(From Hansell, D. M., Lynch, D. A., McAdams, H. P., et al. [2010].
FIGURE 16.6
FIGURE 16.5 Cystic (saccular) bronchiectasis. Right lateral bronchogram showing cystic bronchiectasis affecting mainly the lower lobe and posterior segment of the upper lobe. (From Hansell, D. M., Lynch, D. A., McAdams, H. P., et al. [2010]. Imaging of diseases of
the chest [5th ed.]. Philadelphia, PA: Elsevier.)
Varicose bronchiectasis. Left posterior oblique projection of left bronchogram in a patient with the ciliary dyskinesia syndrome. All basal bronchi are affected by varicose bronchiectasis.
Imaging of diseases of the chest [5th ed.]. Philadelphia, PA: Elsevier.)
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Computed Tomography Scan
With this technique, increased bronchial wall opacity is often seen. The bronchial walls may appear as follows:
•Thick
•Dilated
•Characterized by ring lines or clusters
•Signet ring–shaped
•Flame-shaped
The CT scan changes may include many findings that are similar to those seen on the chest radiograph. The bronchial walls may appear thick, dilated, or as rings of opacities arranged in lines or clusters. A characteristic appearance in bronchiectasis is the end-on signet ring opacity produced by the ring shadow of a dilated airway with its accompanying artery (Fig. 16.7).
FIGURE 16.7 Signet ring sign in patient with cystic fibrosis. (From Hansell, D. M., Lynch, D. A., McAdams, H. P., et al. [2010]. Imaging of diseases of the chest [5th ed.]. Philadelphia, PA: Elsevier.)
The specific type of bronchiectasis can be confirmed with the CT scan. For example, Fig. 16.8 confirms the presence of cylindrical bronchiectasis. Fig. 16.9 shows varicose bronchiectasis, and Fig. 16.10 shows cystic bronchiectasis. Airways that are filled with secretions produce rounded or flame-shaped opacities that can be identified by following them through adjacent sections to unfilled airways. The CT scan also confirms atelectasis, consolidation, fibrosis, scarring, and hyperinflation.
FIGURE 16.8 Cylindrical bronchiectasis. Examples from two patients. Airways parallel to the plane of section in anterior segment of an upper lobe show changes of cylindrical bronchiectasis; bronchi are wider than normal and fail to taper as they proceed toward the lung periphery (arrows). (From Hansell, D. M., Lynch, D. A., McAdams, H. P., et al. [2010]. Imaging of diseases of the chest [5th ed.].
Philadelphia, PA: Elsevier.)
FIGURE 16.9 Varicose bronchiectasis. Patient with allergic bronchopulmonary aspergillosis and cystic fibrosis. The bronchiectatic airways have a corrugated, or beaded, appearance. (From Hansell, D. M., Lynch, D. A., McAdams, H. P., et al. [2010]. Imaging
of diseases of the chest [5th ed.]. Philadelphia, PA: Elsevier.)
FIGURE 16.10 Cystic bronchiectasis (advanced) in the upper lobes. (From Hansell, D. M., Lynch, D. A., McAdams, H. P., et al. [2010]. Imaging of diseases of the chest [5th ed.]. Philadelphia, PA: Elsevier.)
Finally, it should be mentioned that the CT scan is an excellent tool to use for lung mapping—that is, the ability to map out and determine precisely where chest physiotherapy would be delivered or exactly where surgical resection of lung should be performed.
General Management of Bronchiectasis
For most causes of bronchiectasis, the treatment of the underlying disease is not possible. Because exacerbations are commonly caused by acute bacterial infections, the general treatment plan is aimed at controlling pulmonary infections, airway secretions, and airway obstruction and preventing complications. Antibiotics (tailored to the patient's sputum cultures and sensitivities), bronchodilators, and expectorants are often prescribed during periods of exacerbation. Daily chest percussion, postural drainage, and effective coughing exercises to remove bronchial secretions are routine parts of the treatment. Childhood vaccinations and yearly influenza vaccinations help reduce the prevalence of some infections. Avoidance of upper respiratory tract infections, smoking, and polluted environments also helps reduce susceptibility to pneumonia in these patients. Surgical lung resection may be indicated for patients who respond poorly to therapy or demonstrate massive hemoptysis.
Respiratory Care Treatment Protocols
Oxygen Therapy Protocol
Oxygen therapy is used to treat hypoxemia, decrease the work of breathing, and decrease myocardial work. The hypoxemia that develops in bronchiectasis is usually caused by the pulmonary shunting associated with the disorder. The hypoxemia may not respond well to oxygen therapy when true or capillary pulmonary shunting is present (see Oxygen Therapy Protocol, Protocol 10.1).
