Chronic bronchitis overview

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

## Overview[edit | edit source]

Bronchitis is an inflammation of the bronchi (medium-size airways) in the lungs. Chronic bronchitis is not necessarily caused by infection and is generally part of a syndrome called chronic obstructive pulmonary disease (COPD); it is defined clinically as persistent cough that produces sputum (phlegm) and mucus for at least three months in two consecutive years. Smoking is the most important risk factor. Typically, it progress to debilitating disease if left untreated. The corner stones for medical therapy are, inhaled bronchodilators and steroids. Smoking cessation and decrease environmental exposure to pollutants are effective measures to control its progression and decrease mortality.

## Historical Perspective[edit | edit source]

Bronchitis was first described by Charles Badham in 1808. Rene Laennec described COPD in details and categorized it as emphysema and chronic bronchitis.[1][2]

## Pathophysiology[edit | edit source]

Hyperplasia and hypertrophy of the goblet cells (mucous gland) of the airway are the common pathologic features of chronic bronchitis. Chronic inflammation due to lymphocyte infiltration is seen on microscopy.[3] On microscopic histopathological analysis there is infiltration of the airway walls with inflammatory cells, particularly CD8+ T-lymphocytes and neutrophils.[4] Inflammation is followed by scarring and remodeling that thickens the walls resulting in narrowing of the small airways.

## Causes[edit | edit source]

Chronic bronchitis, as a subtype of COPD, is caused by multiple environmental and genetic factors. Smoking is the leading cause of chronic bronchitis. Other causes include: air pollutants, occupational exposures to dusts and coal, and auto-immune diseases.[5][6][7][8]

## Differentiating Chronic bronchitis from other Diseases[edit | edit source]

Chronic bronchitis must be differentiated from other causes of chronic cough and dyspnea which include: congestive heart failure, chronic asthma, bronchiectasis, and bronchiolitis obliterans.[9][10]

## Epidemiology and Demographics[edit | edit source]

COPD occurs in 34 out of 1000 patients greater than 65 years old[11] or approximately 25 million people if undiagnosed cases are included.[12] COPD is the third cause of death in the U.S.[13] Hispanics are less likely to report COPD than non-Hispanic whites and blacks (4.0% compared with 6.3% and 6.1%, respectively).[14] Chronic bronchitis mortality rates are higher among Caucasian than among African American or persons of all other races. Women were more likely to report COPD than men (6.7% compared with 5.2%).[14][15] Age adjusted death rates of men decreased between 1999 and 2014 but this rate was stable among women.

## Risk Factors[edit | edit source]

Common risk factors in the development of chronic bronchitis include cigarette smoking, air pollution, genetic factors, increasing age, male gender, allergy, and repeated airway infections.[16][17][18][17][19]

## Screening[edit | edit source]

There is no recommendation for routine screening for adults who do not present with features of chronic bronchitis, such as cough, dyspnea or chest pain, because asymptomatic decreases in lung capacity does not require treatment.[20]

## Natural History, Complications, and Prognosis[edit | edit source]

Prognosis may vary depending on the time of diagnosis and severity of airflow obstruction, which may be measured by FEV1, FVC, or FEV1/FVC. Chronic Bronchitis has a wide range of severity from well controlled chronic bronchitis to severe obstructed airways with multiple exacerbations that require hospitalization and even may develop into lung cancer.[21] COPD gradually deteriorates over time and can lead to death if left untreated. Common complications of chronic bronchitis include: recurrent pneumonia, depression, cor pulmonale, anemia, polycythemia. A good prognosis of COPD relies on an early diagnosis and prompt treatment. Most patients will have improvement in lung function once treatment is started.

## Diagnosis[edit | edit source]

Chronic bronchitis is defined clinically as persistent cough that produces sputum (phlegm), for at least three months in two consecutive years. Bronchitis may be indicated by an expectorating cough (also known as a productive cough, i.e. one that produces sputum), shortness of breath (dyspnea) and wheezing. Occasionally chest pains, fever, and fatigue or malaise may also occur.[22]

## History and Symptoms[edit | edit source]

The hallmark of chronic bronchitis is dyspnea. A positive history of chronic productive cough and shortness of breath is suggestive of chronic bronchitis. Some patients describe the dyspnea as air hunger due to the sensation of gasping for air.[23]

### Physical Examination[edit | edit source]

Chronic bronchitis can be diagnostically evaluated by physical examination through auscultation. Physical examination is quite specific and sensitive for severe disease. The signs are usually difficult to detect in cases of mild to moderate diseases. Findings on general physical examination can be cyanosis, tachypnea, use of accessory respiratory muscles, paradoxical indrawing of lower intercostal spaces (known as the Hoover sign), elevated jugular venous pulse and peripheral edema. Pulmonary examination findings include barrel chest (emphysema), wheezing, hyperresonance, crackles and rhonchi.[18]

