Bronchiectasis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Saarah T. Alkhairy, M.D.

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Saarah T. Alkhairy, M.D.

Overview

Bronchiectasis involves cycles of infections and inflammation that result in alveolar damage and inelastic dilated bronchi. Bronchiectasis may be classified based on either severity of localization of the disease. Bronchiectasis can be caused by both, congenital and acquired factors. Bronchiectasis must be differentiated from other diseases that cause dyspnea and cough, such as COPD, asthma, pneumonia, tuberculosis, chronic sinusitis, cough due to gastrointestinal reflux, upper airway cough syndrome, pulmonary carcinoma, and inhaled foreign body. Bronchiectasis is normally diagnosed after months or years of symptoms. The most common symptoms are a chronic cough and daily sputum production. The most common signs of bronchiectasis are coarse crackles, rhonchi, and wheezes on auscultation. There are both routine investigations and special case investigations. Routine investigations include sputum analysis, full blood count, and quantitative immunoglobulin levels. Cystic fibrosis and autoimmune testing are done if the patient is suspected of having an underlying condition. High-resolution computed tomography (HRCT) is the preferred diagnostic tool in identifying bronchiectasis. Along with treatment of bronchiectasis, it is important to treat the underlying condition if one is present. The medical therapy is divided into medical treatment and physiotherapy strategies. Surgical indications are life-threatening hemoptysis or disease that is unresponsive to medical treatment. Primary prevention of bronchiectasis is aimed at the prevention of future development with the avoidance of harmful substances, vaccinations, maintenance of a healthy body mass index (BMI), and the practice of physiologic strategies. To reduce the impact of the disease, patients should lead a healthy lifestyle, use prophylactic treatment when needed, do vaccinations, and practice physiotherapy strategies.

Historical Perspective

In 1819, René Laennec, inventor of the stethoscope, was the first to describe bronchiectasis. In 1880s, Dr. William Osler, a Canadian physican, was the first to research bronchiectasis in detail.

Pathophysiology

Bronchiectasis involves cycles of infections and inflammation that result in alveolar damage and inelastic dilated bronchi. Damage to the airway results in airflow obstruction and impaired clearance of secretions.

Classification

Bronchiectasis may be classified based on either severity of localization of the disease. Based on severity, there are three pathological subtypes of bronchiectasis: Tubular/fusiform, varicose, and saccular. Based on localization, bronchiectasis may be either localized or generalized.

Causes

Bronchiectasis can be caused by both, congenital and acquired factors. Congenital factors include conditions such as kartagener syndrome, cystic fibrosis, young’s syndrome, yellow nail syndrome, alpha 1-antitrypsin deficiency, and primary immunodeficiencies. Acquired factors include post-infectious, AIDS, IBD, APBD, COPD, airway obstructions, alcohol, drugs, and irritants.

Differential Diagnosis

Bronchiectasis must be differentiated from other diseases that cause dyspnea and cough, such as COPD, asthma, pneumonia, tuberculosis, chronic sinusitis, cough due to gastrointestinal reflux, upper airway cough syndrome, pulmonary carcinoma, and inhaled foreign body.

Epidemiology and Demographics

Bronchiectasis affects extremes of age in certain indigenous populations with a slight female dominance. It is difficult to estimate the prevalence because it is often misdiagnosed. In developed countries, it is important to diagnose the underlying cause. The age of onset is adulthood. In developing countries, infection in childhood is a common cause.

Risk Factors

There are some congenital and acquired conditions that cause inflammation and increased mucus secretion and accumulation of the airways. This repeated cycle leads to the increased risk of bronchiectasis.

Screening

There is no routine screening for bronchiectasis. If the patient has an immune deficiency or primary ciliary dyskinesia then pulmonary function tests should be measures four times a year.

Natural History, Complications, and Prognosis

Bronchiectasis is normally diagnosed after months or years of symptoms. Patients have respiratory complications, infection, and hemoptysis. Death can be caused by cardiac and respiratory failure. Bronchiectasis shows a higher mortality with males, advanced age, poor functional status, severe disease based on radiographic findings, and evidence of hypoxemia and hypercapnia.

History and Symptoms

Symptoms of bronchiectasis can take months or even years to develop. The most common symptoms are a chronic cough and daily sputum production.

Physical Symptoms

The most common signs of bronchiectasis are coarse crackles, rhonchi, and wheezes on auscultation.

Diagnostic Studies

Laboratory Findings

There are both routine investigations and special case investigations. Routine investigations include sputum analysis, full blood count, and quantitative immunoglobulin levels. Cystic fibrosis and autoimmune testing are done if the patient is suspected of having an underlying condition.

Chest X-ray

Although the chest x-ray is not used for diagnosing bronchiectasis, it can be used for patients with respiratory symptoms who are suspected in having any of the differential diagnoses.

CT

High-resolution computed tomography (HRCT) is the preferred diagnostic tool in identifying bronchiectasis. Common findings include increased diameter of a bronchus, tree-in-bud abnormalities, and cysts with definable borders.

Other Imaging Findings

The bronchogram is no longer used for the diagnosis of bronchiectasis.

Other Diagnostic Studies

Other diagnostic tools that can be used are pulmonary function tests, electron microscope examination, and bronchoscopy.

Medical Therapy

Along with treatment of bronchiectasis, it is important to treat the underlying condition if one is present. The medical therapy is divided into medical treatment and physiotherapy strategies. The medical treatment consists of patient education and treatment of the acute exacerbations, prophylactic treatment, vaccination, and other therapies. The physiotherapy strategies focuses on airway clearance and pulmonary rehabilitation.

Surgery

Surgical indications are life-threatening hemoptysis or disease that is unresponsive to medical treatment.

Primary Prevention

Primary prevention of bronchiectasis is aimed at the prevention of future development with the avoidance of harmful substances, vaccinations, maintenance of a healthy body mass index (BMI), and the practice of physiologic strategies.

Secondary Prevention

To reduce the impact of the disease, patients should lead a healthy lifestyle, use prophylactic treatment when needed, do vaccinations, and practice physiotherapy strategies.

References

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Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Saarah T. Alkhairy, M.D.

Overview

In 1819, René Laennec, inventor of the stethoscope, described bronchiectasis for the first time. In 1880s, Dr. William Osler, a Canadian physican, has performed detailed researchs on bronchiectasis.

Bronchiectasis Historical Perspective

In 1819, René Laennec, inventor of the stethoscope, described bronchiectasis for the first time.^[1]
René Laennec described bronchiectasis as an “abnormal dilatation of bronchi and bronchioles due to repeated cycles of airway infection and inflammation.”^[2]
In 1880s, Dr. William Osler, a Canadian physican has performed detailed researchs on bronchiectasis.^[3]

References

↑ Roguin, A. (2006). “Rene Theophile Hyacinthe Laennec (1781-1826): The Man Behind the Stethoscope”. Clinical Medicine & Research. 4 (3): 230–235. doi:10.3121/cmr.4.3.230. ISSN 1539-4182.
↑ O’Donnell, Anne E. (2008). “Bronchiectasis”. CHEST Journal. 134 (4): 815. doi:10.1378/chest.08-0776. ISSN 0012-3692.
↑ Wrong, O. (2003). “Osler and my father”. JRSM. 96 (9): 462–464. doi:10.1258/jrsm.96.9.462. ISSN 0141-0768.

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Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Saarah T. Alkhairy, M.D.

Overview

Bronchiectasis may be classified according to its severity into 3 sub types: tubular/fusiform, varicose, and saccular. Bronchiectasis may also be classified according to its location into 2 sub types: localized and generalized.

