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Chronic Bronchitis

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Last Update: November 28, 2022.

Continuing Education Activity

Chronic bronchitis is a type of chronic obstructive pulmonary disease (COPD) that is defined as a productive cough of more than 3 months occurring within a span of 2 years. Patients typically present with chronic productive cough, malaise, and symptoms of excessive coughing, such as chest or abdominal pain. This activity reviews the evaluation and management of chronic bronchitis and explains the role of the interprofessional team in improving care for patients with this condition.


  • Identify the role of cigarette smoking in the etiology of chronic bronchitis.
  • Describe the pathophysiology of chronic bronchitis.
  • Outline the use of the Reid index in the histopathological evaluation of chronic bronchitis.
  • Explain the importance of improving care coordination among the interprofessional team to counsel patients on smoking cessation and improve outcomes in those with chronic bronchitis.
Access free multiple choice questions on this topic.


Chronic bronchitis can be defined as a chronic productive cough lasting more than 3 months and occurring within a span of 2 years. There is a strong causal association with smoking, and it is very often secondary to chronic obstructive pulmonary disease (COPD). [1]


There are many known causes of chronic bronchitis, but the most important causative factor is exposure to cigarette smoke, either due to active smoking or passive inhalation. Many inhaled irritants to the respiratory tract, such as smog, industrial pollutants, and toxic chemicals, can cause chronic bronchitis. Although bacterial and viral infections usually cause acute bronchitis, repeated exposure to infections can cause chronic bronchitis. The predominant viruses that are causative are Influenza types A and B, and the dominant bacterial agents are Staphylococcus, Streptococcus, and Mycoplasma pneumonia. People who have an associated background in respiratory diseases such as asthma, cystic fibrosis, or bronchiectasis have a higher predisposition to develop chronic bronchitis. People who have repeated exposure to environmental pollutants such as dust or airborne chemicals such as ammonia and sulfur dioxide have a higher risk of developing chronic bronchitis. Chronic gastroesophageal reflux is a well-documented but less frequent cause of chronic bronchitis. [1]


The occurrence of Chronic bronchitis in the general population has been documented to vary between 3% to 7% of healthy adults. However, it is estimated to be as high as 74% among those diagnosed to have COPD. Many among those in the general population experiencing symptoms of chronic bronchitis may not have a definitive respiratory diagnosis. It has been documented that subjects under the age of 50 years who are otherwise healthy and have chronic bronchitis are at a higher risk of morbidity and mortality when compared to healthy subjects. The increasing prevalence of chronic bronchitis is thought to be associated with increasing age, tobacco smoking, occupational exposure, and socioeconomic status.[2]


Chronic bronchitis is thought to be caused by overproduction and hypersecretion of mucus by goblet cells. Epithelial cells lining the airway respond to toxic, infectious stimuli by releasing inflammatory mediators such as interleukin 8, colony-stimulating factor, and other pro-inflammatory cytokines. There is also an associated decrease in the release of regulatory substances such as angiotensin-converting enzyme and neutral endopeptidase. The alveolar epithelium is both the target as well as the initiator of the inflammatory process in chronic bronchitis. During an acute exacerbation of chronic bronchitis, the bronchial mucous membrane becomes hyperemic and edematous with diminished bronchial mucociliary function. This, in turn, leads to airflow impediment because of luminal obstruction to small airways. The airways become clogged by debris, and this further increases the irritation. The characteristic cough of bronchitis is caused by the copious secretion of mucus in chronic bronchitis.[3]


Gross pathology reveals boggy mucosa with excessive mucinous secretion, pus, and prominence of bronchial pits overlying the orifice of bronchial mucous glands.

Early changes in chronic bronchitis on microscopic histology show hypersecretion of mucus in large airways with hypertrophy of submucosal glands in the trachea and bronchus. Later an increase in goblet cells in small airways contributes to airway obstruction due to excessive mucous. Submucosal mucous glands occupy an increasing proportion of the bronchial wall. This is measured by Reid's index, which is the ratio of the thickness of the mucous gland layer to the thickness of the wall between epithelium and cartilage. The standard Reid's index is 0.4. In chronic bronchitis, Reid's index is increased. Chronic bronchitis is also associated with varying degrees of dysplasia and squamous metaplasia.[4]

History and Physical

The most common symptom of patients with chronic bronchitis is a cough. The history of a cough typical of chronic bronchitis is characterized to be present for most days in a month lasting for 3 months, with at least 2 such episodes occurring for 2 years in a row. A productive cough with sputum is present in about 50% of patients. The sputum color may vary from clear, yellow, green, or at times blood-tinged. The color of sputum may be dependent on the presence of secondary bacterial infection. Very often, changes in sputum color can be due to peroxidase released by leucocytes in the sputum. Therefore, color alone is not a definite indication of bacterial infection.

