AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Background

Atelectasis refers to collapse of part of the lung. It may include a lung subsegment or the entire lung and is almost always a secondary phenomenon, with no sex or race proclivities; however, it may occur more frequently in younger children than in older children and adolescents. The direct morbidity from atelectasis is transient hypoxemia, which is due to blood flowing through the atelectatic lung. The blood does not pick up oxygen from the corresponding alveoli. This shunting results in transient hypoxemia.

Pathophysiology

Atelectasis has 4 potential causes, which are as follows:

• Airways may have intrinsic obstruction. 
• Airways may be compressed (extrinsic airway obstruction). 
• Lung tissue may be compressed.
• Alveoli may incompletely expand and eventually collapse.

Because the right middle lobe orifice is the narrowest of the lobar orifices and because it is surrounded by lymphoid tissue, it is the most common lobe to become atelectatic.

Intrinsic airway obstruction is the most common cause of atelectasis in children, and asthma is the most common underlying disorder that predisposes patients to atelectasis. Other causes include bronchiolitis, aspiration due to a swallowing disorder, endobronchial tuberculosis, aspiration from gastroesophageal reflux, airway foreign bodies, cystic fibrosis, and increased or abnormal airway secretions for other reasons. Children younger than 10 years are less likely to have developed the interairway canals of Lambert or the interalveolar pores of Kohn. Thus, young children depend more on the feeding airways to move air into the alveoli. When their airways become obstructed, they are more likely to develop atelectasis than older children who have developed these communications.

Extrinsic compression on the airways is most likely to come from enlarged lymph nodes (such as those due to tuberculosis infection), lymphoma and other tumors in the chest, an enlarged heart that compresses the left main or left lower lobe bronchus, and left-to-right intracardiac shunts that increase blood flow through the pulmonary arteries.

In children with hypoventilation for a protracted period, the alveoli may collapse. This may occur in children with neuromuscular disease, those who have had recent thoracic or upper abdominal surgery, those on medications that decrease their minute ventilation (such as narcotics), and those with abnormally small or dysmorphic chest walls, which may be less compliant than the normal chest wall. Such children may also be predisposed to atelectasis because of poor clearance of airway secretions. An ineffective cough allows these secretions to obstruct the airway.

Atelectasis due to compressed lung tissue occurs most commonly when air, blood, pus, or chyle is present in the pleural space. Intrathoracic abdominal contents, chest wall masses, cardiomegaly, and an abnormal chest wall can all compress adjacent lung tissue. If a portion of lung enlarges, such as with congenital emphysema, or if focal overinflation occurs for any other reason, it may compress the adjacent lung, causing atelectasis.

Frequency

United States

No data are available on the frequency of atelectasis.

Mortality/Morbidity

• Most of the morbidity and any mortality is due to the underlying disorder. The primary complication of atelectasis is hypoxemia, which is usually transient. Within 24-48 hours, the lung is able to decrease or shut off blood flow to the atelectatic area. This is probably caused by factors such as serotonin that reacts to the local hypoxia in the alveoli and causes an intense vasoconstriction. If the atelectasis is massive enough, it may cause enough hypoxemia acutely to require supplemental oxygen or ventilatory support.
• Atelectasis is a suggested cause of fever; however, no known physiologic reason supports this. Recent data dispute this old dogma. A study of adults after open-heart surgery showed no correlation between atelectasis and fever and reported that fever appeared as the incidence of atelectasis was decreasing.¹ Patients with temperatures of more than 38.5°C were less likely to have atelectasis on radiography findings than those patients who were afebrile and undergoing radiography as part of the postoperative routine.
• Another concern is the likelihood of infection in the atelectatic portion of the lung. Although the clearance in this portion of the lung is abnormal, the lung is normally a sterile environment. In the otherwise healthy child with atelectasis, infection is unlikely. However, if the child has abnormal secretions or is prone to aspiration, secondary infection of the atelectatic lung may occur. In children with chronically infected lungs, the atelectatic portion is likely to be similarly infected, with decreased ability to clear the infection. This sets up the possibility of bronchiectasis developing in that portion of the lung. Children who remain on assisted ventilation with atelectasis are at risk of developing infection, including infection in the atelectatic portion of the lung. This portion has less intrinsic clearance, which increases the risk of significant infection if organisms enter this portion.

