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Bronchitis

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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]
Synonyms and keywords: Inflammation of bronchus

Overview

Overview

Bronchitis is an inflammation of the bronchi (medium and large size airways).[1] Acute bronchitis is a self-limiting disease usually caused by viruses or bacteria. Chronic bronchitis is a subtype of the chronic obstructive pulmonary disease (COPD), and it is defined as a chronic productive cough for at least three months in two consecutive years, after excluding other causes of chronic cough. The inflammatory response of the bronchial epithelium to infections or irritants that involve the medium and large-sized airways results in thickening of the bronchial and tracheal mucosa. Hallmark features of the pathophysiology of chronic bronchitis include hyperplasia and hypertrophy of the goblet cells of the airway, resulting in an increased mucus secretion, which contributes to the airway obstruction. Microscopically, there is infiltration of the walls of the airway with inflammatory cells, particularly neutrophils. Inflammation is followed by scarring and remodeling that thickens the walls, resulting in narrowing of the small airway. Further progression leads to metaplasia and fibrosis of the lower airway. The consequence of these changes is a limitation of airflow.[2][3][4] Acute bronchitis affects young children and old people. Its overall incidence is approximately 5% in the U.S. There is no racial or gender predilection for this disease.[5][6][7]Although chronic bronchitis is common among geriatric patients, it occurs more commonly among caucasian individuals compared to other races, and there is no sexual predilection.[8] Age, season of the year and the immunization status are the main determining risk factors for acquiring acute bronchitis.[9][6][10] The most potent risk factor in the development of chronic bronchitis is cigarette smoking.[11] Other risk factors are occupational pollutants such as cadmium and silica, air pollutants, and genetic factors such as alpha 1 antitrypsin deficiency[12] Acute bronchitis is a self limiting lower respiratory tract infection that usually presents with cough that lasts for up to 3 weeks.[9][13] Chronic bronchitis gradually worsens over time and can result in death. The rate of deterioration varies between individuals and depends on the level of airflow obstruction. The prognosis is dependent on early recognition and smoking cessation, which improves the outcome significantly. Smoking cessation, good hand hygiene, vaccination, and a reduction in occupational exposure to known risk factors, are important to ensure decreased severity and risk of bronchitis.[10][14]

Causes

Causes

  • Acute Bronchitis: may be caused by either viruses, bacteria or environmental factors.
Viruses: Influenza virus, parainfluenza virus, respiratory syncytial virus, coronavirus, adenovirus, enterovirus, rhinovirus, coxsackievirus, and human metapneumovirus[15][16][17]
Bacteria: Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Bordetella pertussis[6]
Environmental factors: Toxic fume inhalation, tobacco, dust, and aerosols[18]
  • Chronic Bronchitis: may be caused by smoking, air pollutants and occupational exposures in a genetically susceptible person.


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

Overview

Virus are thought to be the most common cause of acute bronchitis. Influenza A and B, parainfluenza, respiratory syncytial virus, coronavirus are the most commonly involved pathogens. Bacteria, such as mycoplasma, chlamydiae and bordetella pertussis, are also found to cause acute bronchitis. Smoking, occupational exposures, air pollutants, and genetic factors are etiologies of chronic bronchitis.

Causes

  • Acute Bronchitis: may be caused by either viruses, bacteria or environmental factors.
Viruses: Influenza virus, parainfluenza virus, respiratory syncytial virus, coronavirus, adenovirus, enterovirus, rhinovirus, coxsackievirus, and human metapneumovirus[1][2][3]
Bacteria: Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Bordetella pertussis[4]
Environmental factors: Toxic fume inhalation, tobacco, dust, and aerosols[5]
  • Chronic Bronchitis: may be caused by smoking, air pollutants, occupational exposures, and genetic factors
Smoking
The primary risk factor for COPD is chronic tobacco smoking. In the United States, 80 to 90% of cases of COPD are due to smoking.[6][7] Exposure to cigarette smoke is measured in pack-years, the average number of packages of cigarettes smoked daily multiplied by the number of years of smoking.[8] The likelihood of developing COPD increases with age and cumulative smoke exposure. Almost all life-long smokers will develop COPD.[9]
Occupational Exposures
Intense and prolonged exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry, and chemicals such as cadmium, isocyanates, and fumes from welding, have been implicated in the development of airflow obstruction, even in nonsmokers.[10] Workers who smoke and are exposed to these particles and gases are even more likely to develop COPD. Intense silica dust exposure causes silicosis, a restrictive lung disease distinct from COPD; however, less intense silica dust exposures have been linked to a COPD-like condition.[11] The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of cigarette smoking.[12]
Air Pollution
Studies in many countries reveal that people who live in large cities have a higher rate of COPD compared to people who live in rural areas.[13] Urban air pollution may be a contributing factor for COPD, as it is thought to slow the normal growth of the lungs, although the long-term research needed to confirm the link has not been performed. Studies of the industrial waste gas and COPD/asthma-aggravating compound, sulfur dioxide, and the inverse relation to the presence of the blue lichen Xanthoria (usually found abundantly in the countryside, but never in towns or cities) suggest that combustive industrial processes do not aid COPD sufferers. In many developing countries, indoor air pollution from cooking fire smoke (often using biomass fuels such as wood and animal dung) is a common cause of COPD, especially in women.[14]
Genetics
Some factor in addition to heavy smoke exposure is required for a person to develop COPD. This factor is probably a genetic susceptibility. COPD is more common among relatives of COPD patients who smoke than unrelated smokers.[15] The genetic differences that make some peoples’ lungs susceptible to the effects of tobacco smoke are mostly unknown. Alpha 1-antitrypsin deficiency is a genetic condition that is responsible for approximately 2% of cases of COPD. In this condition, the body does not make enough of the protein alpha 1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damage caused by protease enzymes, such as elastase and trypsin, that can be released as a result of an inflammatory response to tobacco smoke.[16]

