Bronchiectasis Clinical Presentation

  • Author: Ethan E Emmons, MD; Chief Editor: Zab Mosenifar, MD   more...
 
Updated: May 13, 2011
 

History

The classic clinical manifestations of bronchiectasis are cough and daily mucopurulent sputum production, often lasting months to years. Blood-streaked sputum or hemoptysis may result from airway damage associated with acute infection. Less specific symptoms include dyspnea, pleuritic chest pain, wheezing, fever, weakness, and weight loss.

A rare variant known as dry bronchiectasis manifests as episodic hemoptysis with little-to-no sputum production. Dry bronchiectasis is usually a sequela of tuberculosis and is found in the upper lobes.

Bronchiectasis is a morphologic diagnosis. Thus, it may exist with relatively few symptoms.

Although patients may report repetitive pulmonary infections that require antibiotics over several years, a single episode of a severe infection, often in childhood, may result in bronchiectasis.[7] These include tuberculosis, pertussis, or severe bacterial pneumonia. Today, CF is the most common cause of bronchiectasis in children and young adults.[10]

Exacerbations of bronchiectasis that are caused by acute bacterial infections are often heralded by the onset of increased sputum production over baseline, increased viscidity of sputum, and, occasionally, a foul odor of the sputum. Rarely, low-grade fever may occur. Patients may experience an increase in generalized constitutional symptoms, such as fatigue and malaise, as well as increased dyspnea, shortness of breath, wheezing, or pleuritic pain.

With secondary infection or poorly treated pneumonia, the discrete pathogens are often unknown. However, most patients relate a history of childhood infections that may include tuberculosis, pertussis, or Mycoplasma infection.[7]

Most individuals have never smoked (55%) or have smoked too little to account for their degree of cough, findings of obstruction on spirometry testing, and daily sputum production.

Chronic productive cough is prominent,[71] occurring in up to 98% of patients. Sputum is typically produced on a daily basis in greater than 70% of patients, with one study reporting production in 96% of patients.[72] Some patients produce sputum only with acute upper respiratory tract infections, but otherwise they have quiescent disease.

Sputum is typically mucoid and relatively odorless. During infectious exacerbations, however, sputum becomes purulent and may develop an offensive odor.

In the past, total daily sputum amount has been used to characterize the severity of bronchiectasis, with less than 10 mL defined as mild bronchiectasis, 10-150 mL defined as moderate bronchiectasis, and greater than 150 mL defined as severe bronchiectasis. Today, bronchiectasis is most often classified by radiographic findings. In patients with CF, the volume of sputum produced is generally much greater than that associated with other etiologies of bronchiectasis.

Hemoptysis occurs in 56-92% of patients with bronchiectasis. Hemoptysis is more commonly observed in dry bronchiectasis. Hemoptysis is generally mild and manifested by blood flecks in the patient's usual purulent sputum. This is often the factor that leads patients to consult a physician. Bleeding usually originates from dilated bronchial arteries, which contain blood at systemic (rather than pulmonary) pressures. Therefore, massive hemoptysis may occur but is rarely a cause of death.[10, 72, 73]

Dyspnea may occur in as many as 72% of patients; a 2006 review reported a rate of 62%.[72] Dyspnea typically occurs in patients with extensive bronchiectasis observed on chest radiographs. Marked dyspnea is more likely to be secondary to a concomitant illness, such as chronic bronchitis or emphysema.

Wheezing is commonly reported and may be due to airflow obstruction following destruction of the bronchial tree. Similar to dyspnea, it may also be secondary to concomitant conditions such as asthma.

Pleuritic chest pain is an intermittent finding, occurring in 19-46% of patients.[72] It is most commonly secondary to chronic coughing but also occurs in the setting of acute exacerbation.

Fatigue is commonly reported (73% of patients).[72] Weight loss often occurs in patients with severe bronchiectasis. This is believed to be secondary to increased caloric requirements associated with the increased work of coughing and clearing secretions. Weight loss suggests advanced disease but is not diagnostic of bronchiectasis.

Fever may occur in the setting of acute infectious exacerbations.

Urinary incontinence occurs more frequently in women with bronchiectasis versus age-matched controls (47% vs 12%).[74] The etiology of this is unclear.

Next

Physical Examination

Findings are nonspecific and may be attributed to other conditions. Most commonly, crackles, rhonchi, wheezing, and inspiratory squeaks may be heard upon auscultation. General findings may include digital clubbing, cyanosis, plethora, wasting, and weight loss. Nasal polyps and signs of chronic sinusitis may also be present. In advanced disease, the physical stigmata of cor pulmonale may be observed. Note the following:

  • Crackles and rhonchi are often observed in association with active infections and acute exacerbations
  • Crackles are nonspecific and may occur in as many as 73% of patients[72]
  • Scattered wheezing may be heard in approximately one third of patients; wheezing may be due to airflow obstruction from secretions, destruction of the bronchial tree leading to airway collapsibility, or a concomitant condition[10, 72]
  • Digital clubbing is an inconsistent finding in approximately 2-3% of patients[72] ; it is more frequent in patients with moderate-to-severe bronchiectasis
  • Cyanosis and plethora are rare findings secondary to polycythemia from chronic hypoxia.

Wasting and weight loss are suggestive of advanced disease but are not diagnostic of bronchiectasis. In severe cases, findings are consistent with cor pulmonale. Right-sided heart failure may be observed, including peripheral edema, hepatomegaly, and hypoxia. This can ultimately lead to progressive respiratory failure.[69]

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Contributor Information and Disclosures
Author

Ethan E Emmons, MD  Chief, Pulmonary Disease/Critical Care/Sleep Medicine, Brooke Army Medical Center

Ethan E Emmons, MD is a member of the following medical societies: American College of Chest Physicians and American College of Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Helen M Hollingsworth, MD  Director, Adult Asthma and Allergy Services, Associate Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, Boston Medical Center

Helen M Hollingsworth, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American Thoracic Society, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Daniel R Ouellette, MD, FCCP  Associate Professor of Medicine, Wayne State University School of Medicine; Consulting Staff, Pulmonary Disease and Critical Care Medicine Service, Henry Ford Health System

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians and American Thoracic Society

Disclosure: Boehringer Ingleheim Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; Astra Zeneca Honoraria Speaking and teaching

Chief Editor

Zab Mosenifar, MD  Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Professor and Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society

Disclosure: Nothing to disclose.

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Cylindrical bronchiectasis with signet-ring appearance. Note that the luminal airway diameter is greater than the diameter of the adjacent vessel.
Cystic and cylindrical bronchiectasis of the right lower lobe on a posterior-anterior chest radiograph.
Varicose bronchiectasis with alternating areas of bronchial dilatation and constriction.
This CT scan depicts areas of both cystic bronchiectasis and varicose bronchiectasis.
 
 
 
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