Atelectasis in children

INTRODUCTION — Atelectasis refers to volume loss within the lung, generally to a degree visible on radiographic imaging. It is a common finding on chest radiography, particularly in the inpatient setting. Although it is abnormal, reflecting a pathophysiologic process, it is often asymptomatic and requires no specific intervention. However, patients with risk factors for clinically significant atelectasis may require specific interventions to prevent or treat atelectasis. These include patients undergoing cardiothoracic surgery or those with underlying pulmonary or neuromuscular disease.

The common causes, radiographic appearance, and management of atelectasis in children will be discussed below. Other aspects of atelectasis are discussed in separate topic reviews:

●(See "Radiologic patterns of lobar atelectasis".)

●(See "Atelectasis: Types and pathogenesis in adults".)

PATHOPHYSIOLOGY

Mechanisms — Atelectasis may be caused by:

●Obstruction – Atelectasis is often a consequence of an airway obstruction, which may be within the airway (intraluminal), extrinsic to the airway, or within the airway wall. If the obstruction is complete, the air distal to the obstruction is reabsorbed (particularly if 100% oxygen is administered), causing atelectasis. By contrast, partial obstruction can lead to air trapping and hyperinflation distal to the obstruction ("ball-valve effect"). Hence, patients with areas of complete and partial airway obstruction (eg, with multiple mucus plugs) may lead to both atelectasis and hyperinflation in the same radiograph.

●Inability to reexpand the lung – Atelectasis also may be caused or exacerbated by disorders that interfere with reexpansion of the lung, such as parenchymal compression, neuromuscular disease, or severe scoliosis.

●Increased surface tension – Diseases in which surfactant is reduced/absent (eg, extreme prematurity) or inactivated (eg, acute respiratory distress syndrome or pneumonia) are often complicated by atelectasis; this form is sometimes called adhesive atelectasis. Surfactant reduces surface tension and is essential to prevent the collapse of small alveoli. Alveoli are more prone to collapse than larger airways because the air pressure inside a bubble is inversely proportional to its radius (Laplace relationship).

These and other mechanisms of atelectasis are discussed in more detail separately. (See "Atelectasis: Types and pathogenesis in adults".)

Functional consequences — Consequences of atelectasis may include:

●Increased work of breathing – Most commonly, there is no change in work of breathing. However, extensive atelectasis produces restrictive mechanical changes and may contribute to work of breathing, particularly in the setting of underlying chronic lung disease (eg, in bronchopulmonary dysplasia). (See "Bronchopulmonary dysplasia (BPD): Clinical features and diagnosis".)

●Gas exchange abnormalities – Hypoxemia due to atelectasis is uncommon due to local hypoxic vasoconstriction in atelectatic areas, which redirects blood flow to better-ventilated areas of the lung, partially compensating for the under-ventilated area. This compensatory mechanism becomes less effective when >50 percent of the lung is collapsed. It is also less effective in patients with underlying diffuse parenchymal lung diseases leading to hypoxemia (eg, cystic fibrosis, asthma) or pulmonary hypertension (eg, bronchopulmonary dysplasia).

Natural history — The natural course of atelectasis depends upon its cause. Treatment of the underlying problem often leads to resolution of the atelectasis.

Persistence of atelectasis suggests that there is a fixed obstruction (eg, foreign body) and/or other factors that promote atelectasis, including inadequate respiratory muscle strength, anatomic factors, and/or reduced surfactant. As an example, persistent left lower lobe atelectasis in Duchenne muscular dystrophy may be triggered by pneumonia but is propagated by a combination of cardiomegaly compressing lung parenchyma and the left main bronchus and diaphragm weakness. Similarly, patients with neuromuscular disease or neurocognitive disability often have chronic or recurrent atelectasis.

CAUSES — Common causes of clinically significant atelectasis in children and their mechanism(s) are listed in the table (table 1). Several of these causes involve multiple mechanisms.

CHEST EXAMINATION — Examination findings suggesting atelectasis are:

●Diminished breath sounds – Focal reduction of breath sounds is the most specific physical sign of atelectasis. However, this finding is generally apparent only when large areas of the lung are atelectatic, particularly when the lower lobes are affected. In some cases, the reduction in breath sounds may be appreciated only by comparing the affected side with the unaffected side.