Common Causes

Causes by Organ System

Cardiovascular Heart disease
Chemical / poisoning Acenaphthene, acetaldehyde, acetic acid, acetic anhydride, biphenyl, chlorine dioxide, ethyleneamine, hexamethylene diisocyanate, nitric acid, phosphine, polychlorinated dibenzofurans, selenium poisoning, silver, sulfuric acid, toluene diisocyanate, vanadium poisoning
Dermatologic Yellow nail syndrome
Drug Side Effect Albuterol, alferon N, alfuzosin, artemether and lumefantrin, belimumab, benazepril, budesonide, butorphanol, candesartan, captafol, cardura, cevimeline, ciclesonide, citalopram, clopidogrel, crofelemer, doxazosin, enalapril maleate, escitalopram, exemestane, febuxostat, felodipine, fingolimod, fluoxetine, fluvoxamine, goserelin, ibandronate, infliximab, interferon, ipratropium, irbesartan, isosorbide dinitrate, isosorbide mononitrate, itraconazole, lamotrigine, latanoprost, leflunomide, lumigan, methotrexate, metipranolol, metronidazole topical, minoxidil, moexipril, mycophenolate, mycophenolic acid, nateglinide, nitisinone, oseltamivir, oxcarbazepine, paroxetine, pentamidine isethionate, pirbuterol, pramipexole, repaglinide, risedronate, ropinirole, rosuvastatin, sertraline, sibutramine, simvastatin, tacrolimus, tamsulosin, tarka (medication), telmisartan, thalidomide, tiagabine, tobramycin, tolterodine, topiramate, trandolapril, travoprost, unoprostone, zanamivir
Ear Nose Throat Pharyngitis, sinusitis
Endocrine No underlying causes
Environmental Air pollution, aluminium lung, anthracosis, coal dust, coal worker’s pneumoconiosis, farmer’s lung, mesothelioma, pneumoconiosis, silicosis, smoking
Gastroenterologic Alpha 1-antitrypsin deficiency, cystic fibrosis, gastroesophageal reflux disease, inflammatory bowel disease
Genetic Alpha 1-antitrypsin deficiency, ataxia telangiectasia, cystic fibrosis, Gulf War syndrome, Klinefelter syndrome
Hematologic No underlying causes
Iatrogenic Lung transplantation
Infectious Disease Acute viral nasopharyngitis (common cold), adenovirus, aspergillosis, bordetella pertussis, chickenpox, chlamydia pneumonia, common cold, coronavirus, coxsackievirus, echovirus, encephalitozoon cuniculi infection, enterovirus, flu, group A streptococcal infection, HIV, influenza, measles, moraxella catarrhalis, mycoplasma pneumonia, orthomyxovirus, paragonimiasis, parainfluenza, paramyxovirus, pharyngitis, pneumococcus, respiratory syncytial virus, rhinovirus, trichinellosis
Musculoskeletal / Ortho Prune belly syndrome
Neurologic Ataxia telangiectasia, Gulf War syndrome
Nutritional / Metabolic Hypoglycemia
Obstetric/Gynecologic No underlying causes
Oncologic Lung cancer, mesothelioma
Opthalmologic No underlying causes
Overdose / Toxicity Marijuana abuse, nicotine addiction
Psychiatric No underlying causes
Pulmonary Acute viral nasopharyngitis (common cold), alpha 1-antitrypsin deficiency, aluminium lung, anthracosis, aspergillosis, asthma, blue and bloated syndrome, bronchiectasis, bronchiolitis, coal worker’s pneumoconiosis, common cold, COPD, farmer’s lung, flu, influenza, lung cancer, lung transplantation, mesothelioma, yellow nail syndrome
Renal / Electrolyte No underlying causes
Rheum / Immune / Allergy Asthma, Felty’s syndrome, Gulf War syndrome, IgG deficiency, Immunoglobulin G subclass deficiency, MHC class I deficiency, primary immunodeficiency, Sjogren’s syndrome
Sexual No underlying causes
Trauma No underlying causes
Urologic Prune belly syndrome
Miscellaneous Tobacco smoking

