> Table of Contents > Atelectasis
Bruce Jay Gardner, MD
Fahad Pervez, MD
image BASICS
  • Incomplete expansion of lung tissue with resultant loss of lung volume and function, leading to impaired airway mucus clearance
  • Broadly categorized as:
    • Obstructive: blockage within an airway
    • Nonobstructive: loss of contact between the parietal and visceral pleurae, replacement of lung tissue by scarring or infiltrative disease, surfactant dysfunction, and parenchymal compression
  • Symptoms depends on the rapidity with which bronchial occlusion occurs, the size of the lung area affected, and the presence or absence of lung disease and comorbidities.
  • Reduced respiratory gas exchange can lead to hypoxemia and other pulmonary complications.
  • Affects all ages; mean age is 60 years.
  • Male = female. No racial predilection.
  • Round atelectasis (see “Initial Tests (lab, imaging)”) is high in asbestos workers (65-70%).
  • Incidence of lobar atelectasis depends on the collateral ventilation within each individual lung lobe.
Postoperative atelectasis is extremely common, affecting up to 90% of surgical patients, especially after major cardiac or GI procedures.
  • Obstructive (resorptive) atelectasis is more common and is caused by intrinsic respiratory blockage
    • Due to luminal blockage (foreign body, mucus plug, asthma, cystic fibrosis, trauma, tumor) or airway wall abnormality (congenital malformation, emphysema)
    • Distal to the obstruction, air is reabsorbed from the alveoli into the deoxygenated venous system, causing complete collapse of the alveolar tissue.
    • There are three collateral ventilation systems in each lobe: the pores of Kohn, canals of Lambert, and fenestrations of Boren. The patency and formation of the systems depends on multiple factors including age, lung disease, and FiO2.
    • Age: Due to the late development of collaterals in children, atelectasis is frequently diagnosed after foreign body aspiration.
    • Emphysema: The fenestra of Boren in emphysematous patients often becomes enlarged; this enlargement can lead to a delay in atelectasis despite an obstructing lesion or mass.
    • FiO2: Oxygen rapidly dissociates from alveoli to deoxygenated vessels in an obstructed airway. The 79% nitrogen in atmospheric air has a slower rate of dissociation from the alveoli, and thereby prevents collapse by maintaining positive pressure inside the alveoli. With increased FiO2, the concentration of nitrogen is decreased predisposing patients to rapid development of atelectasis at the onset of obstruction.
  • Nonobstructive atelectasis
    • Passive atelectasis: results from pleural membrane separation of the visceral and parietal layers
      • Pleural effusion, pneumothorax
    • Compression atelectasis: alveoli compression leading to diminished resting volume (functional residual capacity [FRC]):
      • Space-occupying lesions, lymphadenopathy, cardiomegaly, abscess, chest wall pressure
    • Adhesive atelectasis: surfactant dysfunction resulting in increased surface tension and alveoli collapse
      • Respiratory distress syndrome, acute respiratory distress syndrome (ARDS), radiation exposure, smoke inhalation, uremia
    • Cicatrization: pleural or parenchymal scarring
      • Granulomatous disease, toxic inhalation, druginduced fibrosis (e.g., amiodarone), radiation exposure
    • Replacement atelectasis: diffuse tumor manifestation resulting in complete lobar collapse
      • Bronchioalveolar cell carcinoma
  • Rounded atelectasis: distinct form of atelectasis following asbestos exposure
  • Others
    • Hypoxemia due to pulmonary embolus
    • Muscular weakness (anesthesia, neuromuscular disease)
  • General anesthesia: positive fluid balance, ≥4 units blood transfusion, use of nasogastric tube, long-acting muscle relaxants, hypothermia, postoperative epidural anesthesia, ventilator settings with high tidal volume and plateau pressure
  • Surgical procedures: cardiothoracic, upper GI, neurosurgery, oromaxillofacial, ENT, vascular
  • Patient risk factors for developing postoperative atelectasis:
    • Age >60 and <6 years, chronic obstructive pulmonary disease (COPD), obstructive sleep apnea, CHF, alcohol abuse, pulmonary hypertension, albumin <3.5 g/dL, hemoglobin <10 g/dL, BMI >27 kg/m2 (weak evidence), ASA class II + functional dependence in activities of daily living (ADL), heart failure, smoking
  • Intensive care and prolonged immobilization
  • Brock syndrome: recurrent right middle lobe collapse secondary to airway disease, infection, or a combination thereof. The right middle lobe airway is long and thin and has the poorest drainage and clearance of the lobes, resulting in trapped mucus.