Race

Other than any racial predilections for the underlying disorders, no racial predilection for atelectasis has been reported (see Cystic Fibrosis and Asthma).

Sex

Atelectasis has no sex predilection.

Age

Atelectasis is probably more common in children younger than 10 years because their airways are typically narrower and are more likely to become obstructed by secretions, airway inflammation, or both. In addition, these smaller airways are more easily compressed. These children are also less likely to have collateral ventilation.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

History

• Most symptoms are related to the underlying disorder.
• Atelectasis alone only causes tachypnea as the child attempts to compensate for decreased tidal volume by increasing the frequency of respiration.
• If the atelectasis is large enough, the child may grunt in an attempt to create auto–positive end-expiratory pressure (PEEP), both to improve oxygenation and to attempt to open the atelectatic areas.
• If a child has underlying cardiopulmonary or neuromuscular disease and is on a monitor, sudden decreases in oxygen desaturation may be a sign of atelectasis. Atelectasis is one of the most common causes of sudden decreases in oxygen saturation in children.

Physical

• Most findings upon physical examination are related to the underlying disorder.
• Breath sounds may be decreased in the atelectatic portion of the lung, although the segment involved may be so small that the changes cannot be perceived. Also, the atelectatic portion may be in a segment inaccessible to the stethoscope.
• If the atelectatic portion and chest wall are large enough, dullness to percussion may be detected.
• The atelectasis may also occur in the right middle lobe or lingula in an adolescent girl. Because both are anteriorly located, the physician must listen to the anterior chest of the patient to hear these lobes. If the physician feels awkward about examining this area and fails to do so, the lobes are not correctly evaluated, and any corresponding abnormalities are not heard.

Causes

• Obstruction of an airway or diminished distention of alveoli may cause atelectasis.
• The most common causes involving airway obstruction include the following:
• • Airway obstruction due to a mucous plug or other airway secretions, such as with bronchiolitis
  • Bronchospasm airway secretions and airway inflammation in patients with asthma
  • Abnormal airway secretions in cystic fibrosis
  • Airway foreign body
  • Extrinsic compression on an airway (eg, compression due to an enlarged or aberrant vessel)
  • Enlarged lymph nodes that compress the airway 
  • Masses in the chest that compress the airway or alveoli
  • Cardiomegaly or enlarged pulmonary vessels that compress adjacent airways
• Causes of diminished alveolar distention include the following:
• • Small or dysmorphic chest wall
  • Neuromuscular diseases
  • Anesthesia or sedation
  • Pain from upper abdominal surgery
  • Abdominal distention
  • Chest wall or upper abdominal pain

DIFFERENTIALS

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Lab Studies

• Laboratory studies should include measurement of oxygenation, either by oximetry or arterial blood gas.
• Pulmonary function studies may detect unrecognized airflow obstruction, restrictive disease, or decreased respiratory muscle pressures.

Imaging Studies

• CT scanning
• • Chest CT scanning may help evaluate for compression of the airway.
  • CT scanning may also detect any underlying pathology that predisposes to atelectasis. It may also reveal diffuse disease not suggested by plain radiography.
• Chest radiography: Plain chest radiography is often the first study to reveal atelectasis.

Procedures

Flexible or rigid bronchoscopy may help distinguish intrinsic obstruction from extrinsic compression. These tests can also better define the nature of any intrinsic obstructing lesion.

Bronchoscopy offers the advantage of potential treatment. This can include removal of secretions with a rigid or flexible bronchoscope or removal of a foreign body, generally with a rigid bronchoscope.

