eMedicine Specialties > Pediatrics: General Medicine > Pulmonology

Atelectasis, Pulmonary

Updated: Sep 8, 2009

Introduction

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 due to blood flowing through the lung, which does not have normal air flow. The blood does not pick up oxygen from the corresponding alveoli. This shunting results in transient hypoxemia.

Atelectasis. Left lower lobe collapse. The opacity is in the posterior inferior location.

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. This is referred to as right middle lobe syndrome.

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 those 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

History

Most symptoms of pulmonary atelectasis 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
- Abnormal airway clearance, such as with ciliary dyskinesia syndrome
- 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
- Severe scoliosis
- Neuromuscular diseases
- Anesthesia or sedation
- Pain from upper abdominal surgery
- Abdominal distention
- Chest wall or upper abdominal pain

Differential Diagnoses

Pneumonia

Workup

Laboratory Studies

Laboratory studies in pulmonary atelectasis should include measurement of oxygenation, either by oximetry or ABG.
Pulmonary function studies may detect unrecognized airflow obstruction, restrictive disease, or decreased respiratory muscle pressures.

Imaging Studies

CT scanning

ChestCT 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

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.
A recent study determined that noninvasive medical treatment can be simply and easily used to substitute bronchoscopic treatment in small hospitals.²
If the child with atelectasis 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.
DNAse has been used in cystic fibrosis to facilitate transport of the abnormal secretions. DNAse has been successfully used in other patients with acute atelectasis. However, the success of the medication depends on the amount of DNA in the secretions, which is generally not known beforehand. Although N -acetyl cysteine has been used as a mucolytic both in nebulizer and bronchoscope forms, success has not been validated in controlled studies. Furthermore, it has the potential to cause significant bronchospasm.

Consultations

A pediatric pulmonologist may help diagnose 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

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.³

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.

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.

Albuterol (Ventolin HFA, Proventil HFA, ProAir HFA)

Relaxes bronchial smooth muscle by action on beta2-receptors with little effect on cardiac muscle contractility. First-line bronchodilator that should be used with spacer if using metered dose inhaler.

Dosing

Adult

2-5 inhalations (90 mcg/actuation) PO qid or q2-3h prn cough or wheeze

Pediatric

Administer as in adults
When MDI is used with valved holding chamber, a nebulizer has no advantage

Interactions

Actions are antagonized by beta-antagonists (eg, propranolol); concomitant administration of sympathomimetics may enhance cardiovascular side effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause tremor or tachycardia

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.

Prednisone (Deltasone) or prednisolone (Prelone, Orapred)

Corticosteroids that are first-line therapies in the United States.
Both are available in tab and syr; Orapred is available in PO dissolving tab. When choosing syr for children, prednisolone syr is more palatable than prednisone syr.

Dosing

Adult

5-60 mg/d PO qd or divided bid/qid

Pediatric

2 mg/kg/d PO divided bid; not to exceed 30-40 mg PO bid; tapering schedule necessary if used >10 d

Interactions

Barbiturates, phenytoin, or rifampin may decrease prednisone effectiveness

Contraindications

Documented hypersensitivity; serious infections (excluding meningitis and septic shock) and fungal infections; varicella infections; diabetes (caution)

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Administer with meals to decrease GI upset; early onset adverse effects include glucose intolerance, hypertension, agitation, and indigestion; late-onset adverse effects include immune suppression and increased susceptibility to sepsis, adrenal suppression, hypertension, urinary calcium loss and osteopenia, and gastric irritation and bleeding; lower dose as quickly as possible to reduce adverse effects and complications; prolonged use might be advisable on an alternate-day schedule

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.

Fluticasone (Flovent HFA, Flovent Diskus)

Fluticasone decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. Available as aerosol, Flovent HFA (44 mcg/actuation, 110 mcg/actuation, or 220 mcg/actuation), also available as Flovent Powder for Inhalation (Diskus) that delivers 50 mcg/actuation, 100 mcg/actuation, or 250 mcg/actuation.