  • Early mobilization, deep breathing exercises, coughing, and frequent changes in body position
  • Preoperative physical therapy lowered rates of atelectasis, PNA, and LOS in elective cardiac surgery without improving other postoperative pulmonary complications or mortality (1)[A]. Further large RCTs are needed before conclusions can be made regarding the effect of chest physiotherapy and incentive spirometry.
  • Mechanical ventilation settings with high tidal volumes (Vt >10 mL/kg), high plateau pressures (>30 cm H2O), and without positive end-expiratory pressure (PEEP) are associated with postoperative pulmonary complications such as pneumonia and respiratory failure:
    • Ventilator-induced lung injury can be minimized by using low Vt and plateau pressures at sufficient PEEP while maintaining lower FiO2 during anesthetic induction and intraoperatively.
  • Application of continuous positive airway pressure (CPAP) during anesthesia induction and reversal of anesthesia-induced atelectasis after intubation by a recruitment maneuver may decrease postoperative pulmonary complications (2)[C].
  • COPD and asthma
  • Trauma
  • ARDS, neonatal respiratory distress syndrome, pulmonary edema, pulmonary embolism
  • Neuromuscular disorders (muscular dystrophy, spinal muscular atrophy, spinal cord injury), cystic fibrosis
  • Respiratory syncytial virus (RSV), bronchiolitis
  • Bronchial stenosis, pulmonic valve disease, pulmonary hypertension
  • Pneumonia, pleural effusion, pneumothorax
  • Signs of hypoxia or cyanosis
  • Tracheal or precordial impulse displacement toward the affected side; dullness to percussion
  • Bronchial breathing if airway is patent
  • Wheezing or absent breath sounds if airway is occluded
  • Diminished chest expansion
See “Etiology and Pathophysiology.”
Initial Tests (lab, imaging)
  • CBC and sputum culture if infection suspected
  • ABG: despite hypoxemia, the PaCO2 level is usually normal or low
  • Chest x-ray (CXR), PA and lateral
    • Raised diaphragm, flattened chest wall, movement of fissures and mediastinal structures toward the atelectatic region
    • Unaffected lung may show compensatory hyperinflation.
    • Wedge-shaped densities: obstructive atelectasis
    • Small, linear bands (Fleischner lines) often at lung bases: discoid (subsegmental or plate) atelectasis
    • Lobar collapse
      • Direct signs: displacement of fissures and opacification of the collapsed lobe. Right upper lobe collapse may display the inverted S sign of Golden, suggesting neoplastic shift of the minor fissure.
      • Indirect signs: displacement of the hilum, mediastinal shift toward the side of collapse, loss of volume of ipsilateral hemithorax, elevation of ipsilateral diaphragm, crowding of the ribs, compensatory hyperlucency of remaining lobes, and silhouetting of the diaphragm or heart border
    • P.89

    • Air bronchograms: Evidence of pleural fluid or air may indicate compressive atelectasis.
    • Adhesive atelectasis may present as a diffuse reticular granular pattern, progressing to a pulmonary edema pattern, and finally to bilateral opacification in severe cases.
    • Pleural-based round density on CXR: round atelectasis
    • Complete atelectasis of entire lung: opacification of the entire hemithorax and an ipsilateral shift of the mediastinum
Follow-Up Tests & Special Considerations
  • Chest CT or MRI may be indicated to visualize airway and mediastinal structures and identify cause of atelectasis.
  • Pulmonary function tests (PFTs) may detect restrictive disease, decreased respiratory muscle pressures, or airflow obstruction.
  • Low serum albumin (<3.5 g/L) is a powerful marker of increased risk for postoperative pulmonary complications, including atelectasis.
Diagnostic Procedures/Other
Bronchoscopy can be considered in unexplained or refractory cases.
  • Prevention following surgery or general anesthesia using PEEP (2)[C]
  • Treat the underlying cause.
  • Ensure patient is lying on the unaffected side to promote drainage:
    • Maximize mobility and encourage frequent coughing and deep breathing.
  • Incentive spirometry every hour while awake
    • Lack of evidence for incentive spirometry preventing postoperative pulmonary complications after coronary artery bypass graft (CABG) (3)[A]
  • Initiate intubation and mechanical ventilation with PEEP in severe respiratory distress or hypoxemia:
    • Lower tidal volume (6 mL/kg) and lower end-inspiratory values (<30 mm Hg) are associated with reduced mortality.
    • PEEP 15 to 20 mL may be necessary to maintain arterial O2 saturation in surfactant-impaired states.
  • Postsurgical measures include positive airway pressure, continuous or intermittent.