Airway Clearance Therapy Protocol
A number of airway clearance therapy modalities may be used to enhance the mobilization of bronchial secretions, including the following:
•Directed cough
•Exercise breathing programs
•Autogenic breathing
•Forced expiration
•Chest physiotherapy (CPT) (postural drainage [PD], hand or mechanical chest clapping)
•Suctioning
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•Positive expiratory pressure (PEP)
•Oscillatory PEP (e.g., flutter valve acapella device)
•High-frequency chest wall compression
Chest percussion has become more practical and very effective with the advent of high-frequency chest compression devices such as the pneumovest. However, such compression devices are moderately expensive and chest wall discomfort and claustrophobia may limit their usefulness (see Airway Clearance Therapy Protocol, Protocol 10.2).
Lung Expansion Therapy Protocol
Attempts to keep distal lung units inflated may involve the use of deep breathing and coughing and incentive spirometry (see Lung Expansion Therapy Protocol, Protocol 10.3).
Aerosolized Medication Therapy Protocol
Both sympathomimetic and parasympatholytic agents are commonly used in selected patients with bronchiectasis to induce bronchial smooth muscle relaxation, particularly in patients with spirometrically proved reversible airway obstruction (see Protocol 10.4: Aerosolized Medication Therapy Protocol, and Appendix II on the Evolve site).
The use of corticosteroids is discouraged. There are insufficient data to support the use of nebulized hypertonic saline, inhaled dornaxe (DNase), or acetylcysteine in patients with bronchiectasis. Many centers require use of direct physician order to use them.
Mechanical Ventilation Protocol
Invasive and noninvasive mechanical ventilation may be necessary to provide and temporarily help improve alveolar ventilation and eventually return patients to their baseline condition and/or spontaneous breathing. Because acute ventilatory failure superimposed on chronic ventilatory failure is often seen in patients with severe bronchiectasis, continuous mechanical ventilation is justified when the acute ventilatory failure is thought to be reversible—for example, when acute pneumonia exists as a complicating factor (see Ventilator Initiation and Management Protocol, Protocol 11.1, and Ventilation Weaning Protocol, Protocol 11.2).
Medications Commonly Prescribed by the Physician
Expectorants
Expectorants sometimes are ordered when oral liquids and aerosol therapy alone are not sufficient to facilitate expectoration (see Appendix V on the Evolve site). Their clinical effectiveness is doubtful.
Administration of Antibiotics
Antibiotics are commonly administered to treat associated respiratory tract infections (see Appendix III on the Evolve site).
Case Study Bronchiectasis
Admitting History and Physical Examination
A 31-year-old obese male patient consulted his physician regarding an increasingly productive cough. He reported a “bad case” of right lower lobe pneumonia 7 years ago and several episodes of “pulmonary infection” since that time. On those occasions, he usually received an antibiotic, and until 6 months ago the infections responded readily to treatment. However, 6 months ago he noticed that his chronic cough had become increasingly severe and more or less constant and for the first time his cough became productive. Recently, he had produced as much as a cup of thick, tenacious, yellowwhite sputum per day. Within the past 2 to 3 days, he noticed a small amount of dark blood mixed with the sputum. He also noticed some dyspnea on exertion, but he was largely sedentary, and this had not been particularly troublesome. His medical history revealed chronic sinusitis since adolescence but was otherwise unremarkable.
Physical examination revealed an obese male adult in no apparent distress. Vital signs were within normal limits. His oral temperature was 98.4°F. He coughed frequently during the examination and produced a moderate amount of thick, yellow, blood-streaked sputum. Coarse crackles were heard over the right lower lung fields posteriorly. His SpO2 on room air while
at rest was 85%.
Laboratory results showed a mild leukocytosis but were otherwise normal. An outpatient sputum culture indicated the presence of H. influenzae. An HRCT scan of the chest revealed cystic dilations of the right lower lobe (RLL) bronchus. The respiratory therapist assigned to assess and treat the patient at this time recorded the following in the patient's chart.
Respiratory Assessment and Plan
S Productive cough, hemoptysis, worse in past 6 months. Mild dyspnea on exertion.
O Vital signs: Normal. Afebrile. SpO2 85%. Observed moderate amount of mucopurulent, blood-
streaked sputum. Coarse crackles over RLL. Outpatient sputum culture: H. influenzae. HRCT scan suggests saccular dilation of RLL bronchi.