### Laboratory Findings[edit | edit source]

Cronic bronchitis has irreversible airflow limitation, especially during forced expiration. This is due to the destruction of lung tissue and increase in resistance to flow in the conducting airways. Thus, it doesn't show an improvement in FEV1 post bronchodilator administration, unlike asthma. This characteristic feature is used as an diagnostic criteria for COPD (i.e. a COPD is diagnosed by spirometry if FEV1/FVC < 70% for a matched control).[24] Arterial blood gas may show hypoxemia with or without hypercapnia depending on the disease severity. pH may be normal due to renal compensation. A pH less than 7.3 usually indicate severe respiratory compromise. A blood sample taken from an artery (i.e. Arterial Blood Gas (ABG)), can be tested for blood gas levels which may show hypoxemia and/or hypercapnia (respiratory acidosis if pH is also decreased). A blood sample taken from a vein may show a high blood count (reactive polycythemia), a reaction to long-term hypoxemia.

### Electrocardiogram[edit | edit source]

Electrocardiographic findings in chronic bronchitis includes: P pulmonale, Right ventricular strain, Right ventricular hypertrophy, and S1S2S3 pattern.[25]

### X Ray[edit | edit source]

Generally, chest x ray is not recommended for chronic bronchitis diagnosis, but it is common to order it to rule out other causes of dyspnea and productive cough such as: pneumonia and heart failure. The common findings for chronic bronchitis include: hyperinflation and hyperlucency of the lungs.[18]

### CT[edit | edit source]

CT scan is not generally required for chronic bronchitis but it is helpful to rule out other causes of dyspnea and chronic cough.

### Echocardiography[edit | edit source]

Echocardiography is helpful to diagnose pulmonary hypertension in patients with long standing chronic bronchitis.

## Treatment[edit | edit source]

The main goal of chronic bronchitis treatment is to improve the lung function and slow down the loss of its function. In this regard the treatment plan is divided in to two main categories:

1. Reduce symptoms: by relief of dyspnea and improve exercise tolerance
2. Reduce risks: by treating exacerbations, preventing disease progression and reducing mortality

### Medical Therapy[edit | edit source]

Inhaled bronchodilators and steroids are the corner stones of medical therapy for chronic bronchitis.

### Primary Prevention[edit | edit source]

Smoking cessation, control of air pollutants and decreased job exposure to dusts or fumes are the main preventative measures for chronic bronchitis.[26]

### Secondary Prevention[edit | edit source]

Smoking cessation and decreased occupational exposure are the corner stones to decreasing the mortality and morbidity of chronic bronchitis.