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Medical Care

• Antibiotics are not necessary in the child with asthma. Oral corticosteroids, together with frequent inhaled bronchodilators and continued high-dose inhaled corticosteroids, address the underlying inflammation and bronchospasm.
• If the child has cystic fibrosis, aggressive antibiotic therapy is indicated in conjunction with chest physical therapy and postural drainage. A mucous plug from other causes may respond to chest physical therapy and postural drainage. See Cystic Fibrosis for a more detailed discussion of the therapy for this disorder. Instillation of DNAse, either through a nebulizer or through a bronchoscope, may help remove the secretions more rapidly and completely.
• Children with neuromuscular disease, children who have undergone surgery, and children with chest pain benefit from chest physical therapy to reduce the likelihood of developing further atelectasis; whether these procedures treat the existing atelectasis is not clear. In children with neuromuscular disease, using the mechanical ex-insufflator (CoughAssist Device) is helpful in preventing atelectasis and may produce enough of a cough to clear the airways.
• If pain is causing the atelectasis, adequate pain therapy is mandatory. Administering adequate pain therapy is probably more important than the possibility of decreased minute ventilation from the pain therapy in this situation.

Surgical Care

If the patient is severely affected by the atelectasis and response to therapy of the underlying disorder is suboptimal, bronchoscopic removal of secretions, mucous plugs, or both may be helpful. Both N-acetyl cysteine and rhDNase have been used with some success in facilitating the removal of mucous plugs in the airways. Both have been used in patients with cystic fibrosis and have had some success in patients without cystic fibrosis as well.

Consultations

A pediatric pulmonologist may help detect and treat the underlying disorder and may also be helpful if bronchoscopy is necessary.

Activity

As long as the child's oxygenation status is not compromised, activity should not be limited.

MEDICATION

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Tailor therapy to the underlying disorder whenever possible. Antibiotics are not necessary if the child has asthma and uses oral corticosteroids, frequent inhaled bronchodilators, or high-dose inhaled corticosteroids to address the underlying inflammation and bronchospasm. For more information, see Asthma. The National Asthma Education and Prevention Program (NAEPP) provides detailed information regarding managing children or adults with asthma. For more information see the NAEPP guidelines.

If the child has cystic fibrosis, aggressive antibiotic therapy is indicated in conjunction with chest physical therapy and postural drainage. In children with cystic fibrosis, reducing the load of Pseudomonas species in airways facilitates airway clearance. See Cystic Fibrosis for a more complete discussion on the indications for antibiotics, antibiotics used, and dosing schedule in these patients.

Drug Category: Bronchodilators

These agents decrease muscle tone in the small and large airways in the lungs, thereby increasing ventilation. They are used in children with asthma and are potentially helpful in children with cystic fibrosis.

Drug Category: Systemic corticosteroids

These agents effectively reduce airway inflammation in asthma and cystic fibrosis, which allows easier mobilization of secretions. These also reduce airway reactivity, which might increase propensity to atelectasis.

Drug Category: Inhaled corticosteroids

These agents are safer than systemic corticosteroids for long-term anti-inflammatory effect. Dosing is based on the severity of asthma. Some of the most commonly used inhaled corticosteroids in the United States are listed below.

Drug Category: Corticosteroid and bronchodilator combinations

These agents elicit long-acting beta2-adrenergic agonistic and anti-inflammatory effects for persistent asthma.

FOLLOW-UP

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Further Inpatient Care

• The child should be kept in the hospital while in need of supplemental oxygen and therapy that cannot be adequately or appropriately administered at home. Treatment may include antibiotics and chest physical therapy. Children with neuromuscular disease may benefit from using a mechanical ex-insufflator, which is often part of their long-term home management.

Further Outpatient Care

• Continued therapy is necessary to attempt to eliminate the atelectasis and to prevent further episodes.
• If the child has asthma, prolonged taper of systemic steroids may help eliminate the airway swelling that predisposed the patient to atelectasis. Inhaled corticosteroids help control the asthma and prevent further episodes. Early recognitions of exacerbations of asthma and early therapy also prevent future problems.
• If the child has cystic fibrosis, see Cystic Fibrosis for a more detailed discussion of the therapy of the disease.
• If the child has neuromuscular disease or an abnormal chest wall, attempts to clear the airways, such as with chest physical therapy and postural drainage, help prevent atelectasis. The mechanical ex-insufflator is very helpful in mobilizing secretions in children with an ineffective cough. Some children benefit from positive pressure ventilation to maintain airway and alveolar patency. This should be performed in conjunction with a pediatric pulmonologist.
• If aspiration due to gastroesophageal reflux or swallowing dysfunction predisposes to atelectasis, these causes should be addressed. Pharmacotherapy of gastroesophageal reflux is available. Speech therapists and occupational therapists can often assist with swallowing dysfunction.