Classification

Based on Severity

Based on severity, bronchiectasis may be classified as follows:

Type	Features
Tubular or fusiform (cylindrical) bronchiectasis (follicular bronchiectasis)	Most common type. It is characterized by development of mildly inflamed bronchi that fail to taper distally^[1]^[2]
Varicose bronchiectasis	The bronchial walls appear beaded because areas of dilation are mixed with areas of constriction
Saccular (cystic) bronchiectasis	These are characterized by severe, irreversible ballooning of the bronchi peripherally, with or without air-fluid levels

Based on Location

Based on localization, bronchiectasis may be classified as follows:

Location	Features
Localized	Confined to one lobe only
Generalized	Involves more than one lobe

References

↑ Mysliwiec, V, Pina, JS (1999). “Bronchiectasis: the ‘other’ obstructive lung disease”. POSTGRADUATE MEDICINE. 106 (1): 252–63.
↑ O’Donnell, Anne E. (2008). “Bronchiectasis”. Chest. 134 (4): 815–823. doi:10.1378/chest.08-0776. ISSN 0012-3692.

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Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Saarah T. Alkhairy, M.D.

Overview

Bronchiectasis involves cycles of infections and inflammation that result in alveolar damage and inelastic dilated bronchi. Damage to the airway results in airflow obstruction and impaired clearance of secretions.

Pathophysiology

The following events summarize the pathophysiology of bronchiectasis:^[1]

Dilation of the bronchial walls results in airflow obstruction and impaired clearance of secretions.
The dilated areas interrupt normal air pressure of the bronchial tubes, causing sputum to pool inside the dilated areas instead of being pushed upward.
The sputum contains elastase, interleukin-8, tumor necrosis factor alpha (TNF-a), and prostanoids.
The pooled sputum provides an environment favorable to the growth of infectious pathogens.
Recurrent infections are followed inflammation and infiltration of neutrophils, macrophages, and T-lymphocytes.
The more infection that the lungs experience, leads to the sustained inflammation, consequently, damage to the alveoli in the lungs.
With more injury to the lung tissue, the elasticity in the bronchial tubes is reduced and the tubes are dilated, which creates a perpetual destructive cycle

Cole’s Cycle

The following events summarize Cole’s cycle (Cole’s “vicious cycle hypothesis”), which is the most widely known model of the development of bronchiectasis:^[2]

Two factors are required for the development of bronchiectasis:
- Persistent infection
- Host defense derangement
Impaired mucociliary clearance due to the genetic susceptibility may cause environmental insult.
Insults result in persistence of microbes in the sinobronchial tree.
The microbial infection can cause chronic inflammation, which may result in tissue damage and impaired mucociliary motility.
Inflammation ensues more infection, which in turn ensues more inflammation.

Immune Response

Bronchiectasis involves the activity of reactive oxygen species (ROS), elastases, and matrix metalloproteinases (MMPs):
- Reactive oxygen species (ROS)
  - A by product for the metabolism of oxygen
  - Increased concentration may result in cell structure damage

Elastase
- Protease that catalyzes the breaks down of elastin.
- Elastin plus collagen determine the mechanical properties of connective tissue.

Matrix metalloproteinases (MMPs)
- Responsible for the degradation of the majority of the extracellular proteins during normal tissue turn over.
- Inflammation may result in epithelial injury and mucus secretion via increased concentrations of ROS, elastase ciliotoxin, and mucus secretogogues.
- Epithelial injury and mucus hypersecretion lead to chronic bronchial infection, reduced mucociliary clearance, and plugging of the airway – which all eventually leads to airway damage and bronchiectasis.

The diagram below depicts the immune response for bronchiectasis:

Schematic representation of a vicious circle of events which occurs during chronic bronchial infection. IL: interleukin; TNF: tumour necrosis factor; LT: leukotriene; MMP: matrix metalloproteinase
European Respiratory Journal

Gross Pathology

Bronchiectasis Source:Case courtesy of Dr Yale Rosen, Radiopaedia.org, rID: 9307

References

↑ Morrissey BM (2007). “Pathogenesis of bronchiectasis”. Clin Chest Med. 28 (2): 289–96. PMID 17467548.
↑ King PT (2009). “The pathophysiology of bronchiectasis”. Int J Chron Obstruct Pulmon Dis. 4: 411–9. PMC 2793069. PMID 20037680.CS1 maint: PMC format (link)

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Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Saarah T. Alkhairy, M.D., Ogheneochuko Ajari, MB.BS, MS [3]

Overview

Bronchiectasis can be caused by both, congenital and acquired factors. Congenital factors include conditions such as Kartagener syndrome, cystic fibrosis, Young’s syndrome, yellow nail syndrome, alpha 1-antitrypsin deficiency, and primary immunodeficiencies. Acquired factors include post-infectious, AIDS, IBD, ABPA, COPD, airway obstructions, alcohol, drugs, and irritants.

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

Commom causes

Causes by Organ System

Cardiovascular	Immotile cilia syndrome, Kartagener syndrome, Marfan syndrome, primary ciliary dyskinesia, pulmonary artery aneurysm
Chemical/Poisoning	Ammonia, chlorine gas, irritants, nitrogen dioxide, silicates, talc
Dental	No underlying causes
Dermatologic	Systemic lupus erythematosus, yellow nail syndrome
Drug Side Effect	Drug use, heroin
Ear Nose Throat	Young’s syndrome
Endocrine	No underlying causes
Environmental	Bronchiolitis obliterans, smoke
Gastroenterologic	Alpha 1-antitrypsin deficiency, bronchial cyst, Crohn’s disease, cystic fibrosis, hiatus hernia, inflammatory bowel disease, irritable bowel syndrome, tracheoesophageal fistula, ulcerative colitis
Genetic	Alpha 1-antitrypsin deficiency, autosomal dominant polycystic kidney disease, Bloom syndrome, chronic granulomatous disease, Crohn’s disease, cystic fibrosis, diffuse panbronchiolitis, DiGeorge syndrome, hyper-IgE syndrome, immotile cilia syndrome, Kartagener syndrome, Marfan syndrome, Nezelof syndrome, primary ciliary dyskinesia, severe combined immunodeficiency, WHIM syndrome, X-linked agammaglobulinemia
Hematologic	Immunoglobulin M deficiency
Iatrogenic	Bone marrow transplantation, heart-lung transplant, lung transplantation
Infectious Disease	Adenovirus, allergic bronchopulmonary aspergillosis, bordetella pertussis, chronic bronchitis, herpes simplex virus, histoplasmosis, HIV AIDS, immotile cilia syndrome, influenza, Kartagener syndrome, klebsiella , laryngeal papillomatosis, measles, mycobacterium avium complex, mycobacterium tuberculosis, mycoplasma pneumoniae, pertussis, pneumonia, primary ciliary dyskinesia, pseudomonas aeruginosa, recurrent aspiration pneumonia, respiratory syncytial virus, staphylococcus aureus, tuberculosis, whooping cough
Musculoskeletal/Orthopedic	Marfan syndrome
Neurologic	Foreign body aspiration, pulmonary aspiration
Nutritional/Metabolic	Alpha 1-antitrypsin deficiency, cystic fibrosis
Obstetric/Gynecologic	Young’s syndrome
Oncologic	Airway adenoma, endobronchial teratoma, tumor
Ophthalmologic	Marfan syndrome
Overdose/Toxicity	No underlying causes
Psychiatric	Drug use, heroin
Pulmonary	Airway adenoma, airway obstruction, alpha 1-antitrypsin deficiency, bronchial cyst, bronchiolitis obliterans, bronchocentric granulomatosis, bronchomalacia, cartilage deficiency, chronic bronchitis, chronic obstructive pulmonary disease, cystic fibrosis, diffuse panbronchiolitis, ectopic bronchus, endobronchial teratoma, foreign body aspiration, immotile cilia syndrome, Kartagener syndrome, lipoid pneumonia, Mounier-Kuhn syndrome, pneumonia, primary ciliary dyskinesia, pulmonary artery aneurysm, pulmonary aspiration, recurrent aspiration pneumonia, sarcoidosis, tracheobronchial amyloidosis, tracheobronchomalacia, tracheobronchomegaly, tracheoesophageal fistula, tuberculosis, Williams-Campbell syndrome, yellow nail syndrome, Young’s syndrome
Renal/Electrolyte	Autosomal dominant polycystic kidney disease, systemic lupus erythematosus
Rheumatology/Immunology/Allergy	Allergies, ankylosing spondylitis, autoimmune diseases, Bruton’s agammaglobulinemia, chronic granulomatous disease, common variable immunodeficiency, connective tissue disease, Crohn’s disease, DiGeorge syndrome, hyper-IgE syndrome, hypogammaglobulinaemia, immunoglobulin M deficiency, inflammatory bowel disease, MHC class I deficiency, Nezelof syndrome, primary immunodeficiency, relapsing polychondritis, rheumatoid arthritis, sarcoidosis, selective deficiency of immunoglobulin G, selective immunoglobulin A deficiency, severe combined immunodeficiency, Sjögren’s syndrome, systemic lupus erythematosus, ulcerative colitis, WHIM syndrome, x-linked agammaglobulinemia
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Miscellaneous	Alcohol