Dosing

Adult

Doses may be higher for patient with poor asthma control
HFA:
Previously on bronchodilators alone: 88-132 mcg inhaled PO bid; may increase to 440 mcg bid; higher doses may be necessary
Previously on inhaled corticosteroids: 88-220 mcg inhaled PO bid; may increase to 440 mcg bid or higher
Previously on PO corticosteroids: 440 mcg inhaled PO bid; may increase to 880 mcg bid or higher
Powder for inhalation:
Previously on bronchodilators alone: 100 mcg inhaled PO bid; may increase to 500 mcg bid or higher
Previously on inhaled corticosteroids: 100-250 mcg inhaled PO bid; may increase to 500 mcg bid or higher
Previously on PO corticosteroids: 500-1000 mcg inhaled PO bid or higher

Pediatric

Doses may be higher for patient with poor asthma control
<4 years: Not yet FDA-approved for young children, but emerging data suggest administering HFA formulation via holding chamber and mask; 44-88 mcg inhaled PO bid; may increase to 110-220 mcg inhaled PO bid; when stabilized decrease to lowest possible dose providing control
HFA; 4-11 years: 88 mcg inhaled PO bid; higher doses may be required
Powder; 4-11 years: 50 mcg inhaled PO bid; may increase to 100 mcg bid or higher
HFA or powder: Adolescents: Administer as in adults

Interactions

Drugs metabolized by CYP450 3A4 isoenzyme (eg, ketoconazole) might increase fluticasone concentrations

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Budesonide (Pulmicort Flexhaler)

Budesonide is relatively new to US market but has been extensively used in Europe. It has recently been released in a nebulizer solution approved for use in children as young as 12 mo.
Budesonide decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. Available as Pulmicort Flexhaler, powder for inhalation (90 mcg/actuation and 180 mcg/actuation, each actuation delivers 80 mcg/actuation and 160 mcg respectively) or Pulmicort Respules inhalation susp (0.25 mg/2 mL, 0.5 mg/2 mL, or 1 mg/2 mL). Nebulization has been used in children aged 1-8 y.

Dosing

Adult

Doses may be higher for patient with poor asthma control
Flexhaler: 360 mcg inhaled bid initially; may increase to 720 mcg bid

Pediatric

Doses may be higher for patient with poor asthma control
Flexhaler:
<6 years: Not established
180 mcg inhaled bid initially, for some 360 mcg bid may be appropriate; not to exceed 360 mcg bid
Respules (Age 12 mo to 8 y):
Previously on bronchodilators alone: 0.5 mg/d inhaled via nebulization administered qd or divided bid
Previously on inhaled corticosteroids: 0.5 mg/d inhaled via nebulization administered qd or divided bid; may increase to 1 mg/d
Previously on PO corticosteroids: 1 mg/d inhaled via nebulization administered qd or divided bid

Interactions

The manufacturer recommends not mixing the Respules with any other nebulized medications, they should be administered as separate treatments; ketoconazole and other inhibitors of CYP450 3A may interfere with budesonide metabolism and increase serum levels; cimetidine caused a slight decrease in budesonide clearance

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Suppression of HPA, suppression of linear growth, or Cushing syndrome may occur; caution with untreated systemic infections, ocular herpes simplex, or respiratory tuberculosis; rinse mouth after use to reduce likelihood of PO candidiasis; use with spacer; all clinical studies on the Respules were performed with a mask tightly fitting over the nose and mouth or with a mouthpiece in the mouth; these are the recommended methods of delivery; the "blow-by" technique frequently used for nebulizer medications in children is strongly discouraged; the Respules should not be used in an ultrasonic nebulizer

Beclomethasone

Decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. Available as 40 mcg/actuation or 80 mcg/actuation.

Dosing

Adult

Previously on bronchodilators alone: 40-80 mcg inhaled PO bid initially; may increase up to 320 mcg bid; higher doses may be necessary
Previously on inhaled corticosteroids: 40-160 mcg inhaled PO bid; may increase up to 320 mcg bid; higher doses may be necessary

Pediatric

<5 years: Not established
5-11 years:
Previously on bronchodilators alone or inhaled corticosteroids:
40 mcg inhaled PO bid; may increase to 80-160 mcg bid; higher doses may be necessary
Adolescents: Administer as in adults

Interactions

Coadministration with ketoconazole may increase plasma levels but does not appear to be clinically significant

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Suppression of the HPA, suppression of linear growth, or Cushing syndrome may occur; caution with untreated systemic infections, ocular herpes simplex, or respiratory tuberculosis; rinse mouth after use to reduce likelihood of PO candidiasis; use with spacer