In/Out Patient Meds

• Therapy should be geared to the underlying disorder whenever possible.
• If the child has asthma, then oral steroids, frequent inhaled bronchodilators, and high-dose inhaled steroids may help the underlying inflammation and bronchospasm. Antibiotics are not necessary.
• If the child has cystic fibrosis, see Cystic Fibrosis for a discussion of appropriate therapy.

Transfer

• Patients should be transferred to a tertiary care facility if they require a level of support that the referring institution is unequipped for or does not frequently perform in children.

Deterrence/Prevention

• The appropriate long-term management of asthma should reduce the likelihood of the child developing atelectasis.
• In children with cystic fibrosis, adequate use of the airway clearance mechanisms, sometimes in conjunction with antibiotics, can reduce the likelihood of atelectasis developing.
• In children with neuromuscular disease, using a mechanical ex-insufflator (CoughAssist Device) can mobilize those secretions that predispose to atelectasis.
• Routine use of chest physical therapy and postural drainage after extubation has not been shown to reduce the incidence of atelectasis.

Complications

• Complications arising from the underlying disorder
• Hypoxemia
• Secondary infection of the atelectatic lung
• Bronchiectasis in the atelectatic portion of a chronically infected lung

Prognosis

• In most cases, the prognosis for the atelectasis is the same as the prognosis for the underlying disorder. If caused by a readily reversible disorder, the atelectasis should be reversible as well.
• In children with significant neuromuscular disease and lower lobe atelectasis, the atelectasis may be very difficult to resolve.

Patient Education

• Educating the patient and the parents about the underlying disorders and the need to prevent complications is crucial.
• For excellent patient education resources, visit eMedicine's Lung and Airway Center and Procedures Center . Also, see eMedicine's patient education articles Collapsed Lung and Bronchoscopy.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

1. Engoren M. Lack of association between atelectasis and fever. Chest. Jan 1995;107(1):81-4. [Medline].
2. Bagley CE, Gray PH, Tudehope DI, Flenady V, Shearman AD, Lamont A. Routine neonatal postextubation chest physiotherapy: a randomized controlled trial. Journal of Paedtrics & Child Health. November 2005;41:592-7. [Medline].
3. De Boeck K, Willems T, Van Gysel D. Outcome after right middle lobe syndrome. Chest. Jul 1995;108(1):150-2. [Medline].
4. Hendriks T, de Hoog M, Lequin MH, Devos AS, Merkus PJ. DNAse and atelectasis in non-cystic fibrosis pediatric patients. Critical Care. August 2005;9:351-6. [Medline].
5. Miske LJ, Hickey EM, Kolb SM, et al. Use of the mechanical in-exsufflator in pediatric patients with neuromuscular disease and impaired cough. Chest. Apr 2004;125(4):1406-12. [Medline].
6. Schindler MB. Treatment of atelectasis: where is the evidence?. Crit Care. Aug 2005;9(4):341-2. [Medline].
7. Slattery DM, Waltz DA, Denham B, et al. Bronchoscopically administered recombinant human DNase for lobar atelectasis in cystic fibrosis. Pediatr Pulmonol. May 2001;31(5):383-8. [Medline].
8. Stiller K. Physiotherapy in intensive care: towards an evidence-based practice. Chest. Dec 2000;118(6):1801-13. [Medline].
9. Woodring JH. Determining the cause of pulmonary atelectasis: a comparison of plain radiography and CT. AJR Am J Roentgenol. Apr 1988;150(4):757-63. [Medline].
10. Wu KH, Lin CF, Huang CJ, Chen CC. Rigid ventilation bronchoscopy under general anesthesia for treatment of pediatric pulmonary atelectasis caused by pneumonia: A review of 33 cases. Int Surg. Sep-Oct 2006;91(5):291-4. [Medline].

Article Last Updated: Sep 13, 2007