Causes in Alphabetical Order

Causes Based on Mode of Infection

Bronchiectasis may be either congenital or acquired. Acquired bronchiectasis is more common than congenital bronchiectasis.

Congenital

The following table lists the congenital causes of bronchiectasis:

Causes	Description
Kartagener syndrome	Bronchiectasis is secondary to the impaired mobility of cilia in the lungs^[1]
Cystic fibrosis (CF)	A small number of patients develop severe localized bronchiectasis Development of bronchiectasis is mainly due to the increased risk of chronic sinopulmonary infections^[2]
Young’s Syndrome	Similar to CF and may be a genetic variant Development of bronchiectasis is mainly due to the increased risk of chronic sinopulmonary infections^[3]
Yellow Nail Syndrome	This is a rare disorder characterized by pleural effusions, lymphedema, and yellow dystrophic nails, chronic bronchitis, sinus infections, and bronchiectasis
Alpha 1-Antitrypsin Deficiency (AAD)	The pathophysiology of development of bronchiectasis among these patients is yet to be understood^[4]
Primary Immunodeficiencies	Bronchiectasis is caused by the weakened immune system’s response to severe, recurrent pulmonary infections^[5]

Acquired

Acquired bronchiectasis is more common than congenital bronchiectasis. The following table lists the acquired causes of bronchiectasis:

Causes	Description
Post Infectious (viral, bacterial, fungal, atypical mycobacterial)	Such as tuberculosis (either from bronchial stenosis or secondary traction from fibrosis), pneumonia, measles, pertussis
Acquired Immunodeficiency Syndrome (AIDS)	AIDS is caused by untreated HIV viral infection. Development of bronchiectasis is due to development of opportunistic pulmonary infections^[6]
Inflammatory Bowel Disease (IBD)	The exact pathogenesis is unknown for the link between inflammatory bowel disease and bronchiectasis Bronchiectasis is more common among patients with ulcerative colitis than those with Crohn’s disease
Allergic Bronchopulmonary Aspergillosis (ABPA)	Development of bronchiectasis is associated with inhalation of fungus spores^[7]
Connective Tissue Diseases such as Rheumatoid arthritis	Patterns of lung injury are common in connective tissue disease – which eventually leads to bronchiectasis
Airway obstructions	Such as tumors or enlarged lymph nodes These obstructions can block the airways leading to bronchiectasis
Chronic Obstructive Pulmonary Disease (COPD)	The mucus build up from COPD can lead to bronchiectasis
Environmental exposures such as ammonia	The environmental irritants cause inflammation in the airways that can lead to bronchiectasis
Alcoholism	Heavy drinking causes a deficiency of the antioxidant glutathione in the lungs, which increases the susceptibility of various lung diseases including bronchiectasis
Drug use such as heroin	Various drugs cause inflammation in the airways that can lead to bronchiectasis
Various allergies	Allergies cause inflammation in the airways that can lead to bronchiectasis^[8]

References

↑ Morillas HN, Zariwala M, Knowles MR (2007). “Genetic Causes of Bronchiectasis: Primary Ciliary Dyskinesia”. Respiration. 72 (3): 252–63. PMID 17534128.
↑ Dalrymple-Hay MJ, Lucas J, Connett G, Lea RE (1999). “Lung resection for the treatment of severe localized bronchiectasis in cystic fibrosis patients”. Acta Chir Hung. 38 (1): 23–5. PMID 10439089.
↑ Handelsman DJ, Conway AJ, Boylan LM, & Turtle JR (1984). “Young’s syndrome. Obstructive azoospermia and chronic sinopulmonary infections”. NEJM. 310 (1): 3–9.
↑ Shin MS, Ho KJ (1993). “Bronchiectasis in patients with alpha 1-antitrypsin deficiency. A rare occurrence?”. Chest. 104: 1384–86.
↑ Notarangelo LD, Plebani A, Mazzolari E, Soresina A, Bondioni MP (2007). “Genetic causes of bronchiectasis: primary immune deficiencies and the lung”. Respiration. 74 (3): 264–75. PMID 17534129.
↑ Sheikh S, Madiraju K, Steiner P, Rao M (1997). “Bronchiectasis in pediatric AIDS”. Chest. 112 (5): 1202–7. PMID 9367458.
↑ Ferguson HR, Convery RP (2002). “An unusual complication of ulcerative colitis”. Postgrad. Med. J. 78: 503.
↑ Lamari NM, Martins ALQ, Oliveira JV, Marino LC, Valério N (2006). “Bronchiectasis and clearence physiotherapy: emphasis in postural drainage and percussion”. Braz. j. cardiovasc. surg. (in Portuguese). 21 (2).

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Differentiating Bronchiectasis from other Disorders

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Saarah T. Alkhairy, M.D.

Overview

Bronchiectasis must be differentiated from other diseases that cause dyspnea and cough, such as COPD, asthma, pneumonia, tuberculosis, chronic sinusitis, lung cancer, postnasal drip and inhaled foreign body.