A
•Postpneumonic bronchiectasis RLL (history and HRCT scan)
•Excessive airway secretions and sputum production (coarse crackles and sputum expectoration)
•Acute bronchial infection and hemoptysis (yellow, blood-streaked sputum, culture results)
•Moderate hypoxemia (SpO2)
P Oxygen Therapy Protocol (O2 via 2 L/min nasal cannula). Airway Clearance Therapy Protocol (CPT and PD, cough and deep breathing, q6h).
The physician prescribed antibiotics and administered pneumococcal vaccine. The patient was discharged from the hospital after 3 days with considerable improvement. However, he was still producing a small amount of thin clear sputum. He was instructed to seek prompt medical attention for all future pulmonary infections. His wife was instructed in manual chest percussion and postural drainage techniques.
About 6 months later, the patient arrived at the emergency department complaining of a productive cough, pain on the
left side of the chest (made worse by deep breathing), shaking chills and fever for 3 days, and noticeable swelling of both ankles. Since his previous visit, he had been doing his manual CPT and PD only one or two times per week. He had gained 30 lb and had taken a new job as a painter's apprentice. He admitted to smoking an occasional cigarette. There had been no known recent infectious disease exposure.
Physical examination revealed a young man in obvious respiratory distress. His vital signs were blood pressure 160/100, heart rate 110 beats/min and regular, respiratory rate 20 breaths/min, and oral temperature 101.5°F. His sputum was foulsmelling (a fecal odor), thick, and yellow-green. His cough was strong. Auscultation revealed coarse crackles over both bases. There was mild clubbing of fingers and toes. The physician wrote “bronchiectasis” in the working diagnosis section of the patient's chart.
Although an HRCT scan was ordered, it had not yet been taken. The patient's WBC was 23,500 mm3, with 80%
segmented neutrophils and 10% bands. Room air ABG showed pH 7.51, PaCO2 28 mm Hg,
21 mEq/L, PaO2 45 mm Hg, and SaO2 87%. His SpO2 at rest on room air was 86%; it fell to 78% when he got out of bed to go to the
bathroom.
The respiratory therapist recorded the following note in the patient's emergency department chart.
Respiratory Assessment and Plan
S Cough, pleuritic left-sided chest pain, chills, fever, leg swelling. 30 lb weight gain. Smoking. O HR 110; RR 20; BP 160/100; T 101.5°F. Sputum thick, yellow-green, foul-smelling. Coarse crackles both bases. Strong cough. Clubbing of digits. WBC 23,500 (80% neutrophils, 10%
bands). Room air ABG pH 7.51; PaCO2 28;
21; PaO2 45, and SaO2 87%; SpO2 (room air,
rest) 86%, falls to 78% with mild exertion. A
•Bronchiectasis (old chart record)
•Excessive airway secretions (thick sputum, coarse crackles)
•Good ability to mobilize secretions (strong cough)
•Infection likely (fever, yellow-green sputum, leukocytosis)
•Acute alveolar hyperventilation with moderate hypoxemia (ABG)
•Possible pneumonia
P Review CXR. Oxygen Therapy Protocol (2 L/min per nasal cannula). Airway Clearance Therapy Protocol (CPT and PD q4h). Obtain sputum for Gram stain and culture. Check I&O. Repeat ABG in a.m. Review deep breathing and cough, flutter valve, and pulmonary rehabilitation strategies with patient and his wife. Train in use of pneumovest chest percussion device. Offer smoking cessation and weight reduction programs.
Discussion
The main challenge facing the respiratory therapist caring for the patient with bronchiectasis is the efficient removal of excessive airway secretions. Over the years, postural drainage and percussion, good systemic hydration, and judicious use of antibiotics have been the hallmarks of therapy. More recently, intermittent (rare) use of mucolytics, percussive ventilation, and the Lung Expansion Therapy Protocol (see Protocol 10.3) has become more common. Pneumococcal prophylaxis is, of course, important, as is prompt attention to parenchymal pulmonary infections such as pneumonia. The clinical distinction between chronic bronchiectasis and cystic fibrosis is a subtle one at the bedside, and the latter condition must always be ruled out in patients with bronchiectasis. The goal of long-term therapy in bronchiectasis is prevention of lung parenchyma–destroying pulmonary infections and avoidance of frequent hospitalizations. Hemoptysis is often a sign of more deep-seated infection requiring antibiotic therapy. At the time of the second admission, severe infection was suspected, and intravenous antibiotic therapy was started.
