Bronchitis Empiric Therapy 

Bronchitis Empiric Therapy 

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Empiric therapeutic regimens for bronchitis are outlined below, including those for acute bronchitis, chronic bronchitis, and acute bacterial exacerbation of chronic bronchitis. [1, 2, 3, 4, 5, 6, 7, 8, 9]

See Bronchitis and Chronic Obstructive Pulmonary Disease for full discussions of these topics.

Patients typically present with a cough that lasts more than 5 days and may be associated with sputum production. Cough usually resolves within 3 weeks but may linger for up to 8 weeks.

Acute bronchitis is typically caused by viruses.

There is limited evidence to support the use of antibiotics for treating acute bronchitis in otherwise healthy adults. Antibiotic administration does not significantly alter presence of productive cough or activity limitations at follow-up doctor visits; however, there is a trend toward increased adverse effects with their use. [6]

There may be a role for antibiotic treatment of acute bronchitis in the elderly with multiple comorbidities.

Symptomatic treatment includes the use of cough suppressants (dextromethorphan or codeine), mucolytics, and bronchodilators (albuterol).

Patients without underlying heart or lung disease who present with a persistent cough lasting more than 14 days should be evaluated for pertussis.

Chronic bronchitis is typically defined as cough and sputum production on most days of the month for at least 3 months of the year for 2 consecutive years. Chronic bronchitis results from excessive airway mucus due to increased production (ie, inflammation, oxidative stress, infection) and decreased clearance (ie, poor ciliary function, airway occlusion, respiratory muscle weakness). It is a phenomenon with variable presentations that is most common in individuals with inhalation exposures, such as smoking, and often coincides with chronic obstructive pulmonary disease (COPD).

Empiric antibiotic therapy is not recommended.

Although chronic macrolide therapy, known for its anti-inflammatory properties, reduces COPD exacerbations, it does not show any additional benefit in patients with baseline chronic bronchitis.

Reduce mucus production.

Smoking cessation and avoidance of environmental irritants will decrease goblet cell stimulation and hyperplasia.

Anticholinergics decrease mucus secretion via their action on the muscarinic receptors; however, use with caution as they may dehydrate airways making secretions more difficult to expectorate.

Inhaled glucocorticoids reduce inflammation and thus mucus production.

PDE-4 inhibitors (eg, roflumilast) may decrease COPD exacerbations in patients with concomitant chronic bronchitis by decreasing mucus secretions; however, evidence is limited.

Facilitate mucus elimination.

Physical maneuvers such as chest physical therapy or flutter valve may help to augment shear stressors to aid mucus breakdown and clearance (minimal evidence available).

Methylxanthines and short-acting beta agonists increase airway lumen diameter, intensify ciliary beat frequency, and promote mucus hydration via activation of the cystic fibrosis transmembrane regulator.

Inhale hypertonic saline directly rehydrate airways and promotes cough (minimal evidence to show benefit).

Expectorants (eg, guaifenesin) vagally medicate increase in airway secretions improving mucus clearance in the short term (no long-term benefit found).

Bacterial pathogens are identified in less than half of all ABECB cases. The Anthonisen Criteria is typically used to qualify severity of acute exacerbations. Three clinical factors are considered: dyspnea, sputum volume, and sputum purulence. Antibiotic treatment is recommended for moderate (2 of 3 symptoms) or severe (all 3 symptoms) exacerbations. Change in sputum color has also been recognized to be a strong predictor of presence of potentially pathologic microorganisms in ABECB. Green and yellow sputum are more likely than white sputum to be culture positive.


No antibiotics recommended

Outpatient symptomatic therapy and monitor for worsening symptoms

Moderate ABECB and/or any one of the following: age < 65 years, FEV1 >50% predicted, no cardiac disease, or < 3 exacerbations per year:

Azithromycin 500 mg PO on first day then 250 mg PO daily for next 4 days or

Clarithromycin 250-500 mg PO BID for 7-14 days or

Doxycycline 100 mg PO BID for 7 days or

Trimethoprim-sulfamethoxazole (160 mg/800 mg) 1 DS tablet PO BID for 10-14 days or

Cefuroxime 250-500 mg PO q12h for 10 days or

Cefdinir 300 mg PO BID for 5-10 days or

Cefpodoxime 200 mg PO q12h for 10 days

If recent antibiotic exposure within 3 months, use alternative class.