Bronchiectasis Differential Diagnosis

The following table lists the most common differential diagnoses of bronchiectasis based on chronic cough:^[1]^[2]

Organ system		Diseases	Clinical manifestations								Diagnosis				Other features
			Symptoms							Physical exam	Diagnosis
			Onset	Duration	Productive cough	Hemoptysis	Weight lost	Fever	Dyspnea	Ascultation	Lab findings	Imaging	PFT	Gold standard
Respiratory	Upper airway diseases	Laryngopharyngeal reflux^[3]^[4]	Chronic	Variable	+	−	−	−	+	Hoarseness Stridor	Decreased levels of salivary epidermal growth factor (EGF) Increased levels of NKTR Biopsy may be helpful	X−Ray may be helpful Endoscopy examination may be helpful as well	Normal function	24 hour−dual sensor pH probe	Throat clearing Globus sensation
Respiratory	Upper airway diseases	Rhinosinusitis^[5]^[6]	Acute, subacute, chronic, recurrent	Acute: Less than 4 weeks Subacute: 4−12 weeks Chronic: More than 12 weeks Recurrent: 4 or more episodes or acute rhinosinusitis per year	+	−	−	+	+	Clear chest	In complicated acute bacterial rhinosinusitis, endoscopic cultures or sinus aspirate is indicated Nasal culture may also be helpful	Air−fluid level, mucosal edema and bony erosion of sinus on CT MRI for distinguish the etiology	Normal function	Clinical diagnosis: Nasal congestion, obstruction, and purulent rhinorrhea	Erythema in periorbital area
Organ system		Diseases	Clinical manifestations								Diagnosis				Other features
			Symptoms							Physical exam	Diagnosis
			Onset	Duration	Productive cough	Hemoptysis	Weight lost	Fever	Dyspnea	Ascultation	Lab findings	Imaging	PFT	Gold standard
Respiratory	Lower airway	Asthma^[7]	Chronic	Years	+ Clear mucoid or yellow sputum	−	−	−	+	Wheezing (expiratory) Rales Rhonchi	Eosinophilia Total serum IgE in test for allergy may be helpful	Normal airways in chest X−ray CT if there any abnormality in chest X−Ray	FEV1/FVC ratio <70% and FEV1 >15% increase after 15 minutes of 2 puffs of beta 2 sympathomimetic drug After physical active FEV1 decreases by >15% After inhaled corticosteroid (ICS)FEV1 increased by >15%	Airflow limitation on spirometry	Family history Seasonal variation
		Chronic Bronchitis^[8]^[9]	Chronic	Most of the days for three months in the las two years.	+ Clear sputum	−	−	+	+	Wheezing Rhonchi	CBC and ABG may be helpful	Chest X−Ray to exclude other diseases CT may also be helpful	FEV1/FVC ratio < 70% Post bronchodilatador FEV1 > 80% Reduced FVC after bronchodilatador administration Decread vital capacity Increased total lung capacity	Demostration of airflow limitation on spirometry	Smoker’s cough Cigarette smoking Pollution
		Non−asthmatic eosinophilic bronchitis^[10]^[11]	Chronic	More than 8 weeks	+ Eosinophilic sputum	−	−	−	+	Wheezing Shortness of breath	High levels of IgE Airway eosinophilia in sputum induction or bronchial wash fluid from bronchoscopy (bronchoalveolar lavage)	Normal chest X−Ray	FEV1/FVC >70% No response of short acting bronchodilator	Bronchial biopsy Eosinophilia	Exposure to an occupational cause
		Bronchiectasis^[12]	Chronic	Months to years	+ Mucopurulent sputum	+	−	−	+	Crackles Wheezing Shortness of breath	Complete blood count (CBC) IgG, IgM and IgA Sputum culture for fungi, bacteria and mycobacteria	Linear atelectasis and dilated airways in chest X−Ray	FEV1/FVC <70% Normal FVC Low levels of FEV1	CT of chest	Digital clubbing Recurrent pleurisy
		Emphysema ^[13]	Chronic	Months to years	+ Mucoid or purulent sputum	−	−	+	+	Shortness of breath Wheezing Prolonged expiration Crackles	Testing for alpha 1−antitrypsin may be helpful	Chest X−Ray to exclude other diseases CT may also be helpful	FEV1/FVC <70% Post bronchodilator FEV1 >80	Detection of early emphysema in CT of chest	Exposure of tobacco and air pollution
Organ system		Diseases	Clinical manifestations								Diagnosis				Other features
			Symptoms							Physical exam	Diagnosis
			Onset	Duration	Productive cough	Hemoptysis	Weight lost	Fever	Dyspnea	Ascultation	Lab findings	Imaging	PFT	Gold standard
Respiratory	Parenchyma	Pneumoconioses^[14]^[15]	Acute, Chronic	Years	−	−	+	+	+	Wheezing Rhonchi Crackles	CBC and ABG may be helpful	Small oppacities and fibrosis observed in chest X−ray CT and FDG−PET may be helpful	FEV1/FVC <70% FEV1 <80%	Exposure history and chest radiograph	Fibrogenic: Silica, asbestos Inert: Iron, barium Granulomatous: Beryllium Giant cell pneumonia: Cobalt
		Lung cancer^[16]^[17]	Chronic	Years	+	+	+	+/−	+	Hoarseness	The following investigations may be helpful: Complete blood count (CBC) ALT, AST Calcium Alkaline phosphatase LDH Creatinine	Contrast−enhanced CT of chest and upper abdomen	Not specific	Tissue biopsy (sample should be sufficient for molecular testing)	Risk factor: Cigarette smoking Types Small cell lung cancer (SCLC) Non−small cell lung cancer (NSCLC)
		Interstitial lung disease^[18]^[19]	Chronic	Variable	−	+	+	−	+	Wheezing Crackles or velcro rales Inspiratory high−pitched rhonchi	The following investigations may be helpful: Hepatic function test Renal function test CBC Serological testing	Nodular, reticular or both pattern in chest X−ray CT in patients with diffuse pulmonary lung disease	Reduction in FVC, RV, FRC, TLC and FEV1 on spirometry FEV1/FVC normal or increase Lung volumes Diffusion capacity (DLCO reduced)	Lung biopsy when lab, imaging, and PFT has indeterminate result	Clubbing is common in asbestosis and idiopathic pulmonary fibrosis
		Tuberculosis (TB)^[20]^[21]	Chronic	More than 2 or 3 weeks	+	+	+	+	+	Pleural effusion Crackles Whispered pectoriloquy Decreased fremitus Rhonchi	Sputum acid−fast bacilli (AFB) smear may be positive Mycobacterial culture may be positive Molecular testing may be helpful	Reactivation of TB is observed as infiltration in the upper lobe in chest X−Ray In patients with HIV, Tb is observed as lobar infiltration, adenopathy, lung mass named tuberculoma, small fibronodular lesions, and/or pleural effusion on chest X−Ray CT can detect early nodal process	Decreased FEV1 Reduced FVC	Isolation of Mycobacterium tuberculosis from some secretion	Etiology: Mycobacterium tuberculosis Complications: Pneumothorax, bronchiectasis, pulmonary destruction and chronic pulmonary aspergillosis
		Cystic fibrosis (CF)^[22]^[23]	Chronic	Variable	+	−	+	+/−	+	Barrel−shaped chest Wheezing Tachypnea	Respiratory tract culture may be helpful for diagnosing secondary bacterial infection Bronchoalveolar lavage for cytology may be helpful ≥ 60 mmol/L Sweat chloride test CFTR mutation in molecular testing may be positive	Hyperinflation, atelectasis, and infiltrates on chest X−Ray Severe patients present bronchietasis, “tram tracks” peribronchial cuffing in chest X−Ray The extension of bronchietasis can be defined by CT	RV/TLC ratio increased FEV1/FVC ratio <70% Low levels of FEV1 High levels of TLC RV increased	Sweat chloride test	Evidence of CFTR dysfunction
Organ system		Diseases	Clinical manifestations								Diagnosis				Other features
			Symptoms							Physical exam	Diagnosis
			Onset	Duration	Productive cough	Hemoptysis	Weight lost	Fever	Dyspnea	Ascultation	Lab findings	Imaging	PFT	Gold standard
[[[Heart\|Cardiac]]		Mitral Stenosis^[24]^[25]	Chronic	Variable	+ Pink frothy	+	−	−	+	Crackles Hoarseness	Not specifc	Electrocardiogram may be helpful Enlargement of left atrium and appendage in chest radiograph	FVC reduced	Resting transthoracic echocardiography	Stress testing Cardiac catheterization
[[[Heart\|Cardiac]]		Pulmonary hypertension^[26]^[27]	Chronic	More than 2 years	−	+	+	−	+	Hoarseness	The following investigations may be helpful: HIV serology Antinuclear antibody (ANA) Rheumatoid factor (RF) Anti−neutrophil cytoplasmic antibody (ANCA)	Enlargement of the central pulmonary artery and right heart in chest X−Ray Pulmonary artery systolic pressure can be estimated in echocardiography	Low levels of FEV1 Decreased FVC DLCO reduced	Mean pulmonary artery pressure more than 25 mmHg at rest	Chest pain Ascites Syncope Peripherial edema
Gastrointestinal		Gastroesophageal reflux^[28]^[29]	Chronic	Variable	+	−	+	−	+	Wheezing Hoarseness	Not specific	Upper endoscopy may be helpful Barium esophagram may be helpful	Normal function	PH testing	−−
Organ system		Diseases	Clinical manifestations								Diagnosis				Other features
			Symptoms							Physical exam	Diagnosis
			Onset	Duration	Productive cough	Hemoptysis	Weight lost	Fever	Dyspnea	Ascultation	Lab findings	Imaging	PFT	Gold standard
Autoimmune		Goodpasture syndrome^[30]^[31]	Chronic	Variable	−	+	−	−	+	Shortness of breath	The following investigations may be helpful: Complete blood count (CBC) ANCA positive Anti−GBM in ELISA or western blot	Pulmonary infiltratation in chest X−Ray CT scan for parenchymal involvement	Increased DLCO Decreased TLC Decreased FVC	Renal biopsy	Hematuria Proteinuria
		Wegener’s disease (GPA) ^[32]^[33]	Chronic	Months	+	+	+	+	+	Hoarseness Stridor Wheezing	The following investigations may be helpful: ANCA, P−ANCA, C−ANCA BUN Creatinine Complete blood count Urinalysis Lung biopsy	Nodules, pulmonary infiltrates, reticular margins, pleural opacities and cavities in chest X−Ray Nodules, cavities and stellate−shaped peripherial pulmonary in chest CT Bronchoscopy may be helpful	Low levels of DLCO Reduce lung volumes	Tissue biopsy	Nasal crusting, sinus pain, chronic rhinosinusitis, nasal obstruction and discharge in upper airway Saddle nose deformity Purpura in lower extremities
		Sarcoidosis^[34]^[35]	Chronic	Years	−	−	+	+	+	Wheezing Squeaky sounds	The following investigations may be helpful: Complete blood count (CBC) Urinalysis BUN Liver function test Calcium Alkaline phosphatase levels Electrolytes Histopathologic detection	On chest X−Ray: Stage 1: Bilateral hiliar adenopathy Stage 2: Reticular opacities and hiliar adenopathy Stage 3: Shrink hiliar nodules and reticular opacities Stage 4: Lost of volume	Reduced FVC Decreased of TLC	Clinical diagnosis, histopathologic detection of noncaseating granulomas and exclusion of other diseases	Young adults Skin, joint and eye lesions
		Microscopic polyangitis (MPA)^[36]	Chronic	Variable	+	+	+	+	+	Hoarseness Stridor Wheezing	The following investigations may be helpful: ANCA positive BUN Creatinine Complete blood count Urinalysis	Cavitation, nodules, and alveolar opacities in chest X−ray Head and chest CT may be helpful Electromyography/nerve conduction study may also be helpful	Reduced lung volumes	Tissue biopsy	Nerve damage Rhinosinusitis Purpura involving lower extremities
		Churg−Strauss^[37]^[38]	Chronic	Variable	+	+	+	+	+	Wheezing Rales Rhonchi Expiratory sounds(related to asthma)	Peripherial eosinophilia In active phase CRP and erytrocyte sedimentation rate high Elevated IgE ANCA positive	Infiltrates in chest X−Ray Ground glass opacities, tree−in−bud sign and small nodules in chest CT	Lung volumes decreased FVC reduced FEV1/FVC ratio <70%	Tissue biopsy	Asthma Eosinophilia Rhinosinusitis