Causes in Alphabetical Order

Causes Based on Classification

Acute Bronchitis

The following factors exacerbate bronchitis:

Chronic Bronchitis

Chronic bronchitis is a long-term condition. People have a cough that produces excessive mucus. To be diagnosed with chronic bronchitis, a patient must have a cough with mucus most days of the month for at least 3 months.

References

  1. ↑ Jonsson JS, Sigurdsson JA, Kristinsson KG, Guthnadóttir M, Magnusson S (1997). “Acute bronchitis in adults. How close do we come to its aetiology in general practice?”. Scand J Prim Health Care. 15 (3): 156–60. PMID 9323784.
  2. ↑ Boivin G, Abed Y, Pelletier G, Ruel L, Moisan D, Côté S, Peret TC, Erdman DD, Anderson LJ (2002). “Virological features and clinical manifestations associated with human metapneumovirus: a new paramyxovirus responsible for acute respiratory-tract infections in all age groups”. J. Infect. Dis. 186 (9): 1330–4. doi:10.1086/344319. PMID 12402203.
  3. ↑ Louie JK, Hacker JK, Gonzales R, Mark J, Maselli JH, Yagi S, Drew WL (2005). “Characterization of viral agents causing acute respiratory infection in a San Francisco University Medical Center Clinic during the influenza season”. Clin. Infect. Dis. 41 (6): 822–8. doi:10.1086/432800. PMID 16107980.
  4. ↑ Wenzel RP, Fowler AA (2006). “Clinical practice. Acute bronchitis”. N. Engl. J. Med. 355 (20): 2125–30. doi:10.1056/NEJMcp061493. PMID 17108344.
  5. ↑ Irwin RS, Madison JM (2000). “The diagnosis and treatment of cough”. N. Engl. J. Med. 343 (23): 1715–21. doi:10.1056/NEJM200012073432308. PMID 11106722.
  6. ↑ MedicineNet.com – COPD causes
  7. ↑ 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)
  8. ↑ “Definition of pack year – NCI Dictionary of Cancer Terms”.
  9. ↑ Template:Cite doi
  10. ↑ 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)
  11. ↑ Hnizdo E, Vallyathan V (2003). “Chronic obstructive pulmonary disease due to occupational exposure to silica dust: a review of epidemiological and pathological evidence”. Occup Environ Med. 60 (4): 237–43. doi:10.1136/oem.60.4.237. PMC 1740506. PMID 12660371. Unknown parameter |month= ignored (help)
  12. ↑ Loscalzo, Joseph; Fauci, Anthony S.; Braunwald, Eugene; Dennis L. Kasper; Hauser, Stephen L; Longo, Dan L. (2008). Harrison’s Principles of Internal Medicine (17th ed.). McGraw-Hill Professional. ISBN 0-07-146633-9.
  13. ↑ Halbert RJ, Natoli JL, Gano A, Badamgarav E, Buist AS, Mannino DM (2006). “Global burden of COPD: systematic review and meta-analysis”. Eur. Respir. J. 28 (3): 523–32. doi:10.1183/09031936.06.00124605. PMID 16611654. Unknown parameter |month= ignored (help)
  14. ↑ 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)
  15. ↑ Silverman EK, Chapman HA, Drazen JM; et al. (1998). “Genetic epidemiology of severe, early-onset chronic obstructive pulmonary disease. Risk to relatives for airflow obstruction and chronic bronchitis”. Am. J. Respir. Crit. Care Med. 157 (6 Pt 1): 1770–8. PMID 9620904. Unknown parameter |month= ignored (help)
  16. ↑ MedlinePlus Encyclopedia 000091

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Classification

Classification

Bronchitis is classified into two major categories based on symptom chronicity:

Differential diagnosis

Differential diagnosis

Organ System Disease Symptoms Signs Laboratory findings Diagnostic modality Management
Cardiac HFpEF Exertional dyspnea, reduced exercise tolerance, orthopnea, paroxysmal nocturnal dyspnea, edema Elevated JVP, fine crackles, edema Increased BNP Echocardiography (normal EF) Control of volume overload and hypertension,

treatment of underlying condition (obesity, AF, coronary artery disease, anemia)

HFrEF Exertional dyspnea, reduced exercise tolerance, orthopnea, paroxysmal nocturnal dyspnea, edema Elevated JVP, fine crackles, edema Increased BNP Echocardiography (reduced EF) Diuretics, ACE inhibitors, ARBs, beta blockers, nitrates
Pericardial disease Exercise intolerance, dyspnea, fatigue Elevated JVP, pericardial knock, kussmaul’s sign, pulsus paradoxus – Echocardiography, ECG Diuretics, pericardiectomy
Hypertrophic cardiomyopathy Dyspnea, chest pain, palpitation, lightheadedness Systolic murmur – Echocardiography, ECG Beta blockers, verapamil
Valvular disease

(MR, TR)

Edema, fatigue, exercise intolerance, dyspnea, lightheadedness Cardiac murmur – Echocardiography, ECG Valve repair or replacement, diuretics, beta blockers
Pulmonary Chronic airway disease Cough, dyspnea, chest pain, exercise intolerance Tachypnea, respiratory distress, cyanosis, edema, rhonchi and crackles Hypoxemia, hypercapnea, polycythemia, PFT, chest imaging Bronchodilators, corticosteroids, anticholinergics
Interstitial lung diseaee Exercise intolerance, cough Crackles, clubbing, cyanosis Hypoxemia PFT, Chest imaging, lung biopsy Corticosteroids, bronchodilators
Pulmonary hypertension Dyspnea, fatigue, chest pain, syncope, palpitation Edema, clubbing, elevated JVP, TR murmur Elevated BNP, elevated d-dimer Echocardiography, cardiac cathaterization Diuretics, calcium channel blockers, endothelin receptor antagonist, phosphodiesterase 5 inhibitor
Sleep apnea Snoring, somnolence, headache, fatigue, irritability Tachypnea, hypertension, tachycardia Hypoxemia, polycythemia Polysomnography Weight reduction, CPAP
Asthma Dry cough, dyspnea, wheezing Wheezing, tachypnea Hypoxemia PFT Bronchodilators, corticosteroids, anticholinergics


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

Overview

Bronchitis must be differentiated from other diseases that cause cough such as asthma, pneumonia, bronchiectasis and CHF.

Differential Diagnosis

The Bronchitis must be differentiated from other diseases that may cause cough, dyspnea and wheezing[1].

Disease Findings
Pneumonia Presents with acute fever, cough and shortness of breath, although pulmonary infiltrate on chest x-ray is an imaging finding.[2]
Asthma Presents with cough, dyspnea and wheezing and typically is a chronic condition which typically starts during childhood.[3]
Bronchiectasis Presents copious purulent sputum, coarse crackles, clubbing and CT findings suggestive of bronchiectasis.[3]
Gastroesophageal Reflux Disease May present with chronic dry cough but the typical symptom is heart burn.[4][5]
Congestive heart failure Features with orthopnea, paroxysmal nocturnal dyspnea, fine crackles on auscultation and chest x-ray findings of cardiac enlargement and pulmonary congestion (Kerley B lines, and pleural effusion).

References

  1. ↑ Albert RH (2010). “Diagnosis and treatment of acute bronchitis”. Am Fam Physician. 82 (11): 1345–50. PMID 21121518.
  2. ↑ 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.
  3. ↑ 3.0 3.1 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.
  4. ↑ Singh A (2009). “Asthma in older adults”. CMAJ. 181 (12): 929. doi:10.1503/cmaj.109-2049. PMC 2789137. PMID 19969583.
  5. ↑ Irwin RS, Baumann MH, Bolser DC, Boulet LP, Braman SS, Brightling CE, Brown KK, Canning BJ, Chang AB, Dicpinigaitis PV, Eccles R, Glomb WB, Goldstein LB, Graham LM, Hargreave FE, Kvale PA, Lewis SZ, McCool FD, McCrory DC, Prakash UB, Pratter MR, Rosen MJ, Schulman E, Shannon JJ, Smith Hammond C, Tarlo SM (2006). “Diagnosis and management of cough executive summary: ACCP evidence-based clinical practice guidelines”. Chest. 129 (1 Suppl): 1S–23S. doi:10.1378/chest.129.1_suppl.1S. PMC 3345522. PMID 16428686.