It is of prime importance to elicit a complete history from the patient, including information regarding possible exposure to inhaled irritants or chemicals, as well as full details regarding smoking habits. Fever is uncommon in chronic bronchitis and, when present, can be suggestive of associated influenza or pneumonia. Generalized malaise is a commonly associated symptom. Rarely patients may complain of chest pain or abdominal muscle pain caused by continuous forceful coughing. When there is inflammation of the airway, there can be an associated wheeze.

Uncomplicated chronic bronchitis presents with a cough, and there is no evidence of airway obstruction physiologically. When patients have chronic asthmatic bronchitis, there is usually a wheeze present due to a hyperactive airway leading to intermittent bronchospasm. When there is obstructive bronchitis which is the more severe end of the spectrum of the disease, there is small airway disease which at times results in emphysema.[1]


The most critical factor in the diagnosis of chronic bronchitis is a typical history to exclude other possible diseases of the lower respiratory tract. 

The investigations which assist in confirming the diagnosis of chronic bronchitis are a complete blood count with differential. A serum procalcitonin level can help in distinguishing associated bacterial from non-bacterial infections. A chest x-ray in the elderly and when physical findings suggest pneumonia is important. A culture of the sputum when a bacterial infection is suspected is indicated. The additional investigations are a helpful measurement of oxygen saturation and pulmonary function test.[3]

Treatment / Management

The primary aim of treatment for chronic bronchitis is to relieve symptoms, prevent complications and slow the progression of the disease. The primary goals of therapy are aimed at reducing the overproduction of mucus, controlling inflammation, and lowering cough. These are achieved by pharmacological as well as nonpharmacological interventions. [5][6][7]

The mainstay of pharmacological interventions are the following:

  1. Bronchodilators: Short and long-acting β-adrenergic receptor agonists, as well as anticholinergics, help by increasing the airway lumen, increasing ciliary function, and by increasing mucous hydration.
  2. Glucocorticoids: Reduce inflammation and mucus production. Inhaled corticosteroids reduce exacerbation and improve quality of life. However, it is administered under medical supervision and for short periods of time, as long-term usage can induce osteoporosis, diabetes, and hypertension.
  3. Antibiotic therapy: is not indicated in the treatment of chronic bronchitis; however, macrolide therapy has been shown to have an anti-inflammatory property and hence may have a role in the treatment of chronic bronchitis.
  4. Phosphodiesterase-4 inhibitors: decrease inflammation and promote airway smooth muscle relaxation by preventing the hydrolysis of cyclic adenosine monophosphate, a substance when degraded, leads to the release of inflammatory mediators.

Non Pharmacological Measures

The most critical nonpharmacological intervention is smoking cessation. Smoking cessation improves mucociliary function and decreases goblet cell hyperplasia. Smoking cessation has also been shown to reduce airway injury resulting in lower levels of exfoliated mucus in tracheobronchial cells.

Pulmonary rehabilitation is an important part of treatment for chronic bronchitis is pulmonary rehabilitation which consists of education, lifestyle modification, regular physical activity, and avoidance of exposure to known pollutants either at work or living environment.[8]

Differential Diagnosis

  • Acute sinusitis
  • Alpha 1 antitrypsin (ATT) deficiency
  • Asthma
  • Bacterial pharyngitis
  • Bronchiectasis
  • Bronchiolitis
  • Bronchitis
  • Chronic obstructive pulmonary disease (COPD)
  • Chronic sinusitis
  • Influenza


The presence of chronic bronchitis is known to cause worsening airflow obstruction and a deterioration in lung function. Large epidemiological studies have shown that chronic mucus hypersecretion was associated with a decline in FEV1. Patients with chronic bronchitis symptoms had a threefold increased risk of developing new COPD compared to the asymptomatic population. Chronic bronchitis increases mortality. Those suffering from chronic bronchitis were found to have higher levels of serum IL8 and C reactive protein, which indicates that systemic inflammatory response could increase the risk of cardiac disease and other comorbidities. Chronic bronchitis also leads to a lessened quality of life.[8]

Enhancing Healthcare Team Outcomes

The management of chronic bronchitis is complex and lifelong. There is no cure for the disorder, and the patients are prone to many complications. Thus, the condition is best managed with an interprofessional team that consists of a primary care physician, respiratory physiotherapist, nurse practitioner, pulmonologist, infectious disease expert, radiologist, and internist. Chronic bronchitis has a significant impact on morbidity and quality of life. Smoking is a major contributor; hence smoking cessation needs to form an important strategy for prevention. Alteration in lifestyle and regular vaccination for influenza as well as pneumonia can reduce the morbidity in those who have chronic bronchitis. The overall prognosis for most patients is poor, with many patients being disabled from progressive shortness of breath.[9][10][11]