Cough

The differential diagnosis according to cough for bronchiectasis is shown in the table below:

Organ system		Diseases	Clinical manifestations								Diagnosis				Other features
			Symptoms							Physical exam	Diagnosis
			Onset	Duration	Productive cough	Hemoptysis	Weight lost	Fever	Dyspnea	Ascultation	Lab findings	Imaging	PFT	Gold standard
Respiratory	Upper airway diseases	Epiglottitis^[39]^[40]	Abrupt or acute	12-24 hours	–	–	–	✔	✔	Stridor Hoarseness	Elevated white blood count in CBC Blood culture may show bacterial growth Epiglottal culture in intubated patients may show bacterial growth	Enlarge epiglottis (>8 mm), loss of vallecular air space and distended hypopharynx in neck X-ray	Normal function	Direct visualization of erythematous and edematous epiglottis	Tripod posture Drooling Tenderness of the anterior part of the neck Etiology: Haemophilus influenzae
		Croup^[41]	Acute	3-5 days	✔	–	–	–	✔	Stridor Crackles	Low White blood cell count (WBC) in CBC	Subglottic narrowing (steeple sign) in postero-anterior radiograph chest	Decresed tidal volume	Clinical diagnosis. Laboratory findings and imaging are not necessary for diagnosis	Barking cough Etiology: Parainfluenza virus type 1 (most common)
		Pertussis^[42]^[43]	Acute	Two weeks	✔ Whooping sound	–	✔	–	✔	Clear chest	Polymerase chain reaction (PCR) shows Bordetella pertussis Serologic testing	Atelectasis Lymphadenopathy	Normal function	Culture	Etiology: Bordetella pertussis Phases: Catarrhal, paroxysmal and convalescent
		Laryngopharyngeal reflux^[3]^[4]	Chronic	Variable	✔	–	–	–	✔	Hoarseness Stridor	Decreased levels of salivary epidermal growth factor (EGF) Increased levels of NKTR Biopsy	X-Ray Endoscopy examination	Normal function	24 hour-dual sensor pH probe	Throat clearing Globus sensation
		Common Cold^[44]	Acute	3-10 days	✔	–	–	✔	–	Rales Wheezing	Bacterial culture is not indicated	Chest X-Ray in patients with signs of consolidation	Normal function	Clinical diagnosis	Conjunctival injection Nasal congestion
		Seasonal Influenza ^[45]	Acute	5-10 days	–	–	–	✔	✔	Shorteness of breath	RT-PCR Antigen detection test	Reticular or reticulonodular opacities in chest X-Ray	Normal function	Clinical diagnosis	Etiology: A or B Influenza virus
		Rhinosinusitis^[5]^[6]	Acute, subacute, chronic, recurrent	Acute: Less than 4 weeks Subacute: 4-12 weeks Chronic: More than 12 weeks Recurrent: 4 or more episodes or acute rhinosinusitis per year	✔	–	–	✔	✔	Clear chest	In complicated acute bacterial rhinosinusitis, endoscopic cultures or sinus aspirate is indicated Nasal culture	Air-fluid level, mucosal edema and bony erosion of sinus on CT MRI for distinguish the etiology	Normal function	Clinical diagnosis: Nasal congestion, obstruction, and purulent rhinorrhea	Erythema in periorbital area
	Lower airway	Asthma^[7]	Chronic	Years	✔ Clear mucoid or yellow sputum	–	–	–	✔	Wheezing (expiratory) Rales Rhonchi	Eosinophilia is observed in complete blood count (CBC) Total serum IgE in test for allergy	Normal airways in chest X-ray CT if there any abnormality in chest X-Ray	FEV1/FVC ratio <70% and FEV1 >15% increase after 15 minutes of 2 puffs of beta 2 sympathomimetic drug After physical active FEV1 decreases by >15% After inhaled corticosteroid (ICS)FEV1 increased by >15%	Airflow limitation on spirometry	Family history Seasonal variation
		Acute Bronchitis^[46]	Acute	From 5 days to 1 or 3 weeks	✔	–	–	–	✔	Wheezing Rhonchi	Sputum culture is not indicated PCR in bacterial infection	Chest X-ray to exclude other diseases	FEV1 < 80%	Clinical diagnosis	Majority of cases are caused by respiratory viruses
		Chronic Bronchitis^[8]^[9]	Chronic	Most of the days for three months in the las two years.	✔ Clear sputum	–	–	✔	✔	Wheezing Rhonchi	Blood test Arterial blood gas (ABG)	Chest X-Ray to exclude other diseases CT	FEV1/FVC ratio < 70% Post bronchodilatador FEV1 > 80% Reduced FVC after bronchodilatador administration Decread vital capacity Increased total lung capacity	Demostration of airflow limitation on spirometry	Smoker’s cough Cigarette smoking Pollution
		Non-asthmatic eosinophilic bronchitis^[10]^[11]	Chronic	More than 8 weeks	✔ Eosinophilic sputum		–	–	✔	Wheezing Shortness of breath	High levels of IgE Airway eosinophilia in sputum induction or bronchial wash fluid from bronchoscopy (bronchoalveolar lavage)	Normal chest X-Ray	FEV1/FVC >70% No response of short acting bronchodilator	Bronchial biopsy eosinophilia	Exposure to an occupational cause
		Bronchiectasis^[12]	Chronic	Months to years	✔ Mucopurulent sputum	✔		–	✔	Crackles Wheezing Shortness of breath	Complete blood count (CBC) IgG, IgM and IgA Sputum culture for fungi, bacteria and mycobacteria	Linear atelectasis and dilated airways in chest X-Ray	FEV1/FVC <70% Normal FVC Low levels of FEV1	CT of chest	Digital clubbing Recurrent pleurisy
		Emphysema ^[13]	Chronic	Months to years	✔ Mucoid or purulent sputum	–	–	✔	✔	Shortness of breath Wheezing Prolonged expiration Crackles	Blood test Testing for alpha 1-antitrypsin	Chest X-Ray to exclude other diseases CT	FEV1/FVC <70% Post bronchodilator FEV1 >80	Detection of early emphysema in CT of chest	Exposure of tobacco and air pollution
		Foreing body aspiration^[47]^[48]^[49]	Acute	Variable	✔	✔	–	✔	✔	Wheezing Decreased breath sounds	No specific	Hyperinflated lungs, atelectasis, and mediastinitis Shift in chest radiograph when the object is radio-opaque CT	Not specific	Bronchoscopy	In children <1 year and adults >75 years Organic materials in children Inorganic materials in adults
		Bronchiolitis^[50]^[51]	Acute	8-15 days	✔	–		✔	✔	Wheezing Crackles Increased respiratory rate	Complete blood count (CBC) Urinalysis (in infants) Urine culture ( in infants)	Chest X-Ray	Normal function or obstructive changes (FEV1/FVC <70%) Air trapping in Lung volumes Reduced Diffusing capacity of carbon monoxide ( DLCO)	Clinical diagnosis	Etiology: Respiratory syncytial virus, Rhinovirus Children <2 years
	Parenchyma	Pneumonia^[52]^[53]	Acute	Variable	✔ Mucopurulent sputum	–	–	✔	✔	Crackles Egophony Decreased bronchial sounds	Leftward shift leukocytosis Blood culture in hospitalized patients Sputum culture in hospitalized patients	Consolidation, cavitation, and infiltrated interstitial in chest X-ray Anatomical changes observed in chest CT	Not specific	Infiltration observed in chest X-ray	Community-acquired pneumonia Healthcare-associated pneumonia
