Pediatric Bronchitis Medication

  • Author: Patrick L Carolan, MD; Chief Editor: Michael R Bye, MD   more...
 
Updated: Mar 29, 2011
 

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; either a beta-adrenergic agonist, such as albuterol or metaproterenol, or theophylline may be effective. Beta-adrenergic agents are less toxic, have a more rapid onset of action than theophylline, and do not require monitoring of levels. Inhaled corticosteroids may be effective.

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.

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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.

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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.

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Bronchodilators

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)

 

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).).

Metaproterenol sulfate

 

Metaproterenol is a beta agonist for bronchospasms that relaxes bronchial smooth muscle by action on beta2 receptors with little effect on cardiac muscle contractility.

Theophylline (Theo-24, Uniphyl)

 

Potentiates exogenous catecholamines and stimulates endogenous catecholamine release and diaphragmatic muscular relaxation, which, in turn, stimulates bronchodilation. It partially acts by inhibiting phosphodiesterase, elevating cellular cyclic AMP levels, or antagonizing adenosine receptors in the bronchi, resulting in relaxation of smooth muscle.

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Antibiotics

Class Summary

Studies 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. 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.

Erythromycin (EES, E-Mycin, Ery-Tab)

 

Erythromycin inhibits RNA-dependent protein synthesis, possibly by stimulating the dissociation of peptidyl tRNA from ribosomes, inhibiting bacterial growth. This agent is used for prophylaxis in patients who are allergic to penicillin and will be undergoing dental, oral, or respiratory tract procedures.

Clarithromycin (Biaxin)

 

Clarithromycin reversibly binds to P site of 50S ribosomal subunit of susceptible organisms. It may inhibit RNA-dependent protein synthesis by stimulating dissociation of peptidyl tRNA from ribosomes, inhibiting bacterial growth.

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.

Tetracycline (Sumycin)

 

Tetracycline inhibits bacterial protein synthesis by binding with 30S and, possibly, 50S ribosomal subunits of susceptible bacteria. It is used to treat bacterial infections caused by susceptible gram-positive and gram-negative organisms, as well as mycoplasmal, chlamydial, and rickettsial infections. It is less effective than erythromycin in mycoplasmal, chlamydial, and Bordetella pertussis infections.

Doxycycline (Vibramycin)

 

Doxycycline is a broad-spectrum bacteriostatic antibiotic that inhibits protein synthesis.

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.

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Antivirals

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.

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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.

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Contributor Information and Disclosures
Author

Patrick L Carolan, MD  Adjunct Associate Professor, Departments of Pediatrics, Family Practice, and Community Health, University of Minnesota Medical School; Medical Director of Minnesota Sudden Infant Death Center; Attending Staff, Department of Emergency Services, Children's Hospitals and Clinics of Minnesota

Patrick L Carolan, MD is a member of the following medical societies: American Academy of Pediatrics and International Society of SIDS Researchers

Disclosure: Nothing to disclose.

Specialty Editor Board

Thomas Scanlin, MD  Chief, Division of Pulmonary Medicine and Cystic Fibrosis Center, Department of Pediatrics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School

Thomas Scanlin, MD is a member of the following medical societies: American Association for the Advancement of Science, American Society for Biochemistry and Molecular Biology, American Thoracic Society, Society for Pediatric Research, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

Charles Callahan, DO  Professor, Deputy Chief of Clinical Services, Walter Reed Army Medical Center

Charles Callahan, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American College of Osteopathic Pediatricians, American Thoracic Society, Association of Military Surgeons of the US, and Christian Medical & Dental Society

Disclosure: Nothing to disclose.

Mary E Cataletto, MD  Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital

Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians

Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Michael R Bye, MD  Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons; Attending Physician, Pediatric Pulmonary Medicine, Morgan Stanley Children's Hospital of New York Presbyterian, Columbia University Medical Center

Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

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