Review Questions


Mejza F, Gnatiuc L, Buist AS, Vollmer WM, Lamprecht B, Obaseki DO, Nastalek P, Nizankowska-Mogilnicka E, Burney PGJ., BOLD collaborators. BOLD study collaborators. Prevalence and burden of chronic bronchitis symptoms: results from the BOLD study. Eur Respir J. 2017 Nov;50(5) [PMC free article: PMC5699921] [PubMed: 29167298]
Ferré A, Fuhrman C, Zureik M, Chouaid C, Vergnenègre A, Huchon G, Delmas MC, Roche N. Chronic bronchitis in the general population: influence of age, gender and socio-economic conditions. Respir Med. 2012 Mar;106(3):467-71. [PubMed: 22197577]
Jetmalani K, Thamrin C, Farah CS, Bertolin A, Chapman DG, Berend N, Salome CM, King GG. Peripheral airway dysfunction and relationship with symptoms in smokers with preserved spirometry. Respirology. 2018 May;23(5):512-518. [PubMed: 29141272]
Imran S, Shan M, Muazam S. A Comparative Histological Study of Submucosal Gland Hypertrophy in Trachea of Mice Exposed to Cigarette and Shisha Smoke. J Coll Physicians Surg Pak. 2018 Mar;28(3):192-195. [PubMed: 29544574]
Song DJ, Song WJ, Kwon JW, Kim GW, Kim MA, Kim MY, Kim MH, Kim SH, Kim SH, Kim SH, Kim ST, Kim SH, Kim JK, Kim JH, Kim HJ, Kim HB, Park KH, Yoon JK, Lee BJ, Lee SE, Lee YM, Lee YJ, Lim KH, Jeon YH, Jo EJ, Jee YK, Jin HJ, Choi SH, Hur GY, Cho SH, Kim SH, Lim DH. KAAACI Evidence-Based Clinical Practice Guidelines for Chronic Cough in Adults and Children in Korea. Allergy Asthma Immunol Res. 2018 Nov;10(6):591-613. [PMC free article: PMC6182199] [PubMed: 30306744]
Perotin JM, Launois C, Dewolf M, Dumazet A, Dury S, Lebargy F, Dormoy V, Deslee G. Managing patients with chronic cough: challenges and solutions. Ther Clin Risk Manag. 2018;14:1041-1051. [PMC free article: PMC5995432] [PubMed: 29922064]
Smith DRM, Dolk FCK, Pouwels KB, Christie M, Robotham JV, Smieszek T. Defining the appropriateness and inappropriateness of antibiotic prescribing in primary care. J Antimicrob Chemother. 2018 Feb 01;73(suppl_2):ii11-ii18. [PMC free article: PMC5890733] [PubMed: 29490061]
Arkhipov V, Arkhipova D, Miravitlles M, Lazarev A, Stukalina E. Characteristics of COPD patients according to GOLD classification and clinical phenotypes in the Russian Federation: the SUPPORT trial. Int J Chron Obstruct Pulmon Dis. 2017;12:3255-3262. [PMC free article: PMC5680946] [PubMed: 29138554]
Reddel HK, Gerhardsson de Verdier M, Agustí A, Anderson G, Beasley R, Bel EH, Janson C, Make B, Martin RJ, Pavord I, Price D, Keen C, Gardev A, Rennard S, Sveréus A, Bansal AT, Brannman L, Karlsson N, Nuevo J, Nyberg F, Young SS, Vestbo J. Prospective observational study in patients with obstructive lung disease: NOVELTY design. ERJ Open Res. 2019 Feb;5(1) [PMC free article: PMC6355976] [PubMed: 30723727]
Kania A, Krenke R, Kuziemski K, Czajkowska-Malinowska M, Celejewska-Wójcik N, Kuźnar-Kamińska B, Farnik M, Bokiej J, Miszczuk M, Damps-Konstańska I, Grabicki M, Trzaska-Sobczak M, Sładek K, Batura-Gabryel H, Barczyk A. Distribution and characteristics of COPD phenotypes - results from the Polish sub-cohort of the POPE study. Int J Chron Obstruct Pulmon Dis. 2018;13:1613-1621. [PMC free article: PMC5963485] [PubMed: 29844667]
Golpe R, Suárez-Valor M, Martín-Robles I, Sanjuán-López P, Cano-Jiménez E, Castro-Añón O, Pérez de Llano LA. Mortality in COPD patients according to clinical phenotypes. Int J Chron Obstruct Pulmon Dis. 2018;13:1433-1439. [PMC free article: PMC5936010] [PubMed: 29750029]

Disclosure: Allen Widysanto declares no relevant financial relationships with ineligible companies.

Disclosure: George Mathew declares no relevant financial relationships with ineligible companies.

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Bookshelf ID: NBK482437PMID: 29494044


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