		Pneumoconioses^[14]^[15]	Acute, Chronic	Years	–	–	✔	✔	✔	Wheezing Rhonchi Crackles	Arterial blood gas Complete blood count (CBC)	Small oppacities and fibrosis observed in chest X-ray CT FDG-PET	FEV1/FVC <70% FEV1 <80%	Exposure history and chest radiograph	Fibrogenic: Silica, asbestos Inert: Iron, barium Granulomatous: Beryllium Giant cell pneumonia: Cobalt
		Lung cancer^[16]^[17]	Chronic	Years	✔	✔	✔	–	✔	Hoarseness	Complete blood count (CBC) ALT, AST Calcium Alkaline phosphatase LDH Creatinine	Contrast-enhanced CT of chest and upper abdomen	Not specific	Tissue biopsy (sample should be sufficient for molecular testing)	Risk factor: Cigarette smoking Types Small cell lung cancer (SCLC) Non-small cell lung cancer (NSCLC)
		Interstitial lung disease^[18]^[19]	Chronic	Variable	–	✔	✔	–	✔	Wheezing Crackles or velcro rales Inspiratory high-pitched rhonchi	Test for hepatic and renal function Hematologic test in differential CBC Serological testing	Nodular, reticular or both pattern in chest X-ray CT in patients with diffuse pulmonary lung disease	Reduction in FVC, RV, FRC, TLC and FEV1 on spirometry FEV1/FVC normal or increase Lung volumes Diffusion capacity (DLCO reduced)	Lung biopsy when lab, imaging, and PFT has indeterminate result	Clubbing is common in asbestosis and idiopathic pulmonary fibrosis
		Tuberculosis (TB)^[20]^[21]	Chronic	More than 2 or 3 weeks	✔	✔	✔	✔	✔	Pleural effusion Crackles Whispered pectoriloquy Decreased fremitus Rhonchi	Sputum acid-fast bacilli (AFB) smear Mycobacterial culture Molecular testing	Reactivation of TB is observed as infiltration in the upper lobe in chest X-Ray In patients with HIV, Tb is observed as lobar infiltration, adenopathy, lung mass named tuberculoma, small fibronodular lesions, and/or pleural effusion chest X-Ray CT can detect early nodal process	Decreased FEV1 Reduced FVC	Isolation of Mycobacterium tuberculosis from some secretion	Etiology: Mycobacterium tuberculosis Complications: Pneumothorax, bronchiectasis, pulmonary destruction and chronic pulmonary aspergillosis
		Cystic fibrosis (CF)^[22]^[23]	Chronic	Variable	✔	–	✔		✔	Barrel-shaped chest Wheezing Tachypnea	Respiratory tract culture for CF Bronchoalveolar lavage for cytology ≥ 60 mmol/L Sweat chloride test CFTR mutation in molecular testing	Hyperinflation, atelectasis, and infiltrates on chest X-Ray Severe patients present bronchietasis, “tram tracks” peribronchial cuffing in chest X-Ray The extension of bronchietasis can be defined by CT	RV/TLC ratio increased FEV1/FVC ratio <70% Low levels of FEV1 High levels of TLC RV increased	Sweat chloride test	Evidence of CFTR dysfunction
Cardiac		Cardiogenic pulmonary edema^[54]^[55]	Acute	Days to weeks	✔ Pink frothy, liquid	–	✔	–	✔	Crackles Increased respiratory rate Wheezing Rhonchi Gurgling sounds	Arterial blood gas BUN Serum creatinin Serum troponin Electrolytes Lactic acid Complete blood count	Cardiomegaly, pleural effusion, interstitial edema, alveolar edema and blood redistribution in lower lobes in chest X-ray	Not specific	Clinical diagnosis Tests are supportive	12-lead ECG Plasma BNP and NT-proBNP Echocardiography
		Mitral Stenosis^[24]^[25]	Chronic	Variable	✔ Pink frothy	✔	–	–	✔	Crackles Hoarseness	Not specifc	Electrocardiogram Enlargement of left atrium and appendage in chest radiograph	FVC reduced	Resting transthoracic echocardiography	Stress testing Cardiac catheterization
		Pulmonary hypertension^[26]^[27]	Chronic	More than 2 years	–	✔	✔	–	✔	Hoarseness	HIV serology Antinuclear antibody (ANA) Rheumatoid factor (RF) Anti-neutrophil cytoplasmic antibody (ANCA)	Enlargement of the central pulmonary artery and right heart in chest X-Ray Pulmonary artery systolic pressure can be estimated in echocardiography	Low levels of FEV1 Decreased FVC DLCO reduced	Mean pulmonary artery pressure more than 25 mmHg at rest	Chest pain Ascites Syncope Peripherial edema
Gastrointestinal		Gastroesophageal reflux^[28]^[29]	Chronic	Variable	✔	–	✔	–	✔	Wheezing Hoarseness	Not specific	Upper endoscopy Barium esophagram	Normal function	PH testing	—
Autoinmune		Goodpasture syndrome^[30]^[31]	Chronic	Variable	–	✔	–	–	✔	Shortness of breath	Complete blood count (CBC) ANCA positive Anti-GBM in ELISA or western blot	Pulmonary infiltratation in chest X-Ray CT parenchimal envolment	Increased DLCO Decreased TLC Decreased FVC	Renal biopsy	Hematuria Proteinuria
		Wegener’s disease (GPA) ^[32]^[33]	Chronic	Months	✔	✔	✔	✔	✔	Hoarseness Stridor Wheezing	ANCA, P-ANCA, C-ANCA BUN Creatinine Complete blood count Urinalysis Lung biopsy	Nodules, pulmonary infiltrates, reticular margins, pleural opacities and cavities in chest X-Ray Nodules, cavities and stellate-shaped peripherial pulmonary in chest CT Bronchoscopy	Low levels of DLCO Reduce lung volumes	Tissue biopsy	Nasal crusting, sinus pain, chronic rhinosinusitis, nasal obstruction and discharge in upper airway Saddle nose deformity Purpura in lower extremities
		Sarcoidosis^[34]^[35]	Chronic	Years	–	–	✔	✔	✔	Wheezing Squeaky sounds	Complete blood count (CBC) Urinalysis BUN Liver function test Calcium Alkaline phosphatase levels Electrolytes Histopathologic detection	On chest X-Ray: Stage 1: Bilateral hiliar adenopathy Stage 2: Reticular opacities and hiliar adenopathy Stage 3: Shrink hiliar nodules and reticular opacities Stage 4: Lost of volume	Reduced FVC Decreased of TLC	Clinical diagnosis, histopathologic detection of noncaseating granulomas and exclusion of other diseases	Young adults Skin, joint and eye lesions
		Microscopic polyangitis (MPA)^[36]	Chronic	Variable	✔	✔	✔	✔	✔	Hoarseness Stridor Wheezing	ANCA positive BUN Creatinine Complete blood count Urinalysis	Cavitation, nodules, and alveolar opacities in chest X-ray Head and chest CT Electromyography/nerve conduction study	Reduced lung volumes	Tissue biopsy	Nerve damage Rhinosinusitis Purpura involving lower extremities
		Churg-Strauss^[37]^[38]	Chronic	Variable	✔	✔	✔	✔	✔	Wheezing Rales Rhonchi Expiratory sounds(related to asthma)	Peripherial eosinophilia In active phase CRP and erytrocyte sedimentation rate high High levels of IgE ANCA positive	Infiltrates in chest X-Ray Ground glass opacities, tree-in-bud sign and small nodules in chest CT	Lung volumes decreased FVC reduced FEV1/FVC ratio <70%	Tissue biopsy	Asthma Eosinophilia Rhinosinusitis
Medication		ACE inhibitors^[56]^[57]	Acute (depend on the medication)	From 2 weeks to 6 months	–	–	–	–	✔	Wheezing	Not required	No required	Normal function	Clinical diagnosis	Resolves in four to five days of stopping the medication Angioedema