Corticosteroid and bronchodilator combinations

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

Fluticasone and salmeterol (Advair HFA, Advair Diskus)

Indicated to treat chronic persistent asthma. Salmeterol component elicits long-acting beta2-adrenergic agonist activity, resulting in bronchiole smooth muscle relaxation. Fluticasone is a corticosteroid that provides anti-inflammatory effects.
Available as powder inhalant containing fluticasone (100 mcg, 250 mcg, or 500 mcg) with salmeterol (50 mcg). HFA preparation in metered dose inhalers has 45, 115 or 230 mcg per puff, each with 21 mcg of salmeterol.

Dosing

Adult

Diskus: 1 inhalation PO q12h; determine dosage strength according to dose of previously administered inhaled corticosteroid
HFA: 2 inhalations PO q12h

Pediatric

Diskus:
<4 years: Not established
4-11 years:
100 mcg/50 mcg inhaled PO q12h
>12 years: Administer as in adults
HFA:
<12 years: Not established
>12 years: Administer as in adults

Interactions

Drugs metabolized by CYP450 3A4 isoenzyme (eg, ketoconazole) might increase fluticasone concentrations; concomitant use of beta-blockers may decrease bronchodilating, and vasodilating effects of beta agonists such as salmeterol; concurrent administration with methyldopa may increase pressor response; coadministration with oxytocic drugs may result in severe hypotension; ECG changes and hypokalemia resulting from diuretics may worsen when coadministered with salmeterol

Contraindications

Documented hypersensitivity; angina, tachycardia, and cardiac arrhythmias associated with tachycardia

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Not indicated to treat acute asthmatic symptoms; black box FDA warning describes that chronic use may result in increased asthma morbidity and mortality, use only as additional therapy for patients not adequately controlled on other asthma-controller medications (eg, low- to medium-dose inhaled corticosteroids) or patients whose disease severity clearly warrants initiation of treatment with 2 maintenance therapies, including salmeterol
Fluticasone may suppress HPA, suppress linear growth, or cause Cushing syndrome; caution with untreated systemic infections, ocular herpes simplex, or respiratory tuberculosis; rinse mouth after use to reduce likelihood of PO candidiasis

Budesonide and formoterol (Symbicort)

Formoterol relieves bronchospasm by relaxing the smooth muscles of the bronchioles in conditions associated with asthma.
Budesonide is an inhaled corticosteroid that alters level of inflammation in airways by inhibiting multiple types of inflammatory cells and decreasing production of cytokines and other mediators involved in the asthmatic response. Available as MDI in 2 strengths; each actuation delivers formoterol 4.5 mcg with either 80 mcg or 160 mcg.

Dosing

Adult

Previously on medium-to-high dose inhaled steroids: 2 inhalations of 4.5/160 PO bid
Previously on low-to-medium dose inhaled steroids: 2 inhalations of 4.5/80 PO bid
Not currently receiving inhaled corticosteroids: 2 inhalations PO bid (strength depends on asthma severity)
Do not exceed 2 inhalations of 4.5/160 daily

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

Budesonide: None reported
Formoterol: Concomitant use of beta-blockers may decrease bronchodilating, and vasodilating effects of beta agonists; concurrent administration with methyldopa may increase pressor response; coadministration with oxytocic drugs may result in severe hypotension; ECG changes and hypokalemia resulting from diuretics, corticosteroids, or theophylline derivatives may worsen; drugs that widen QTc interval (eg, quinidine, procainamide, pimozide, moxifloxacin, sparfloxacin, gatifloxacin, sotalol, thioridazine, amiodarone) may potentiate cardiovascular side effects; concomitant use with other beta-adrenergic agonists may result in additive effects