●Dullness to percussion – Dullness to percussion also may be noted over an area of extensive atelectasis.

●Tracheal deviation – Tracheal deviation may occur with complete atelectasis of one lung, accompanied by greatly diminished or absent breath sounds in the affected hemithorax. This is unusual in children (image 1).

Most other findings are related to an underlying cause of the atelectasis rather than the atelectasis itself. As an example, in patients with asthma and compressive right middle lobe atelectasis, the predominant findings may be wheezes or a combination of wheezes and crackles; changes in breath sounds may not be apparent, because the upper and lower lobes fill the space occupied by the collapsed lobe. Similarly, longstanding airway obstruction (eg, due to an airway foreign body or mucus plug) may be associated with postobstructive atelectasis, pneumonia and localized bronchiectasis. If the obstruction is partial (permitting some airflow), there may be inspiratory (and occasional expiratory) crackles. A more specific sign of partial airway obstruction is phase delay, in which air entry and exit are delayed on the affected side; this is detectable only with a double-headed stethoscope. (See "Airway foreign bodies in children" and "The pediatric physical examination: Chest and abdomen", section on 'Lungs'.)

IMAGING — Atelectasis is generally diagnosed based on the radiographic findings, typically consisting of pulmonary opacification with or without associated adjacent compensatory signs. The appearance of the atelectasis depends upon the size of the area of volume loss and by the imaging modality utilized.

Chest radiograph — Atelectasis is best evaluated with conventional chest radiographs, with two views (anteroposterior and lateral). Inspiratory and expiratory radiographs also may be helpful, particularly if foreign body aspiration is suspected.

Atelectasis may appear as (see "Radiologic patterns of lobar atelectasis"):

●Nonspecific small areas of opacity ("patchy" atelectasis), either unilateral or bilateral

●Subsegmental opacities with linear ("plate-like") or angular margins

●Lobar opacities (right upper, middle, or lower lobe; left upper or lower lobes)

●Unilateral whole-lung opacity with signs of compensatory hyperinflation, pulmonary fissural shift, mediastinal shift

When interpreting the radiograph, look for:

●Signs of foreign body aspiration – This is an especially important consideration in a young child with focal atelectasis and/or those with a history of choking, even if the episode occurred days or weeks before presentation. Most airway foreign bodies are radiolucent and will not be apparent on the radiograph. The key signs consistent with foreign body aspiration may include (see "Airway foreign bodies in children", section on 'Imaging'):

•Hyperinflated lung – Greater lucency of the lung distal to the obstruction (image 2A-B) due to air trapping and hyperinflation distal to a partial obstruction.

•Atelectasis – A foreign body causes atelectasis only if the obstruction is complete and the aspiration was not very recent since the distal air is resorbed over time.

•Mediastinal shift – The mediastinum tends to shift away from the lung field containing the foreign body due to unilateral air trapping distal to the obstruction.

•Focal pneumonia – Infection often develops distal to an obstructed airway.

Foreign bodies may cause little or no radiographic changes, however, so a high suspicion and careful history are important. (See "Airway foreign bodies in children".)

●Signs that distinguish atelectasis from consolidation – Atelectasis (alveolar collapse) can be difficult to distinguish from consolidation (pneumonia). Both can occur together, as in patients with pneumonia and airway involvement. Radiographic clues include:

•Mediastinal shift – Mediastinal shift toward the lesion suggests atelectasis but is not always present (image 1 and image 3A-B).

•Diaphragm position – Elevation of the diaphragm suggests atelectasis (image 4), while a normal or depressed diaphragm is more consistent with consolidation.

•Fissure – Shift of the interlobar fissure toward the lesion (particularly with incurving of the fissure) suggests atelectasis (image 5 and image 6A-B), while a shift away from the lesion suggests consolidation.

•Air bronchograms – Air bronchograms are not seen in an area of atelectasis but may be seen in an area of consolidation.

●Anatomic distribution – The distribution of the atelectasis can provide clues to the etiology, if not already known:

•Unifocal atelectasis is seen in cases of a focal airway obstruction, such as with mucus plug, foreign body aspiration, or congenital lung anomaly. Obstruction of a main bronchus may cause atelectasis of the entire lung (image 7).