The clinical manifestations throughout this case were all based on the clinical scenario associated with excessive bronchial secretions and possible infection (see Fig. 10.11). For example, the thick yellow sputum resulted in decreased ventilation-perfusion ratios, venous admixture, and hypoxemia. These pathophysiologic mechanisms caused clinical manifestations of coarse crackles, an increase in blood pressure and heart rate, and acute alveolar hyperventilation with moderate hypoxemia.
Digital clubbing associated with hypoxemia is another clinical manifestation of bronchiectasis. After the first assessment, the Oxygen Therapy Protocol and Airway Clearance Therapy Protocol were administered appropriately (see Protocols 10.1 and 10.2). The therapist's review of the chest x-ray image allowed him to target the postural drainage therapy. Low-flow oxygen per nasal cannula, aerosolized bronchodilators (albuterol), chest percussion, and postural drainage therapy were selected from these protocols and applied with good results.
Finally, during the second admission, patient noncompliance was evident (i.e., weight gain, resumption of smoking, employment in a dusty workplace, failure to continue CPT and PD), which further complicated the patient's respiratory disorder. Note that both of these SOAPs omit the patient's height and weight (although they do suggest that he is obese). This is important because an exercise/weight reduction program would be helpful to his cough efficiency, the idea was not mentioned. In response to the patient's condition, the whole respiratory care regimen was up-regulated by an increase in frequency of treatments, with a strong emphasis on the patient's responsibility for his own care. In addition, in both of these admissions, no note of the patient's state of systemic or secretion hydration was made. This is an important omission, and a factor worth noting.
Self-Assessment Questions
1.In which of the following forms of bronchiectasis are the bronchi dilated and constricted in an irregular fashion?
1.Fusiform
2.Saccular
3.Varicose
4.Cylindrical
a.2 only
b.3 only
c.2 and 4 only
d.1 and 3 only
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2.Which of the following is(are) common causes of acquired bronchiectasis?
1.Hypogammaglobulinemia
2.Pulmonary tuberculosis
3.Kartagener syndrome
4.Cystic fibrosis
a.1 only
b.2 only
c.3 only
d.3 and 4 only
3.In the primarily obstructive form of bronchiectasis, the patient commonly demonstrates which of the following? 1. Decreased FRC
2.Increased FEF25%–75%
3.Decreased PEFR
4.Increased FEVT
a.1 only
b.3 only
c.1 and 4 only
d.2 and 4 only
4.Which of the following radiologic findings is(are) associated with bronchiectasis that is primarily obstructive? 1. Atelectasis
2.Depressed or flattened diaphragms
3.Long and narrow heart
4.Translucent lung fields
a.1 and 2 only
b.3 and 4 only
c.1 and 4 only
d.2, 3, and 4
5.Which of the following is considered the hallmark of bronchiectasis?
a.Chronic cough and large quantities of foul-smelling sputum
b.Abnormal bronchogram
c.Acute ventilatory failure superimposed on chronic ventilatory failure
d.Presentation as both a restrictive and obstructive pulmonary disorder
6.Which of the following is(are) commonly cultured in the sputum of patients with bronchiectasis? 1. Streptococcus pneumoniae
2. Pseudomonas aeruginosa
3. Haemophilus influenzae
4. Klebsiella
a.3 only
b.4 only
c.1, 2, and 3 only
d.1, 2, 3, and 4
7.When the pathophysiology of bronchiectasis is primarily obstructive, the patient demonstrates which of the following clinical manifestations?
1.Decreased tactile and vocal fremitus
2.Bronchial breath sounds
3.Dull percussion note
4.Rhonchi and wheezing
a.2 only
b.3 only
c.1 and 4 only
d.2 and 4 only
8.Which of the following diagnostic procedures is(are) used to positively diagnose bronchiectasis? 1. Arterial blood gases
2. Bronchography
3.Oxygenation indices
4.Computed tomography
a.2 only
b.3 only
c.1 and 3 only
d.2 and 4 only
9.Which of the following causes of bronchiectasis is(are) related to abnormal secretion clearance? 1. Pertussis
2. Cystic fibrosis
3.Kartagener syndrome
4.Measles
a.1 only
b.2 only
c.3 and 4 only
d.2 and 3 only
10.Which of the following hemodynamic indices is(are) associated with bronchiectasis?
