflow velocity.

Physical Examination

Lungs may sound normal. Crackles, rhonchi, or large airway wheezing, if any, tend to be scattered and bilateral. The pharynx may be injected.

Bronchitis and Asthma

Recurrent episodes of acute or chronic infectious bronchitis are unusual in children and should alert the clinician to the likelihood of asthma. Bronchitis is often repeatedly diagnosed in children in whom asthma has remained undiagnosed for many years.

Similarly, a family history of asthma in parents or siblings may be masked within a history of “recurrent bronchitis.” The diagnosis of "asthmatic bronchitis" or "wheezy bronchitis" is simply asthma.

Bronchitis and Immunodeficiency

Recurrent episodes of acute or chronic bronchitis may be associated with immunodeficiency. Stiehm identifies the 4 most common immunodeficiencies in pediatric patients[39] :

  • Transient hypogammaglobulinemia of infancy (THI)

  • Immunoglobulin G (IgG) subclass deficiency

  • Impaired polysaccharide responsiveness (partial antibody deficiency)

  • Selective IgA deficiency (IgAD)

A summary of immunodeficiency registries in 4 countries listed IgAD in 27.5% of the patients, IgG subclass deficiency in 4.8%, and THI in 2.3%. Patients typically have normal cellular immune systems, phagocyte function, and complement levels. All 4 immunodeficiency states are characterized by recurrent bacterial respiratory infections, such as purulent rhinitis, sinusitis, otitis, and bronchitis. Some patients with selective immunodeficiency may benefit from the use of intravenous immunoglobulin (IVIG), and the long-term prognosis is generally excellent.

Ozkan studied immunoglobulin A (IgA) and IgG deficiency in children who presented with recurrent sinopulmonary infection[40] and found that the overall frequency of antibody defects was 19.1%. IgA deficiency was observed in 9.3%, IgG subclass deficiency was observed in 8.4%, and both IgA and IgG subclass deficiencies were observed in 1.4%. The prevalence of IgA and/or IgG subclass deficiency was 25% in patients with recurrent upper respiratory tract infections, 22% in patients with recurrent pulmonary infections, and 12.3% in patients with recurrent bronchiolitis.

Common variable immunodeficiency is the most frequent of the primary hypogammaglobulinemias. In a Finnish study by Kainulainen et al of patients with common variable immunodeficiency receiving immunoglobulin replacement therapy,[41] sinopulmonary infections were the most common clinical presentation: 66% had recurrent pneumonia, 60% had recurrent maxillary sinusitis, and 45% had recurrent bronchitis.

In the Kainulainen study, the mean interval from the time of onset of symptoms to diagnosis was 8 years. Evidence of chronic lung damage was noted in 17% of patients at the time of diagnosis, highlighting the importance of early recognition in the prevention of chronic pulmonary sequelae.

To improve the recognition of common variable immunodeficiency, the authors suggest consideration of this condition in patients with recurrent sinopulmonary infection. In addition to a low serum IgG concentration, measurement of specific antibody production is recommended to establish the diagnosis.



Diagnostic Considerations

Consider the following in the diagnosis of bronchitis in pediatric patients:

  • Retained foreign body

  • Bronchopulmonary allergy

  • Immunosuppression

Chronic bronchitis is often part of an underlying disease process, such as asthma, cystic fibrosis, dyskinetic cilia syndrome, foreign body aspiration, or exposure to an airway irritant. Recurrent tracheobronchitis may also be seen in patients with tracheostomy or with certain forms of immunodeficiency. In all of these patient groups, chronic bronchitis should not be the primary diagnosis, because it does not describe the pathology of the underlying disorder.

Differential Diagnoses



Approach Considerations

For maximal cost-effectiveness, diagnostic laboratory tests for bronchitis should be performed in a stepwise manner. Patients with uncomplicated acute respiratory illness who are cared for in an outpatient setting need little, if any, laboratory evaluation.