Contraindications

Documented hypersensitivity to adrenergic amines, formoterol, budesonide, or any component of formulation; need for acute bronchodilation (including status asthmaticus)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use only as adjuvant therapy in patients not adequately controlled on other asthma-controller medications; not meant to relieve acute asthmatic symptoms or rapidly-deteriorating symptoms (treat acute episodes with short-acting beta2 agonist)
caution in patients with cardiovascular disease (arrhythmia or hypertension or HF); beta agonists may cause elevation in blood pressure, heart rate and result in CNS stimulation/excitation and may also increase risk of arrhythmias
Use with caution in patients with diabetes mellitus; beta2 agonists may increase serum glucose; use with caution in patients with GI diseases (diverticulitis, peptic ulcer, ulcerative colitis) due to perforation risk; caution in patients with hepatic impairment and patients with hypokalemia (beta2 agonists may decrease serum potassium); caution in myasthenia gravis (exacerbation of symptoms has occurred during initial treatment with corticosteroids); caution following acute MI (corticosteroids associated with myocardial rupture); caution in patients with cataracts and/or glaucoma; increased intraocular pressure, open-angle glaucoma, and cataracts have occurred with prolonged use; high doses and/or long-term use of corticosteroids have been associated with increased bone loss and osteoporotic fractures;
Renal impairment: Caution in renal impairment (fluid retention may occur); beta agonists may result in CNS stimulation/excitation (caution in patients with seizure disorders); changes in thyroid status may necessitate dosage adjustments; metabolic clearance of corticosteroids increases in hyperthyroid patients and decreases in hypothyroid ones; HPA axis suppression may lead to adrenal crisis (withdrawal and discontinuation of corticosteroids should be done slowly and carefully); particular care required when patients transferred from systemic corticosteroids to inhaled products due to possible adrenal insufficiency or withdrawal from steroids, including increase in allergic symptoms (patients receiving >20 mg/d of prednisone (or equivalent) may be most susceptible); steroids do not provide systemic steroid needed to treat patients having trauma, surgery, or infections; asthma-related deaths
US Boxed Warning: Long-acting beta2-agonists may increase risk of asthma-related deaths; rarely paradoxical bronchospasm may occur with use of inhaled bronchodilating agents (should be distinguished from inadequate response); immediate hypersensitivity reactions (urticaria, angioedema, rash, bronchospasm) reported; prolonged use of corticosteroids may increase incidence of secondary infection, mask acute infection (including fungal infections), prolong or exacerbate viral infections, or limit response to vaccines; exposure to chickenpox should be avoided; corticosteroids should not be used to treat ocular herpes simplex or cerebral malaria; close observation is required in patients with latent tuberculosis and/or tuberculosis reactivity restrict use in active tuberculosis (only in conjunction with antituberculosis treatment); may cause psychiatric manifestations, including depression, euphoria, insomnia, mood swings, and personality changes (pre-existing psychiatric conditions may be exacerbated by corticosteroid use); do not exceed recommended dose (serious adverse events, including fatalities, associated with excessive use of inhaled sympathomimetics

Follow-up

Further Inpatient Care

The child with atelectasis 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.

Inpatient & Outpatient Medications

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.

Multimedia

Media file 1: Atelectasis. Left lower lobe collapse. The opacity is in the posterior inferior location.

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Keywords

lung, pulmonary collapse, collapsed lung, asthma, cystic fibrosis, CF, hypoxemia, extrinsic airway obstruction, intrinsic airway obstruction, bronchiolitis, aspiration from swallowing disorder, endobronchial tuberculosis, aspiration from gastroesophageal reflux, airway foreign bodies, increased airway secretions, enlarged lymph nodes, compressed lung tissue, pulmonary atelectasis, transient hypoxemia, lymphoma, hypoventilation, tachypnea, treatment, diagnosis

Contributor Information and Disclosures

Author

Michael R Bye, MD, Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons; Attending Physician, Pediatric Pulmonary Medicine, Morgan Stanley Children's Hospital of New York Presbyterian, Columbia University Medical Center
Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society
Disclosure: Merck Honoraria Speaking and teaching

Medical Editor

Thomas Scanlin, MD, Chief, Division of Pulmonary Medicine and Cystic Fibrosis Center, Department of Pediatrics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School
Thomas Scanlin, MD is a member of the following medical societies: American Association for the Advancement of Science, American Society for Biochemistry and Molecular Biology, American Thoracic Society, Society for Pediatric Research, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Charles Callahan, DO, Professor, Deputy Chief of Clinical Services, Walter Reed Army Medical Center
Charles Callahan, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American College of Osteopathic Pediatricians, American Thoracic Society, Association of Military Surgeons of the US, and Christian Medical & Dental Society
Disclosure: Nothing to disclose.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians
Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Further Reading