•Diffuse or patchy multilobar atelectasis can be seen in generalized lung disease, such as cystic fibrosis, primary ciliary dyskinesia, bronchiolitis, and asthma. The combination of atelectasis and hyperinflation suggests a diffuse airway obstructive process. These disorders may also cause unifocal atelectasis due to a localized mucus plug.

•Left-sided atelectasis can be seen in postcardiac surgery patients, particularly when there has been preoperative cardiomegaly compressing the left bronchus. Left lower lobe atelectasis is also common in older patients with Duchenne muscular dystrophy, caused by cardiomegaly and bronchial compression in combination with diaphragmatic weakness.

•Upper lobe atelectasis is particularly common in younger patients with cystic fibrosis (image 6A-B). The finding of upper lobe atelectasis in an infant should prompt consideration of diagnostic testing for cystic fibrosis (image 3A). Right upper lobe atelectasis also raises the possibility of aspiration because this lobe is vulnerable in the supine position (image 8).

•Migrating or shifting atelectasis (in which the location of the atelectasis changes over time) suggests impaired airway clearance, which is common in patients with severe neurocognitive disability (cerebral palsy with high cough threshold) or neuromuscular disease with ineffective cough clearance. Similarly, in patients with viral bronchiolitis, the distribution of patchy atelectasis often changes in serial radiographs.

Ultrasound — Thoracic ultrasound can detect atelectasis and may help distinguish parenchymal from pleural processes. The finding of pleural fluid in the setting of an opacified hemithorax suggests a diagnosis of pneumonia (see "Epidemiology, clinical presentation, and evaluation of parapneumonic effusion and empyema in children"). Atelectasis can also be an incidental finding on ultrasonography, such as basilar atelectasis noted on abdominal ultrasound.

Computed tomography scan — Compared with conventional radiography, computed tomography (CT) is more sensitive for identifying areas of atelectasis and their distribution. Potential uses include:

●In a patient with known pulmonary disease, CT helps determine the extent of atelectasis and whether it may be contributing to respiratory dysfunction. It can also help guide bronchoscopy.

●In other patients, CT findings may help to clarify the cause of the pulmonary disease by providing precise information about the anatomic distribution of atelectasis and related pulmonary abnormalities.

●If pleural fluid is detected, this suggests a diagnosis of pneumonia; atelectasis alone does not cause a pleural effusion.

Dependent atelectasis (atelectasis seen in posterior portions of the lungs in a supine patient) is a common finding in CT scans performed under anesthesia; it is usually iatrogenic and reversible and does not require specific intervention.

APPROACH TO MANAGEMENT

Incidental atelectasis on imaging — Patients undergoing advanced imaging under sedation or anesthesia often have dependent (posterior) atelectasis. This finding is usually clinically insignificant and resolves spontaneously. However, patients with extensive atelectasis or underlying risk factors may require intervention, similar to the postoperative patients described below.

Atelectasis in acute respiratory illnesses — Atelectasis is common in patients with acute exacerbations of asthma or bronchiolitis. For most such patients with mild disease managed in the outpatient setting, treatment of the underlying disease is sufficient to resolve the atelectasis. (See "Bronchiolitis in infants and children: Treatment, outcome, and prevention" and "Acute asthma exacerbations in children younger than 12 years: Overview of home/office management and severity assessment".)

Similarly, for hospitalized patients, the main focus is on management of the underlying lung disease. However, if interventions such as noninvasive or invasive ventilation are required, the strategy may be adjusted to address the atelectasis (eg, by increasing continuous positive airway pressure [CPAP] or positive end expiratory pressure [PEEP]). This is discussed separately. (See "Bronchiolitis in infants and children: Treatment, outcome, and prevention", section on 'Moderate to severe bronchiolitis (inpatient management)' and "Acute asthma exacerbations in children younger than 12 years: Inpatient management" and "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management" and "Acute exacerbations of asthma in adults: Emergency department and inpatient management".)

Postoperative atelectasis — Atelectasis is common in the postoperative setting due to the effects of anesthesia, splinting from pain, and/or use of opioids. Whether intervention is needed depends on the patient's underlying risk factors and extent of the atelectasis.