Testing in Hospitalized Children

For hospitalized children, serum C-reactive protein screen, respiratory culture, rapid diagnostic studies, and serum cold agglutinin testing (at the appropriate age) help to classify whether the infection is caused by bacteria, atypical pathogens (eg, Chlamydia pneumoniae, Mycoplasma pneumoniae), or viruses. Obtain a blood or sputum culture if antibiotic therapy is under consideration.

For the child admitted to the hospital with a possible chlamydial, mycoplasmal, or viral lower respiratory tract infection for which specific therapy is considered, test nasopharyngeal secretions for these pathogens, using antigen or polymerase chain reaction testing for Chlamydia species and respiratory syncytial, parainfluenza, and influenza viruses or viral culture. Results will guide appropriate antimicrobial selection.

For the child who has been intubated, collect a specimen of deep respiratory secretions for Gram stain, chlamydial and viral antigen assays, and bacterial and viral cultures.

Asthma Testing

A clinical response to daily high-dose oral corticosteroids may be considered as a diagnostic and therapeutic trial to confirm asthma. Evidence of reversible airflow obstruction revealed by pulmonary function testing confirms the diagnosis of asthma.

Cystic Fibrosis Testing

Many states are now using tests for immunoreactive trypsinogen (IRT) coupled with cystic fibrosis transmembrane receptor (CFTR) mutational analyses in newborn screening programs. In newborns with positive results, sweat testing is required to diagnose or rule out cystic fibrosis.

In the United States, sweat chloride analysis using pilocarpine iontophoresis is typically conducted at accredited or affiliated pediatric cystic fibrosis centers. According to recommendations from the US Cystic Fibrosis Foundation (CFF) and the European Cystic Fibrosis Society (ECFS), sweat chloride results for infants aged 6 months or younger are classified as normal (chloride levels ≤29 mmol/L), abnormal (chloride levels ≥60 mmol/L), or intermediate/equivocal (chloride levels 30-59 mmol/L). If results fall within the intermediate/equivocal diagnosis range, the CFF recommends a repeat sweat test within 2 months.

Additional testing may include comprehensive CFTR analysis, fecal elastase evaluation, and pulmonary cultures.[42] Although the sensitivity of newborn screening is high, sweat chloride testing may also be pursued for infants or children with recurrent respiratory tract infection, chronic diarrhea, or failure to thrive who had negative newborn screening results for cystic fibrosis.

Immunodeficiency Testing

For children in whom immunodeficiency is suspected, measurement of total serum immunoglobulins, immunoglobulin G (IgG) subclasses, and specific antibody production is recommended to establish the diagnosis.

Chest Radiography

Chest radiography is typically not warranted but, if obtained, appears normal in most patients with uncomplicated bronchitis. Abnormal findings are minimal and may include atelectasis, hyperinflation, and peribronchial thickening. Focal consolidation is not usually present. These findings are similar to the radiographic findings in patients with asthma. Radiographic findings may help exclude other diseases or complications, particularly when abnormalities in either vital signs or pulse oximetry findings are present.

Pulmonary Function Testing

Pulmonary function tests may show airflow obstruction that is reversible with bronchodilators. Bronchial challenge, such as with exercise or with histamine or methacholine exposure, may demonstrate the airway hyperreactivity characteristic of asthma.


On fiberoptic bronchoscopy, a diagnosis of chronic bronchitis is suggested if the airways appear erythematous and friable. Bronchoalveolar lavage may be useful in establishing an infectious cause. Bronchoalveolar lavage may reveal numerous monocytic or polymorphonuclear inflammatory cells. In children with chronic aspiration of gastric contents, lipids may be present within macrophages.



Approach Considerations

Emergency care for acute bronchitis or exacerbation of chronic bronchitis must focus on ensuring that the child has adequate oxygenation and hydration. Outpatient care is appropriate unless bronchitis is complicated by severe underlying disease. General measures include rest, use of antipyretics, adequate oral fluid intake, and avoidance of smoke.