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References

References

  1. ↑ Bronchitis (Chest Cold) – Get Smart: Know When Antibiotics Work. Centers for Disease Control and Prevention (2015). http://www.cdc.gov/getsmart/community/for-patients/common-illnesses/bronchitis.html Accessed on July 28, 2016
  2. ↑ Cosio MG, Saetta M, Agusti A (2009). “Immunologic aspects of chronic obstructive pulmonary disease”. N. Engl. J. Med. 360 (23): 2445–54. doi:10.1056/NEJMra0804752. PMID 19494220.
  3. ↑ Kumar P, Clark M (2005). Clinical Medicine, 6ed. Elsevier Saunders. pp 900-901. ISBN 0702027634.
  4. ↑ McDonough JE, Yuan R, Suzuki M, Seyednejad N, Elliott WM, Sanchez PG, Wright AC, Gefter WB, Litzky L, Coxson HO, Paré PD, Sin DD, Pierce RA, Woods JC, McWilliams AM, Mayo JR, Lam SC, Cooper JD, Hogg JC (2011). “Small-airway obstruction and emphysema in chronic obstructive pulmonary disease”. N. Engl. J. Med. 365 (17): 1567–75. doi:10.1056/NEJMoa1106955. PMC 3238466. PMID 22029978.
  5. ↑ Macfarlane J, Holmes W, Gard P, Macfarlane R, Rose D, Weston V, Leinonen M, Saikku P, Myint S (2001). “Prospective study of the incidence, aetiology and outcome of adult lower respiratory tract illness in the community”. Thorax. 56 (2): 109–14. PMC 1746009. PMID 11209098.
  6. ↑ 6.0 6.1 6.2 Wenzel RP, Fowler AA (2006). “Clinical practice. Acute bronchitis”. N. Engl. J. Med. 355 (20): 2125–30. doi:10.1056/NEJMcp061493. PMID 17108344.
  7. ↑ Ferri FF. Ferri’s Clinical Advisor 2016, 5 Books in 1. Elsevier Health Sciences; 2015.
  8. ↑ wrongdiagnosis.com > Prevalence and Incidence of COPD Retrieved on Mars 14, 2010
  9. ↑ 9.0 9.1 Gonzales R, Sande MA (2000). “Uncomplicated acute bronchitis”. Ann. Intern. Med. 133 (12): 981–91. PMID 11119400.
  10. ↑ 10.0 10.1 Albert RH (2010). “Diagnosis and treatment of acute bronchitis”. Am Fam Physician. 82 (11): 1345–50. PMID 21121518.
  11. ↑ MedicineNet.com – COPD causes
  12. ↑ MedlinePlus Medical Encyclopedia
  13. ↑ Landau LI (2006). “Acute and chronic cough”. Paediatr Respir Rev. 7 Suppl 1: S64–7. doi:10.1016/j.prrv.2006.04.172. PMID 16798599.
  14. ↑ Braman SS (2006). “Chronic cough due to acute bronchitis: ACCP evidence-based clinical practice guidelines”. Chest. 129 (1 Suppl): 95S–103S. doi:10.1378/chest.129.1_suppl.95S. PMID 16428698.
  15. ↑ Jonsson JS, Sigurdsson JA, Kristinsson KG, Guthnadóttir M, Magnusson S (1997). “Acute bronchitis in adults. How close do we come to its aetiology in general practice?”. Scand J Prim Health Care. 15 (3): 156–60. PMID 9323784.
  16. ↑ Boivin G, Abed Y, Pelletier G, Ruel L, Moisan D, Côté S, Peret TC, Erdman DD, Anderson LJ (2002). “Virological features and clinical manifestations associated with human metapneumovirus: a new paramyxovirus responsible for acute respiratory-tract infections in all age groups”. J. Infect. Dis. 186 (9): 1330–4. doi:10.1086/344319. PMID 12402203.
  17. ↑ Louie JK, Hacker JK, Gonzales R, Mark J, Maselli JH, Yagi S, Drew WL (2005). “Characterization of viral agents causing acute respiratory infection in a San Francisco University Medical Center Clinic during the influenza season”. Clin. Infect. Dis. 41 (6): 822–8. doi:10.1086/432800. PMID 16107980.
  18. ↑ Irwin RS, Madison JM (2000). “The diagnosis and treatment of cough”. N. Engl. J. Med. 343 (23): 1715–21. doi:10.1056/NEJM200012073432308. PMID 11106722.

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