●In patients with normal respiratory muscle strength, the atelectasis typically resolves spontaneously. Recovery is enhanced by use of incentive spirometry, early ambulation, and judicious pain management. (See 'Preventive or general measures' below.)

●Risk factors for clinically significant postoperative atelectasis include:

•Underlying airway disease and anomalies – eg, asthma, bronchiectasis, bronchopulmonary dysplasia, aspiration syndromes, tracheomalacia, and bronchomalacia.

•Neuromuscular disease – eg, severe cerebral palsy (associated with ineffective cough and/or hypoventilation) or muscular dystrophies (causing respiratory muscle weakness).

•Major thoracic or abdominal surgery – Postoperative pain and splinting interferes with lung expansion.

•Severe scoliosis.

•Congenital heart disease – Individuals with congenital heart disease are at risk for postoperative atelectasis if their cardiovascular defect causes external airway compression. In addition, those with heterotaxia syndromes often have impaired mucociliary clearance, which contributes to their atelectasis risk [1].

•Tracheomalacia or bronchomalacia, if severe enough to interfere with effective cough and mucus clearance.

Often, multiple risk factors are present in the same patient.

Patients with these risk factors may require preemptive intervention in the postoperative period, such as chest physiotherapy, inhaled hypertonic saline, mechanical insufflation-exsufflation (MIE), and positive airway pressure therapies (eg, CPAP). For other patients, the decision to intervene depends on the extent of atelectasis and respiratory compromise (hypoxemia, ongoing need for respiratory support). (See 'Interventions' below.)

Atelectasis in patients with neuromuscular disease or scoliosis — Patients with neuromuscular disease or severe scoliosis are at risk for acute or chronic atelectasis. Acute exacerbations may be triggered by surgery (see 'Postoperative atelectasis' above), acute respiratory illness, or immobilization/hospitalization for any reason.

These patients benefit from:

●Early implementation of general measures to prevent atelectasis (ambulation, incentive spirometry). (See 'Preventive or general measures' below.)

●For patients with extensive atelectasis and/or hypoxia, use of MIE (cough assist) devices, sometimes with chest physiotherapy (including oscillating positive expiratory pressure devices) or advanced measures to reexpand the lungs (positive expiratory pressure). (See 'Advanced measures' below and "Respiratory muscle weakness due to neuromuscular disease: Management".)

PREVENTION — Measures to prevent atelectasis are appropriate for certain patients. The intervention depends upon the patient's risk factors and the clinical setting:

●Acute care setting – All hospitalized patients should be assessed for risk factors for atelectasis and encouraged to do some form of preventive measures. Low-risk patients should be encouraged to ambulate.

Postoperative patients and those who are on bedrest should be encouraged to perform incentive spirometry several times a day. Patients who have thoracic, spinal, or abdominal surgeries are particularly at risk; management should include judicious pain control to permit deep inspiration and coughing. (See 'Preventive or general measures' below.)

Patients with neuromuscular disease who are acutely hospitalized for a respiratory illness or surgical intervention often benefit from more intensive preventive measures (chest physiotherapy, performed manually, via airway oscillation device, or with a high-frequency chest compression vest, and/or mechanical insufflation-exsufflation [MIE; "cough assist"] device). (See 'Advanced measures' below.)

●Chronic care setting – For patients with chronic neuromuscular disease (eg, cerebral palsy) or respiratory disease (eg, cystic fibrosis), preventive measures may include regular chest physiotherapy, performed manually or with a high-frequency chest compression device, and/or MIE device.

INTERVENTIONS

Preventive or general measures

Pain management — In the postoperative setting, judicious pain management is an important step to prevent and manage atelectasis. Analgesia should be sufficient to permit coughing and deep inspiration. However, excessive sedation should be avoided because it can interfere with both of these processes.

Incentive spirometry and ambulation — Incentive spirometry is a well-established, safe, and inexpensive technique that is primarily used as a preventive measure but is also a common component of care for mild or moderate atelectasis in the acute or postoperative setting. In the postoperative setting, early ambulation also helps to reexpand the lungs. The efficacy of these measures is marginal, as discussed separately. (See "Strategies to reduce postoperative pulmonary complications in adults", section on 'Lung expansion'.)