Proper care of any underlying disorder is of paramount importance. Recognition of the role of asthma and institution of appropriate therapies are key to the successful treatment of many patients.

Febrile patients should increase oral fluid intake. Instruct the patient to rest until the fever subsides.

Resolution of symptoms, normal findings on physical examination, and normal pulmonary function test results indicate the end of the need for acute treatment. Patients in whom asthma is diagnosed will likely require ongoing therapy for that disease. Patients with defined hypogammaglobulinemia may need periodic immunoglobulin replacement treatments. These are best coordinated with the assistance of a pediatric allergy, immunology or pulmonary specialist.

Pharmacologic Therapy

Acute bronchitis

In otherwise healthy individuals, the use of antibiotics has not demonstrated any consistent benefit in relieving symptoms or improving the natural history of acute bronchitis. Placebo-controlled studies using doxycycline, erythromycin, and trimethoprim-sulfamethoxazole have failed to show significant benefit in patients with acute bronchitis.

In a study of antibiotic prescribing patterns, a retrospective cohort study of ED patients from 2001-2010, using data from the National Hospital Ambulatory Medical Care Survey (NHAMCS), found lower rates of antibiotic prescriptions among pediatric patients with stable rates than among adult patients.[43] This study highlights growing recognition of the limited role for antibiotics in pediatric patients treated for acute bronchitis and related acute respiratory tract infections.

A study that aimed to determine bacterial prevalence rates for 5 common childhood acute respiratory tract infections found that in the United States, antibiotics are prescribed almost twice as often as expected to outpatients aged 18 years and younger.[44, 45]  Another study in the Netherlands by Ivanovska et al reported concerning high antibiotic prescription rates for bronchitis in adolescents compared with children aged 0-4 and 5-11 years.[46]

A research letter reported that physicians are prescribing antibiotics to adults for acute bronchitis at rates between 60% and 80%, despite guidelines and educational efforts that say the rate should be zero.[47, 48]

Medical therapy generally targets symptoms and includes use of analgesics and antipyretics. Antitussives and expectorants are often prescribed but have not been demonstrated to be useful. Few data outside of the research laboratory support the efficacy of expectorants.

The prototype antitussive, codeine, has been successful in some chronic-cough and induced-cough models, but few clinical data address their use in acute bronchitis. The data that are available suggest little benefit. Data show codeine is little or no better than guaifenesin or dextromethorphan in cough suppression.

Preliminary studies suggest a possible role for EPs 7630, an herbal drug preparation derived from Pelargonium sidoides roots, in the treatment of pediatric patients (1-18 y) with acute bronchitis outside the strict indication for antibiotics. Kamin et al demonstrated reduced bronchitis severity symptom scores in patients treated with EPs 7630, with good overall tolerability.[49, 50]

Bronchodilators have failed to demonstrate efficacy in some adult studies of acute bronchitis. Nevertheless, a trial of inhaled albuterol may be worthwhile because it may provide significant relief of symptoms for many pediatric patients.

Chronic bronchitis

Antibiotics should not be the primary therapy. They usually do not result in a cure and may delay the start of more appropriate asthma therapies. However, antibiotics may be appropriate in children with chronic wet cough and symptoms persisting beyond 2-4 weeks, most of whom have protracted bacterial bronchitis.[51]

Bronchodilator therapy should be considered and instituted; a beta-adrenergic agonist, such as albuterol or terbutaline may be effective. Several studies have demonstrated that bronchodilators delivered by metered dose inhalers with spacer device are as, or in some cases more effective, in all age groups than nebulized bronchodilators.