Features that may suggest bronchiectasis in a patient presenting with chronic respiratory symptoms

Digital clubbing
Lack of a significant smoking history (if COPD is suspected)
History of recurrent and/or severe pneumonia or tuberculosis
Presence of either Aspergillus, atypical/nontuberculous Mycobacteria, Pseudomonas aeruginosa, Escherichia coli, or Klebsiella pneumoniae in the sputum

References

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Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Saarah T. Alkhairy, M.D.

Overview

Bronchiectasis affects extremes of age in certain indigenous populations with a slight female dominance. It is difficult to estimate the prevalence because it is often misdiagnosed. In developed countries, it is important to diagnose the underlying cause and in these countries the age of onset mostly is in adulthood. In developing countries, infection in childhood period is a common cause.

Epidemiology and Demographics

Prevalence and Incidence

The true prevalence of bronchiectasis is uknown, given that bronchiectasis remains underdiagnosed and is often misdiagnosed as either asthma or COPD. The estimated prevalence of bronchiectasis in USA is approximately 30 to 40 per 100,000 individuals.^[1]
In USA, the average annual bronchiectasis-associated hospitalization rate approximately 16.5 per 100,000 hospitalizations.^[1]

Age

Bronchiectasis predominantly affect extremes of age.^[1]
The prevalence of bronchiectasis rises steeply from 4-5 per 100,000 adults aged 18-34 years to 250 to 300 per 100,000 individuals aged > 75 years.^[1]

Gender

Predominantly women
The women that are infected with primary Mycobacterium avium complex (MAC) tend to be Caucasian, slender, and older than 60 years. It is given the name of Lady Windermere syndrome which is named after a character in a novel by Oscar Wilde.
Annual increase of about 2.4% in men and 3.0% in women for bronchiectasis-associated hospitalizations.^[1]

Race

There is no known association of increased incidence of the bronchiectasis and a particular race.
Very high prevalence in certain indigenous populations such as Alaskan natives with 10-20/1000 children affected.^[1]

Developed Countries

Before antibiotics, the symptoms on bronchiectasis began in the patient’s first decade of life. In developed countries, the age of onset has move to adulthood (except those with cysts fibrosis).^[2]
It is important to understand the underlying cause before initiating treatment.^[2]

Developing Countries

Infections are an important cause of bronchiectasis because the disease may not be diagnosed or be treated properly in the developing countries.^[3]
Bronchiectasis is a large concern for pediatricians because children are largely affected.^[3]

References

↑ ^1.0 ^1.1 ^1.2 ^1.3 ^1.4 ^1.5 McDonnell MJ, Ward C, Lordan JL, Rutherford RM (2013). “Non-cystic fibrosis bronchiectasis”. QJM. 106 (8): 709–15. doi:10.1093/qjmed/hct109. PMID 23728208.
↑ ^2.0 ^2.1 Bilton, Diana (2008). “Update on non-cystic fibrosis bronchiectasis”. Current Opinion in Pulmonary Medicine. 14 (6): 595–599. doi:10.1097/MCP.0b013e328312ed8c. ISSN 1070-5287.
↑ ^3.0 ^3.1 Karadag, B.; Karakoc, F.; Ersu, R.; Kut, A.; Bakac, S.; Dagli, E. (2005). “Non-Cystic-Fibrosis Bronchiectasis in Children: A Persisting Problem in Developing Countries”. Respiration. 72 (3): 233–238. doi:10.1159/000085362. ISSN 1423-0356.