Older children usually can use an incentive spirometry device, which is essentially an inspiratory flow meter. For young children, incentive spirometry typically consists of blowing bubbles or pinwheels and other play-based techniques. The goal is to fully inflate the lungs. Protocols for incentive spirometry vary but generally involve repeat inhalations (typically 10) with a breath hold, with three to four sessions daily [2].

Advanced measures

Airway clearance techniques

●Chest physiotherapy – Chest physiotherapy refers to percussion and drainage, administered manually, or various forms of high-frequency chest wall compression therapy, administered with a vest or device. These techniques are commonly used and likely of value despite the lack of an evidence base for this modality. Much of the experience with chest physiotherapy comes from patients with cystic fibrosis. (See "Cystic fibrosis: Overview of the treatment of lung disease", section on 'Chest physiotherapy'.)

●Mechanical insufflation-exsufflation (MIE) devices – Children with poor ability to generate a cough may benefit from regular use of an MIE device. This therapy may be delivered via face mask, mouthpiece, or artificial airway, and some devices also provide oscillation of the air column to aid in secretion mobilization. It may be done in the acute setting (eg, to prevent or treat postoperative atelectasis in high-risk patients) or as a chronic intervention (eg, patients with respiratory muscle weakness). It is usually administered then twice daily, with more frequent use during respiratory illnesses. (See "Respiratory muscle weakness due to neuromuscular disease: Management", section on 'Mechanical insufflation-exsufflation'.)

The most robust evidence for use of MIE is for patients with Duchenne or Becker muscular dystrophy; MIE is recommended for those with impaired cough, in addition to other respiratory interventions (see "Duchenne and Becker muscular dystrophy: Management and prognosis", section on 'Respiratory management'). A retrospective study in children with other neuromuscular diseases (primarily spinal muscular atrophy) found that chronic outpatient use of MIE was associated with reduced hospital admissions over a three-year period (decreased from 3.7 to 0.9 admissions) and total hospital days (decreased from median 33.6 days to 2.7 days) [3].

●Intrapulmonary percussive ventilation – Intrapulmonary percussive ventilation is another approach to mobilize secretions. It consists of a pneumatic device that can be connected to a face mask, mouthpiece, or artificial airway that intermittently delivers small tidal volumes at high frequencies (100 to 300 cycles per minute), creating percussions inside the lung.

Data describing efficacy in all age groups are limited, and most data are from retrospective case series [4]. Small randomized trials in children with atelectasis (various causes) found that intrapulmonary percussive ventilation increased secretion clearance [5], improved radiographic manifestations of atelectasis [6], and reduced the need for antibiotics [7]. A systematic review found benefits in children with atelectasis from causes other than cystic fibrosis [4].

●Manually assisted cough – If an MIE is not available for a child with respiratory muscle weakness, cough may be assisted by use of a bag-valve-mask device (eg, Ambu bag) to insufflate the lungs, followed by an abdominal thrust maneuver [8]. This is a second-line approach, used if an MIE device is not available. (See "Respiratory muscle weakness due to neuromuscular disease: Management", section on 'Manual-assisted cough (abdominal thrust)'.)

Positive pressure ventilation — For patients requiring respiratory support, use of increased expiratory pressure helps to reexpand the lungs. The approach depends on the type of respiratory support:

●Noninvasive ventilation – For patients managed with noninvasive ventilation support, use of continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BPAP) helps to expand the lungs. This may be applied in the acute setting (eg, postoperative or during a respiratory illness) or as a chronic measure. This approach is often used for children with neuromuscular disease who have chronic difficulties with atelectasis (ie, associated with significant hypoventilation [CO₂ retention] and/or recurrent pneumonia). (See "Respiratory muscle weakness due to neuromuscular disease: Management", section on 'Noninvasive ventilation'.)

●Intubated patients – For patients on a ventilator, clinically significant atelectasis (eg, with associated hypoxemia) can be addressed by:

•Adjusting ventilator settings to improve lung expansion. A common approach is to increase positive end expiratory pressure (PEEP), although there are few data to support this. Increasing tidal volumes (either with higher peak pressures or higher set tidal volumes) is also reasonable and possibly more effective.

•Positioning the patient so that collapsed lung segments are not dependent.