In the child who continues to cough despite a trial of bronchodilators and in whom the history and physical examination suggest a wheezy form of bronchitis, corticosteroids should be added. Short courses of dexamethasone (1-2 dose schedules) have been shown to be as effective as longer (5 d) courses of prednisolone;[52] this was preferred by caretakers likely due to the reduced need to administer medication and a lower incidence of vomiting. “Stepped-up” courses of inhaled corticosteroids may also be effective for some patients.[53]

If the response to initial therapies is suboptimal or if a persistent wet cough falls within the definitions of protracted bacterial bronchitis, antibiotic therapy with an agent such as a beta-lactamase–resistant antimicrobial (eg, amoxicillin-clavulanate) or a macrolide may be considered. Certain antibiotics, including the macrolides and fluoroquinolones, have the potential to prolong the QT interval and in studies have been associated with a higher risk for lethal arrhythmias.[54]

Subsequent studies have demonstrated no added risk for adverse cardiovascular events among young and middle-aged adults taking azithromycin who do not have cardiovascular risk factors. Due to potential concerns, the US Food and Drug Administration (FDA) updated its warning for azithromycin with information related to the risk of QT interval prolongation and torsades de pointes, a specific, rare heart rhythm abnormality. Care must be exercised when considering these medications, particularly in patients with congenital or acquired forms of long QT syndrome, forms of congenital or acquired heart disease, patients with bradyarrhythmias, hypokalemia, hypocalcemia, or hypomagnesemia and those taking other medications known to be associated with QTc prolongation. Giudicessi and Ackerman (2013) provide a table of factors to consider when assessing this risk.[55]


Referral to a pediatric pulmonologist may be helpful for patients experiencing persistent or recurrent symptoms and whose histories suggest the possibility of tracheobronchial foreign body aspiration, cystic fibrosis, immunodeficiency, or persistent asthma for which appropriate first-line symptom or controller therapies have failed.



Medication Summary

In acute bronchitis, medical therapy generally targets symptoms and includes use of analgesics and antipyretics.

In chronic bronchitis, bronchodilator therapy should be considered and instituted (a beta-adrenergic agonist, such as albuterol or terbutaline). Beta-adrenergic agents are less toxic and have a more rapid onset of action. Stepped-up use of inhaled corticosteroids may also be an effective initial intervention.

In the child who continues to cough despite a trial of bronchodilators and in whom the history and physical examination findings suggest a wheezy form of bronchitis, oral corticosteroids should be added. If the response is suboptimal or if fever persists, antibiotic therapy with an agent such as a macrolide or beta-lactamase–resistant antimicrobial may be considered.

Antibiotics should not be the primary therapy. They usually do not result in a cure and may delay the start of more appropriate asthma therapies.

Analgesic and antipyretic agents

Class Summary

These agents are used to control fever, myalgias, and arthralgias.

Acetaminophen (Tylenol, Aspirin-Free Anacin, Feverall)

This is the treatment of choice for pain in patients who are unable to take aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs).

Ibuprofen (Ibuprin, Advil, Motrin)

This NSAID is the usual treatment of choice for mild-to-moderate pain if no contraindications exist. Ibuprofen reduces inflammatory reactions and pain, probably by decreasing activity of cyclooxygenase, which inhibits prostaglandin synthesis.

Corticosteroids, systemic

Class Summary

These agents are used for short courses (3-10 d) to gain prompt control of inadequately controlled acute asthmatic episodes. Systemic corticosteroids also are used for long-term prevention of symptoms in severe persistent asthma, as well as for suppression, control, and reversal of inflammation. Frequent and repetitive use of beta2-agonists has been associated with beta2-receptor subsensitivity and down-regulation; these processes are reversed with corticosteroids.

Higher-dose corticosteroids have no advantage in severe exacerbations of asthma, and intravenous administration has no advantage over oral therapy, provided that GI tract transit time or absorption is not impaired. The usual regimen is to continue frequent multiple daily dosing until the forced expiratory volume in 1 second (FEV1) or peak expiratory flow (PEF) is 50% of the predicted or personal best values; then, the dose is changed to twice daily. This usually occurs within 48 hours.