## References[edit | edit source]

1. ↑ terms(2016)https://lunginstitute.com/blog/history-of-chronic-bronchitis/accessed on September,13 2016
2. ↑ Klippe HJ, Kirsten D (2009). "[200 years of bronchitis--from 1808 to 2008]". Pneumologie (in German). 63 (4): 228–30. doi:10.1055/s-0028-1119572. PMID 19343614.CS1 maint: Unrecognized language (link)
3. ↑ Hogg JC (2004). "Pathophysiology of airflow limitation in chronic obstructive pulmonary disease". Lancet. 364 (9435): 709–21. doi:10.1016/S0140-6736(04)16900-6. PMID 15325838.
4. ↑ Baraldo S, Turato G, Badin C, Bazzan E, Beghé B, Zuin R, Calabrese F, Casoni G, Maestrelli P, Papi A, Fabbri LM, Saetta M (2004). "Neutrophilic infiltration within the airway smooth muscle in patients with COPD". Thorax. 59 (4): 308–12. PMC 1763819. PMID 15047950.
5. ↑ MedicineNet.com - COPD causes
6. ↑ Young RP, Hopkins RJ, Christmas T, Black PN, Metcalf P, Gamble GD (2009). "COPD prevalence is increased in lung cancer, independent of age, sex and smoking history". Eur. Respir. J. 34 (2): 380–6. doi:10.1183/09031936.00144208. PMID 19196816. Unknown parameter `|month=` ignored (help)CS1 maint: Multiple names: authors list (link)
7. ↑ Devereux, Graham (2006). "Definition, epidemiology, and risk factors". BMJ. 332 (7550): 1142–4. doi:10.1136/bmj.332.7550.1142. PMC 1459603. PMID 16690673. Unknown parameter `|month=` ignored (help)
8. ↑ Kennedy SM, Chambers R, Du W, Dimich-Ward H (2007). "Environmental and occupational exposures: do they affect chronic obstructive pulmonary disease differently in women and men?". Proceedings of the American Thoracic Society. 4 (8): 692–4. doi:10.1513/pats.200707-094SD. PMID 18073405. Unknown parameter `|month=` ignored (help)CS1 maint: Multiple names: authors list (link)
9. ↑ Busse WW (2011). "Asthma diagnosis and treatment: filling in the information gaps". J. Allergy Clin. Immunol. 128 (4): 740–50. doi:10.1016/j.jaci.2011.08.014. PMID 21875745.
10. ↑ Prina E, Ranzani OT, Torres A (2015). "Community-acquired pneumonia". Lancet. 386 (9998): 1097–108. doi:10.1016/S0140-6736(15)60733-4. PMID 26277247.
11. ↑ wrongdiagnosis.com > Prevalence and Incidence of COPD Retrieved on Mars 14, 2010
12. ↑ MORBIDITY & MORTALITY: 2009 CHART BOOK ON CARDIOVASCULAR, LUNG, AND BLOOD DISEASES National Heart, Lung, and Blood Institute
13. ↑ Kenneth D. Kochanek, M.A.; Jiaquan Xu, M.D.; Sherry L. Murphy, B.S.; Arialdi M. Minin˜o, M.P.H.; and Hsiang-Ching Kung, Ph.D., Division of Vital Statistics, Deaths: Final Data for 2009, 2011, 60,National Vital Statistics Reports, http://www.cdc.gov/nchs/data/nvsr/nvsr60/nvsr60_03.pdf
14. ↑ 14.0 14.1 Morbidity and Mortality Weekly Report (MMWR).(2011).https://www.cdc.gov/mmwr/preview/mmwrhtml/mm6146a2.htm Accessed on September 19,2016
15. ↑ Hogg JC, Chu F, Utokaparch S, Woods R, Elliott WM, Buzatu L, Cherniack RM, Rogers RM, Sciurba FC, Coxson HO, Paré PD (2004). "The nature of small-airway obstruction in chronic obstructive pulmonary disease". N. Engl. J. Med. 350 (26): 2645–53. doi:10.1056/NEJMoa032158. PMID 15215480.
16. ↑ PIERCE JA, HOCOTT JB, EBERT RV (1961). "The collagen and elastin content of the lung in emphysema". Ann. Intern. Med. 55: 210–22. PMID 13735539.
17. ↑ 17.0 17.1 Raherison C, Girodet PO (2009). "Epidemiology of COPD". Eur Respir Rev. 18 (114): 213–21. doi:10.1183/09059180.00003609. PMID 20956146.
18. ↑ 18.0 18.1 18.2 Mehta GR, Mohammed R, Sarfraz S, Khan T, Ahmed K, Villareal M, Martinez D, Iskander J, Mohammed R (2016). "Chronic obstructive pulmonary disease: A guide for the primary care physician". Dis Mon. 62 (6): 164–87. doi:10.1016/j.disamonth.2016.03.002. PMID 27087562.
19. ↑ Jeffery PK (2000). "Comparison of the structural and inflammatory features of COPD and asthma. Giles F. Filley Lecture". Chest. 117 (5 Suppl 1): 251S–60S. PMID 10843939.
20. ↑ Amir Qaseem, Timothy J. Wilt, Steven E. Weinberger, Nicola A. Hanania, Gerard Criner, Thys van der Molen, Darcy D. Marciniuk, Tom Denberg, Holger Schunemann, Wisia Wedzicha, Roderick MacDonald & Paul Shekelle (2011). "Diagnosis and management of stable chronic obstructive pulmonary disease: a clinical practice guideline update from the American College of Physicians, American College of Chest Physicians, American Thoracic Society, and European Respiratory Society". Annals of internal medicine. 155 (3): 179–191. doi:10.7326/0003-4819-155-3-201108020-00008. PMID 21810710. Unknown parameter `|month=` ignored (help)CS1 maint: Multiple names: authors list (link)
21. ↑ Mannino DM, Buist AS, Petty TL, Enright PL, Redd SC (2003). "Lung function and mortality in the United States: data from the First National Health and Nutrition Examination Survey follow up study". Thorax. 58 (5): 388–93. PMC 1746680. PMID 12728157.
22. ↑ Vanfleteren LE, Spruit MA, Wouters EF, Franssen FM (2016). "Management of chronic obstructive pulmonary disease beyond the lungs". Lancet Respir Med. doi:10.1016/S2213-2600(16)00097-7. PMID 27264777.
23. ↑ Festic E, Bansal V, Gajic O, Lee AS (2014). "Prehospital use of inhaled corticosteroids and point prevalence of pneumonia at the time of hospital admission: secondary analysis of a multicenter cohort study". Mayo Clin. Proc. 89 (2): 154–62. doi:10.1016/j.mayocp.2013.10.028. PMC 3989069. PMID 24485129.
24. ↑ Brusasco V, Martinez F (2014). "Chronic obstructive pulmonary disease". Compr Physiol. 4 (1): 1–31. doi:10.1002/cphy.c110037. PMID 24692133.
25. ↑ Lazović B, Svenda MZ, Mazić S, Stajić Z, Delić M (2013). "Analysis of electrocardiogram in chronic obstructive pulmonary disease patients". Med Pregl. 66 (3–4): 126–9. PMID 23653989.CS1 maint: Multiple names: authors list (link)
26. ↑ Joy M (2004). "Management of chronic obstructive pulmonary disease". N. Engl. J. Med. 351 (14): 1461–3, author reply 1461–3. PMID 15459997.

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