Severe ABECB and/or anyone of the following: age ≥65 years, FEV1 ≤ 50% predicted, cardiac disease, or ≥3 exacerbations per year [11] :

Consider hospitalization.

Amoxicillin-clavulanate (875 mg/125 mg) 1 tablet PO BID for 7-10 days or

Levofloxacin  750mg PO daily for at least 7 days or

Gemifloxacin 320mg PO daily for 5 days or

Moxifloxacin 400 mg PO daily for 5 days

If at risk for Pseudomonas infection consider sputum culture and treatment with Levaquin 750 mg PO daily for 14 days​ [10] .

If recent antibiotic exposure within 3 months, use alternative class.

Knutson D, Braun C. Diagnosis and management of acute bronchitis. Am Fam Physician. May 15 2002. 65(10):2039-44.

Wenzel RP, Fowler AA 3rd. Clinical practice. Acute bronchitis. N Engl J Med. Nov 16 2006. 355(20):2125-30.

Smucny J, Becker L, Glazier R. Beta2-agonists for acute bronchitis. Cochrane Database Syst Rev. Oct 18 2006. CD001726.

Tan T, Little P, Stokes T. Antibiotic prescribing for self limiting respiratory tract infections in primary care: summary of NICE guidance. BMJ. Jul 23 2008. 337:a437.

Siempos II, Dimopoulos G, Korbila IP, Manta K, Falagas ME. Macrolides, quinolones and amoxicillin/clavulanate for chronic bronchitis: a meta-analysis. Eur Respir J. Jun 2007. 29(6):1127-37.

Smith SM, Fahey T, Smucny J, Becker LA. Antibiotics for acute bronchitis. Cochrane Database of Systematic Reviews. March 2014. 3:1-43. [Full Text].

Kim V, Criner GJ. Chronic bronchitis and chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine. February 2013. 187(3):228-37.

Miravitlles M, Kruesmann F, Haverstock D, Perroncel R, Choudhri SH, Arvis P. Sputum colour and bacteria in chronic bronchitis exacerbations: a pooled analysis. European Respiratory Journal. June 2012. 39(6):1354-60.

Sethi S, Murphy TF. Infection in the Pathogenesis and Course of Chronic Obstructive Pulmonary Disease. New England Journal of Medicine. November 2008. 359(22):2355-365.

American Thoracic Society / European Respiratory Society Task Force. Standards for the Diagnosis and Management of Patients with COPD. [Full Text].

Global Strategy for the Diagnosis, Management and Prevention of COPD, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2016.

Jazeela Fayyaz, DO Pulmonologist, Department of Pulmonology, Unity Hospital

Jazeela Fayyaz, DO is a member of the following medical societies: American College of Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Ravikanth Vydyula, MD Fellow in Pulmonary and Critical Care Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital

Ravikanth Vydyula, MD is a member of the following medical societies: American College of Physicians, American Association of Physicians of Indian Origin

Disclosure: Nothing to disclose.

Maciej P Walczyszyn, MD Fellow in Pulmonary and Critical Care Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital; Hospitalist, Alliance Medical Group, Inc, Waterbury Hospital

Maciej P Walczyszyn, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Klaus-Dieter Lessnau, MD, FCCP Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital

Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Jasmeet Anand, PharmD, RPh Adjunct Instructor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

John J Oppenheimer, MD Clinical Professor, Department of Medicine, Rutgers New Jersey Medical School; Director of Clinical Research, Pulmonary and Allergy Associates, PA

John J Oppenheimer, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology, New Jersey Allergy, Asthma and Immunology society

Disclosure: Received research grant from: quintiles, PRA, ICON, Novartis: Adjudication<br/>Received consulting fee from AZ for consulting; Received consulting fee from Glaxo, Myelin, Meda for consulting; Received grant/research funds from Glaxo for independent contractor; Received consulting fee from Merck for consulting; Received honoraria from Annals of Allergy Asthma Immunology for none; Partner received honoraria from ABAI for none. for: Atlantic Health System.

Bronchitis Empiric Therapy 

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