Prednisolone (Pediapred, Orapred)

Prednisolone works by decreasing inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

Prednisone (Sterapred)

Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte activity. Prednisone stabilizes lysosomal membranes and suppresses lymphocytes and antibody production.


Class Summary

Studies have found that bronchodilators relieve symptoms of bronchitis, and they have been found to be superior to antibiotics in this setting. However, patient numbers in these trials were disappointingly small, given how commonly acute bronchitis is diagnosed.

Albuterol sulfate (Proventil, Ventolin, ProAir)

Terbutaline ( Brethine, Bricanyl, Brethaire, or Terbulin)

A beta-adrenergic agonist useful in the treatment of epinephrine-refractory bronchospasm, albuterol relaxes bronchial smooth muscle by acting on beta2-adrenergic receptors. It has little effect on cardiac muscle contractility. A ready-to-use solution for nebulization is available as 0.083% (2.5 mg/3 mL).).


Class Summary

Antibiotics should not be the primary therapy for patients with acute bronchitis. They usually do not result in a cure and may delay the start of more appropriate asthma therapies. Studies of antibiotic effectiveness have focused on healthy individuals or patients with chronic obstructive lung disease. Patients with chronic obstructive pulmonary disease (COPD) or limited cardiopulmonary reserve, such as patients with asthma, may experience a very limited beneficial effect.

Amoxicillin-clavulanic acid (Augmentin)

Amoxicillin is a semisynthetic bactericidal beta-lactam antibiotic that inhibits cell wall synthesis. This agent contains amoxicillin combined with clavulanate, a beta-lactamase inhibitor.

Azithromycin (Zithromax)

Azithromycin is used to treat mild to moderately severe infections caused by susceptible strains of microorganisms. It is indicated for chlamydial and gonorrheal infections of the genital tract.


Class Summary

Vaccination is the most important preventive measure for influenza; vaccinations offer coverage for influenza A and B and, thereby, provide greater protection from bronchitis in the appropriate populations. Antiviral drugs represent a second line of defense.

Antiviral agents with activity against influenza virus include amantadine, rimantadine, oseltamivir, and zanamivir. Amantadine and rimantadine are not currently recommended by the Centers for Disease Control and Prevention (CDC) for influenza because of widespread resistance among influenza A strains. Oseltamivir (Tamiflu) resistance emerged in the United States during the 2008-2009 influenza season and was found in some strains of H1N1 influenza virus during the 2009-2010 epidemic.

For current recommendations on the use of antiviral drugs for influenza, see the CDC information for health care professionals on antiviral drugs for influenza.

Oseltamivir (Tamiflu)

Oseltamivir inhibits neuraminidase, which is a glycoprotein on the surface of influenza virus that destroys an infected cell's receptor for viral hemagglutinin. By inhibiting viral neuraminidase, oseltamivir decreases release of viruses from infected cells and thus viral spread.

This agent is effective against influenza A and B, although resistance against influenza A emerged in the United States during the 2008-2009 influenza season. Start within 40 hours of symptom onset. Available in capsules and oral suspension.

Zanamivir (Relenza)

Zanamivir is an inhibitor of neuraminidase, which is a glycoprotein on the surface of the influenza virus that destroys the infected cell's receptor for viral hemagglutinin. By inhibiting viral neuraminidase, release of viruses from infected cells and viral spread are decreased. Zanamivir is effective against both influenza A and B. It is inhaled through the Diskhaler oral inhalation device. Circular foil discs that contain 5-mg blisters of drug are inserted into the supplied inhalation device.

Corticosteroids, inhaled

Class Summary

Corticosteroids are the most potent anti-inflammatory agents. Inhaled forms are topically active, poorly absorbed, and least likely to cause adverse effects. No study has shown significant toxicity with inhaled steroid use in children at doses less than the equivalent of 400 mcg/d of beclomethasone. They are used for long-term control of symptoms and for the suppression, control, and reversal of inflammation.