•MIE treatments, delivered via the endotracheal tube once or twice daily.

Details of these strategies are discussed separately. (See "Acute severe asthma exacerbations in children younger than 12 years: Endotracheal intubation and mechanical ventilation" and "Invasive mechanical ventilation in adults with acute exacerbations of asthma" and "Respiratory muscle weakness due to neuromuscular disease: Management", section on 'Invasive mechanical ventilation'.)

Intermittent positive pressure techniques — Other techniques that can be used to expand the lung include (see "Respiratory muscle weakness due to neuromuscular disease: Management", section on 'Lung volume recruitment (assisted inflation maneuvers)'):

●Manual hyperinflation – Manual hyperinflation therapy is performed by a respiratory therapist. Using a manual resuscitator bag with face mask or artificial airway, the therapist administers a deep breath to inflate the lungs to total lung capacity, followed by a breath hold for one to two seconds. Evidence supporting manual hyperinflation is limited, and clinical benefit has not been demonstrated [9].

●Stacked breathing – Alternatively, for cooperative patients with normal respiratory muscle strength, a breath stacking/dynamic hyperinflation technique can be used. This involves initiation of a breath before exhalation of the prior breath is complete, thus increasing lung volume [10].

For patients who are intubated (and also for those with a tracheostomy), each episode of positive pressure treatment should be followed by some form of assisted secretion clearance, such as suctioning or MIE. This is necessary because intubation interferes with cough clearance by preventing closure of glottis and narrowing airway opening, even in an awake patient.

Medications to treat mucus plugging

●Hypertonic saline – Nebulized hypertonic (3%) saline is used to hydrate secretions, especially for patients with a tracheostomy, despite a lack of supportive literature [11]. Use of hypertonic saline for patients with cystic fibrosis is supported by moderate clinical evidence. By contrast, its use in bronchiolitis is not well supported. (See "Cystic fibrosis: Overview of the treatment of lung disease", section on 'Inhaled airway clearance agents' and "Bronchiolitis in infants and children: Treatment, outcome, and prevention", section on 'Nebulized hypertonic saline'.)

●Recombinant human dornase alfa (DNase) – DNase, an endonuclease that decreases the viscosity of purulent sputum, is administered by inhalation. Its primary use is for patients with cystic fibrosis and chronic cough; supportive evidence is primarily from ambulatory patients with cystic fibrosis, without atelectasis. (See "Cystic fibrosis: Overview of the treatment of lung disease", section on 'Inhaled airway clearance agents'.)

DNase has no established benefit for patients without cystic fibrosis, although, theoretically, it might help to dissolve mucus plugs from other disease processes in which there is a high deoxyribonucleic acid (DNA) content in retained secretions. Bronchoscopic/endotracheal instillation of DNase has been reported in case reports of ventilated neonates, asthma, or non-cystic fibrosis-associated bronchiectasis [12]. Although some institutions routinely use DNase for treating atelectasis unrelated to cystic fibrosis in the pediatric intensive care unit, there are no controlled trials to support this practice [13]. In a small comparison trial of nebulized DNase versus hypertonic saline versus normal saline in the treatment of atelectasis in the intensive care setting, there were no differences among these three treatments [11]. Clinical trials in adults with non-cystic fibrosis-related bronchiectasis showed no benefit of DNase. (See "Bronchiectasis in adults: Maintaining lung health", section on 'Mucolytic agents and airway hydration'.)

●Limit anticholinergic agents – Some patients with neuromuscular disease are chronically treated with anticholinergic agents (including systemic glycopyrrolate or atropine or inhaled ipratropium bromide) to manage sialorrhea and/or excessive pulmonary secretions. These agents are effective for managing these issues. However, for patients experiencing difficulties with mucus plugging, and especially those with tracheostomies, anticholinergic agents should be avoided or reduced because they tend to worsen the problem rather than ameliorate it. Use of anticholinergic agents in children with cerebral palsy is discussed separately. (See "Cerebral palsy: Overview of management and prognosis", section on 'Sialorrhea'.)

Bronchoscopy — For patients with an airway foreign body, bronchoscopy is the first-line and definitive treatment. Any associated atelectasis should resolve promptly after removal of the obstruction, although patients with associated postobstructive pneumonia require antibiotics and, sometimes, other measures to promote lung expansion. (See "Airway foreign bodies in children".)