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Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Saarah T. Alkhairy, M.D.

Overview

Common risk factors in the development of bronchiectasis include cystic fibrosis, primary ciliary dyskinesia, exposure to chemical irritants, connective tissue disease, immunodeficiencies, allergic bronchopulmonary aspergillosis (ABPA), and history of childhood infections such as pneumonia, tuberculosis, measles, whooping cough, adenovirus, and Mycoplasma pneumoniae.

Bronchiectasis Risk Factors

The risk factors are mainly the primary causes of bronchiectasis.

The following table lists the most common risk factors of bronchiectasis:^[1]

Risk	Factor Description
Cystic fibrosis	Due to ciliary dysfunction, the mucous secretion accumulates in the airways. This leads to increased infection and damage to the airways.
Primary ciliary dyskinesia	Due to ciliary dysfunction, the mucous secretion accumulates in the airways. This leads to increased infection and damage to the airways.
Childhood infections such as pneumonia, tuberculosis, measles, whooping cough, adenovirus, and Mycoplasma pneumoniae	These infections damage the airways, which leads to more infections
Retained foreign object	This prevents mucus from clearing from the airway
Exposure to chemical irritants	This leads to inflammation and mucous secretion
Connective tissue disease	This leads to pulmonary fibrosis, inflammation of the airways, and traction bronchiectasis
Immunodeficiencies	There are increased infections and mucus secretion
Allergic Bronchopulmonary Aspergillosis (ABPA)	The allergic reaction to the fungus aspergillus causes inflammation of the airways, repeated infections, and accumulation of mucus
Toxic fumes, gases, smoke, and other harmful substances	There cause irritation and inflammation of the airways
Low BMI	It is associated with low immune function, leading to increased infections

References

↑ Morrissey BM (2007). “Pathogenesis of bronchiectasis”. Clin Chest Med. 28 (2): 289–96. PMID 17467548.

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Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Saarah T. Alkhairy, M.D.

Overview

There is no routine screening for bronchiectasis. If the patient has an immune deficiency or primary ciliary dyskinesia then pulmonary function tests should be measures four times a year.

Bronchiectasis Screening

There is no routine screening for bronchiectasis.
If the patient has an immune deficiency or primary ciliary dyskinesia, the forced expiratory volume in one second (FEV1), forced vital capacity (FVC), and peak expiratory flow (PEF) should be measured four times a year.^[1]

References

↑ van der Bruggen-Bogaarts BA, van der Bruggen HM, van Waes PF, Lammers JW (1996). “Screening for bronchiectasis. A comparative study between chest radiography and high-resolution CT”. Chest. 109 (3): 608–11. PMID 8617064.

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Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Saarah T. Alkhairy, M.D.

Overview

Bronchiectasis is normally diagnosed after months or years of symptoms. Patients have respiratory complications, infection, and hemoptysis. Death can be caused by cardiac and respiratory failure. Bronchiectasis shows a higher mortality with males, advanced age, poor functional status, severe disease based on radiographic findings, and evidence of hypoxemia and hypercapnia.

Natural History

There is often a delay between the onset of symptoms and diagnosis
The classic symptoms are cough, daily mucopurulent sputum production, and dyspnea
- These symptoms are usually present for months to years
- The symptoms are manifestations of the lung being repeatedly damaged due to any number of causes

Over the years the patient can develop recurrent infections, massive hemoptysis, and pulmonary hypertension

In about 8-10 years, there is a high mortality rate due to cor pulmonale or respiratory failure

Complications

Recurrent infection
Increased sputum production
Dyspnea
Massive hemoptysis
Pulmonary hypertension
- Decreased air is traveling through the bronchus
- Less oxygen is being distributed everywhere
- Causes pulmonary constriction which increases the pulmonary pressure

Prognosis

Bronchiectasis has been shown to contribute to early mortality^[1]
Early mortality is associated with
- Males^[1]
- Advanced age^[2]
- Poor functional status^[3]
- More severe disease based on radiographic findings^[4]
- Evidence of hypoxemia or hypercapnia^[5]

Infected with Pseudomonas aeruginosa, severe exacerbations, and systemic inflammation are associated with disease advancement
Up to 10% of adults die within 5-8 years of diagnosis (majority being respiratory related)^[6]

References

↑ ^1.0 ^1.1 McDonnell MJ, Ward C, Lordan JL, Rutherford RM (2013). “Non-cystic fibrosis bronchiectasis”. QJM. 106 (8): 709–15. doi:10.1093/qjmed/hct109. PMID 23728208.
↑ Onen ZP, Eris Gulbay B, Sen E, Akkoca Yildiz O, Saryal S, Acican T, Karabiyikoglu G (2007). “Analysis of the factors related to mortality in patients with bronchiectasis”. Respir Med. 101 (7): 1390–97. PMID 17374480.
↑ Onen ZP, Eris Gulbay B, Sen E, Akkoca Yildiz O, Saryal S, Acican T, Karabiyikoglu G (2007). “Analysis of the factors related to mortality in patients with bronchiectasis”. Respir Med. 101 (7): 1390–97. PMID 17374480.
↑ Onen ZP, Eris Gulbay B, Sen E, Akkoca Yildiz O, Saryal S, Acican T, Karabiyikoglu G (2007). “Analysis of the factors related to mortality in patients with bronchiectasis”. Respir Med. 101 (7): 1390–97. PMID 17374480.
↑ Onen ZP, Eris Gulbay B, Sen E, Akkoca Yildiz O, Saryal S, Acican T, Karabiyikoglu G (2007). “Analysis of the factors related to mortality in patients with bronchiectasis”. Respir Med. 101 (7): 1390–97. PMID 17374480.
↑ Onen ZP, Eris Gulbay B, Sen E, Akkoca Yildiz O, Saryal S, Acican T, Karabiyikoglu G (2007). “Analysis of the factors related to mortality in patients with bronchiectasis”. Respir Med. 101 (7): 1390–97. PMID 17374480.

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Diagnosis

Treatment

Case Studies

Case #1

Template:Respiratory pathology Template:Congenital malformations and deformations of respiratory system

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Bronchiectasis

Overview

Historical Perspective

Pathophysiology

Classification

Causes

Differential Diagnosis

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications, and Prognosis

History and Symptoms

Physical Symptoms

Diagnostic Studies

Laboratory Findings

Chest X-ray

CT

Other Imaging Findings

Other Diagnostic Studies

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

References

Overview

Bronchiectasis Historical Perspective

References

Overview

Classification

Based on Severity

Based on Location

References

Overview

Pathophysiology

Cole’s Cycle

Immune Response

Gross Pathology

References

Overview

Causes

Life Threatening Causes

Commom causes

Causes by Organ System

Causes in Alphabetical Order

Causes Based on Mode of Infection

Congenital

Acquired

References

Overview

Bronchiectasis Differential Diagnosis

Cough

Features that may suggest bronchiectasis in a patient presenting with chronic respiratory symptoms

References

Overview

Epidemiology and Demographics

Prevalence and Incidence

Age

Gender

Race

Developed Countries

Developing Countries

References

Overview

Bronchiectasis Risk Factors

References

Overview

Bronchiectasis Screening

References

Overview

Natural History

Complications

Prognosis

References

Diagnosis

Treatment

Case Studies

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