1.Decreased central venous pressure
2.Increased mean pulmonary artery pressure
3.Decreased right ventricular stroke work index
4.Increased right atrial pressure
a.2 only
b.3 only
c.2 and 4 only
d.1 and 3 only
11.Which of the following respiratory care protocols may be of importance in the outpatient care of patients with bronchiectasis?
1.Oxygen Therapy Protocol
2.Airway Clearance Therapy Protocol
3.Lung Expansion Therapy Protocol
4.Aerosolized Medication Therapy Protocol
a.2 and 3 only
b.2 only
c.1 and 2 only
d.1, 2, 3, and 4
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C H A P T E R 1 7
Atelectasis
CHAPTER OUTLINE
Anatomic Alterations of the Lungs
Etiology
Overview of the Cardiopulmonary Clinical Manifestations Associated With Postoperative Atelectasis
General Management of Postoperative Atelectasis
General Considerations
Respiratory Care Treatment Protocols
Case Study: Postoperative Atelectasis
Self-Assessment Questions
CHAPTER OBJECTIVES
After reading this chapter, you will be able to:
•List the anatomic alterations of the lungs associated with atelectasis.
•Describe the specific causes of atelectasis.
•List the respiratory disorders associated with atelectasis.
•List the cardiopulmonary clinical manifestations associated with postoperative atelectasis.
•Describe the general management of atelectasis.
•Describe the clinical strategies and rationales of the SOAP presented in the case study.
•Define key terms and complete self-assessment questions at the end of the chapter and on Evolve.
KEY TERMS
Absorption Atelectasis
Air Bronchograms
Alveolar Degassing
Alveolar Flooding
Incentive Spirometry (IS)
Optimal PEEP Trial
Primary Atelectasis
Primary Lobule
Therapeutic Bronchoscopy
Anatomic Alterations of the Lungs
Atelectasis is an abnormal condition of the lungs characterized by the partial or total collapse of previously expanded alveoli, thus resulting in the prevention of respiratory exchange of carbon dioxide and oxygen in that part of the lung and reduced lung compliance. The failure of the lungs to expand at birth, most commonly seen in premature infants or those narcotized by maternal anesthesia, is known as primary atelectasis. Atelectasis may be limited to the smallest lung unit— that is, the alveolus or primary lobule,1 or it may involve an entire lung or a segment or lobe of the lung (Fig. 17.1).
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FIGURE 17.1 Alveoli in postoperative atelectasis. (A) Total alveolar collapse. (B) Partial alveolar collapse.
The major pathologic and anatomic alterations associated with atelectasis include partial or total collapse of the following:
•Alveoli of primary lobules (microatelectasis or subsegmental atelectasis)—very common
•Lung segment—fairly common
•Lung lobe—less common
•Entire lung—rare
Etiology
As shown in Box 17.1, there are many respiratory disorders associated with atelectasis. The etiologic factors linked to these disorders, and the subsequent atelectasis that ensues, can be further grouped into pulmonary conditions that (1) reduce alveolar ventilation (e.g., pulmonary edema [alveolar flooding], acute respiratory distress syndrome, ventilatorinduced lung injury [VILI] or ventilator-associated lung injury [VALI],2 smoke inhalation, thermal injuries),3 (2) promote alveolar degassing secondary to airway obstruction (e.g., cystic fibrosis, bronchiectasis, Guillain-Barré syndrome, myasthenia gravis), or (3) compress the lung tissue (e.g., flail chest, pneumothorax, pleural disease).
Box 17.1
Cardiorespiratory Disorders Associated With Atelectasis
•Bronchiectasis
•Cystic fibrosis
•Pulmonary edema
•Pulmonary embolism
•Flail chest
•Fluid overload
•Pneumothorax
•Pleural diseases
•Kyphoscoliosis
•Cancer of the lung
•Acute respiratory distress syndrome*
•Guillain-Barré syndrome*
•Myasthenia gravis*
•Meconium aspiration syndrome
•Respiratory distress syndrome
•Pulmonary air leak syndrome
•Respiratory syncytial virus
•Bronchopulmonary dysplasia
•Diaphragmatic hernia
•Near drowning
•Smoke inhalation and thermal injuries
*Common secondary anatomic alteration of the lungs associated with this disorder.
In this chapter, postoperative atelectasis is used as a prototype of the atelectasis process. Postoperative atelectasis is commonly seen after upper abdominal and thoracic surgical procedures. Lung expansion is often decreased after surgery because of postoperative alveolar hypoventilation (anesthesia), external thoracic compression such as from wound