For other patients with persistent atelectasis, flexible bronchoscopy is a last resort; it should only be considered if the atelectasis is severe and less invasive measures have failed. The procedure can be performed at bedside in the intubated patient (image 7). As an example, bronchoscopy may be indicated for a patient with postoperative whole-lung atelectasis that is suspected to be related to a mucus plug, if all of the above measures including intensive noninvasive airway clearance therapies have failed.

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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Atelectasis (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Definition – Atelectasis refers to volume loss within the lung, generally to a degree visible on radiographic imaging. It is a common finding on chest radiography, particularly in the inpatient setting. (See 'Introduction' above.)

●Causes – Common causes of clinically significant atelectasis in children and their mechanism(s) are listed in the table (table 1). Multiple mechanisms may be involved in the same patient. Atelectasis is often a consequence of an airway obstruction (eg, mucus plug or airway foreign body). Complete obstruction leads to distal atelectasis, while partial obstruction leads to hyperinflation. (See 'Causes' above and 'Mechanisms' above.)

●Physical findings – Focal reduction of breath sounds is the most specific physical sign of atelectasis and is often accompanied by dullness to percussion. However, these findings are not apparent in many cases, especially if obscured by other findings related to an underlying cause of the atelectasis, such as wheezing or crackles. Tracheal deviation may occur if the atelectasis involves an entire lung. (See 'Chest examination' above.)

●Imaging – Atelectasis is best evaluated with conventional chest radiographs, with two views (anteroposterior and lateral). Inspiratory and expiratory radiographs also may be helpful. The radiograph may provide clues to the cause of the atelectasis (eg, foreign body aspiration), help to distinguish atelectasis from pneumonia, and evaluate any underlying lung disease. (See 'Chest radiograph' above.)

●Clinical approach

•Acute respiratory illness – In patients with normal respiratory muscle strength, atelectasis caused by a reversible process typically resolves spontaneously. Treatment is focused on managing the underlying process (eg, asthma, bronchiolitis, or foreign body). Hospitalized patients sometimes require interventions that help with the atelectasis, such as chest physiotherapy, positioning, or respiratory support with lung expansion strategies. (See 'Atelectasis in acute respiratory illnesses' above.)

•Postoperative – Atelectasis is common in the postoperative setting due to the effects of anesthesia, splinting from pain, and/or use of opioids. Whether intervention is needed depends on the patient's underlying risk factors and extent of the atelectasis (eg, chronic lung disease, postoperative pain, or respiratory muscle weakness). (See 'Postoperative atelectasis' above.)

•Neuromuscular disease – Patients with neuromuscular disease are at risk for acute or chronic atelectasis. Acute exacerbations may be triggered by surgery, acute respiratory illness, or immobilization/hospitalization for any reason. Such patients may benefit from positive airway pressure therapies (eg, mechanical insufflation-exsufflation [MIE]), sometimes with inhaled medications (eg, hypertonic saline). Rarely, bronchoscopy may be warranted to remove a mucus plug. These interventions are briefly summarized above and discussed in greater detail separately. (See 'Interventions' above and "Respiratory muscle weakness due to neuromuscular disease: Management" and "Flexible bronchoscopy in adults: Indications and contraindications", section on 'Therapeutic indications'.)

●Prevention

•Postoperative setting – For patients at risk for postoperative atelectasis (eg, major thoracic surgery or underlying lung disease), strategies to prevent atelectasis include incentive spirometry, early ambulation, and judicious pain control. Patients with neuromuscular disease may benefit from prophylactic use of MIE therapy starting in the immediate postoperative period. These issues are briefly described above and are discussed in greater detail separately. (See 'Preventive or general measures' above and "Strategies to reduce postoperative pulmonary complications in adults", section on 'Postoperative strategies' and "Respiratory muscle weakness due to neuromuscular disease: Management".)

•Chronic care setting – Patients with chronic neuromuscular or respiratory disease often benefit from chronic measures to prevent and manage atelectasis including regular chest physiotherapy and/or MIE therapy, as discussed separately. (See "Respiratory muscle weakness due to neuromuscular disease: Management".)