Inhaled forms reduce the need for systemic corticosteroids. They block late asthmatic responses to allergens; reduce airway hyperresponsiveness; inhibit cytokine production, adhesion protein activation, and inflammatory cell migration and activation; and reverse beta2-receptor down-regulation and subsensitivity (in acute asthmatic episodes with long-term beta2-agonist use).

Beclomethasone (Qvar)

Beclomethasone inhibits bronchoconstriction mechanisms, causes direct smooth muscle relaxation, and may decrease the number and activity of inflammatory cells, which, in turn, decrease airway hyperresponsiveness. It is available in a metered-dose inhaler (MDI) that delivers 40 or 80 mcg/actuation.

Fluticasone (Flovent HFA, Flovent Diskus)

Fluticasone has extremely potent vasoconstrictive and anti-inflammatory activity. It is available in an MDI (44-mcg, 110-mcg, or 220-mcg per actuation) and Diskus powder for inhalation (50-mcg, 100-mcg, or 250-mcg per actuation).

Budesonide inhaled (Pulmicort Flexhaler, Pulmicort Respules)

Budesonide reduces inflammation in airways by inhibiting multiple types of inflammatory cells and decreasing production of cytokines and other mediators involved in the asthmatic response. It is available as Flexhaler powder for inhalation (90 mcg/actuation [delivers approximately 80 mcg/actuation]) and Respules suspension for inhalation.

Anti-inflammatory Agent



Questions & Answers


What is pediatric bronchitis?

What is the pathophysiology of pediatric acute bronchitis?

What is the pathophysiology of pediatric chronic bronchitis?

What causes pediatric acute bronchitis?

What causes pediatric protracted bacterial bronchitis?

What causes pediatric plastic bronchitis?

What is the prevalence of pediatric bronchitis?

What is the prognosis of pediatric bronchitis?

What is included in patient education about pediatric bronchitis?


Which clinical history findings are characteristic of pediatric bronchitis?

Which physical findings are characteristic of pediatric bronchitis?

When should asthma be considered in children with recurrent bronchitis?

Which immunodeficiencies are related to recurrent pediatric bronchitis?


Which conditions are included in the differential diagnoses of pediatric bronchitis?

What are the differential diagnoses for Pediatric Bronchitis?


How is bronchitis diagnosed?

What is included in the workup of pediatric bronchitis in hospitalized children?

How is a diagnosis of asthma confirmed in pediatric bronchitis?

How is cystic fibrosis diagnosed in pediatric bronchitis?

How is immunodeficiency diagnosed in pediatric bronchitis?

What is the role of chest radiography in the workup of pediatric bronchitis?

What is the role of pulmonary function testing in the workup of pediatric bronchitis?

What is the role of bronchoscopy in the workup of pediatric bronchitis?


How is pediatric bronchitis treated?

What is the role of medications in the treatment of pediatric acute bronchitis?

What is the role of medications in the treatment of pediatric chronic bronchitis?

Which specialist consultations are beneficial to patients with pediatric bronchitis?

What are the possible complications of pediatric bronchitis?


Which medications are used in the treatment of pediatric bronchitis?

Which medications in the drug class Anti-inflammatory Agent are used in the treatment of Pediatric Bronchitis?

Which medications in the drug class Corticosteroids, inhaled are used in the treatment of Pediatric Bronchitis?

Which medications in the drug class Antivirals are used in the treatment of Pediatric Bronchitis?

Which medications in the drug class Antibiotics are used in the treatment of Pediatric Bronchitis?

Which medications in the drug class Bronchodilators are used in the treatment of Pediatric Bronchitis?

Which medications in the drug class Corticosteroids, systemic are used in the treatment of Pediatric Bronchitis?

Which medications in the drug class Analgesic and antipyretic agents are used in the treatment of Pediatric Bronchitis?