First Line
Pharmacotherapy should be tailored to address underlying cause:
  • Antibiotics for infection
  • Chemo/radiation therapy for tumor
  • Steroids for asthma
  • Effective analgesia to permit deep inspiration and coughing
  • Mucolytics can be considered to promote airway clearance (NAC and saline most commonly studied).
Pediatric Considerations
  • RhDNase may be effective clearing mucinous secretions in refractory mucous plugging in children.
  • Chest physiotherapy (i.e., percussion, drainage, deep insufflation, and saline lavage) is a common treatment modality in the hospital setting. Caution must be practiced when interpreting the possible positive effects as the number of patients studied is small, the results are not consistent across trials, data on safety are insufficient, and there may be limited applicability to current guidelines.
  • Application of continuous distending pressure has some benefit in the treatment of preterm infants with respiratory distress syndrome and has the potential to reduce lung damage particularly if applied early (4)[A].
Second Line
Bronchofibroscopy in aspiration of inspissated secretions to improve airway clearance has been efficacious in several studies. However, debate continues regarding its efficacy in the treatment of atelectasis.
Pediatric Considerations
In obstructive atelectasis, bronchoscopy remains controversial. In the presence of a mucus plug or cast, bronchoscopy may be beneficial.
  • Appropriate surgical resection for underlying disease (e.g., tumor, severe lymphadenopathy)
  • Bronchoscopy
Admission Criteria/Initial Stabilization
Ensure adequate oxygenation (may start with 100% FiO2 then taper) and humidification
Patient Monitoring
  • Depends on underlying cause and comorbidities
  • In uncomplicated cases of atelectasis associated with asthma or infection, outpatient monitoring is appropriate.
Maximize patient mobility and encourage frequent coughing and deep breathing.
  • For postoperative atelectasis, spontaneous resolution usually occurs within 24 hours but can persist for days after surgery.
  • The prognosis of lobar atelectasis secondary to endobronchial obstruction depends on treatment of the underlying disease or malignancy.
  • Surgical therapy is needed only for resectable causes or if chronic infection and bronchiectasis supervene.
1. Hulzebos EH, Smit Y, Helders PP, et al. Preoperative physical therapy for elective cardiac surgery patients. Cochrane Database Syst Rev. 2012;(11):CD010118.
2. Baltieri L, Santos LA, Rasera I Jr, et al. Use of Positive pressure in the bariatric surgery and effects on pulmonary function and prevalence of atelectasis: randomized and blinded clinical trial. Arq Bras Cir Dig. 2014;27(Suppl 1):26-30.
3. Freitas ER, Soares BG, Cardoso JR, et al. Incentive spirometry for preventing pulmonary complications after coronary artery bypass graft. Cochrane Database Syst Rev. 2012;(9):CD004466.
4. Ho JJ, Henderson-Smart DJ, Davis PG. Early versus delayed initiation of continuous distending pressure for respiratory distress syndrome in preterm infants. Cochrane Database Syst Rev. 2002;(2):CD002975.
Additional Reading
  • Brower RG. Consequences of bed rest. Crit Care Med. 2009;37(10 Suppl):S422-S428.
  • Ferreyra G, Long Y, Ranieri VM. Respiratory complications after major surgery. Curr Opin Crit Care. 2009;15(4):342-348.
  • Guimarães MM, El Dib R, Smith AF, et al. Incentive spirometry for prevention of postoperative pulmonary complications in upper abdominal surgery. Cochrane Database Syst Rev. 2009;(3):CD006058.
  • McCunn M, Sutcliffe AJ, Mauritz W, et al. Guidelines for management of mechanical ventilation in critically injured patients. Trauma Care. 2004;14(4):147-151.
  • Mavros MN, Velmahos GC, Falagas ME. Atelectasis as a cause of postoperative fever: where is the clinical evidence? Chest. 2011;140(2):418-424.
  • Qaseem A, Snow V, Fitterman N, et al. Risk assessment for and strategies to reduce perioperative pulmonary complications for patients undergoing noncardiothoracic surgery: a guideline from the American College of Physicians. Ann Intern Med. 2006;144(8):575-580.
  • Tusman G, Böhm SH, Warner DO, et al. Atelectasis and perioperative pulmonary complications in high-risk patients. Curr Opin Anaesthesiol. 2012;25(1):1-10.
  • Wu KH, Lin CF, Huang CJ, et al. Rigid ventilation bronchoscopy under general anesthesia for treatment of pediatric pulmonary atelectasis caused by pneumonia: a review of 33 cases. Int Surg. 2006;91(5):291-294.
J98.11 Atelectasis
Clinical Pearls
  • No strong clinical evidence supports atelectasis as an early cause of postoperative fever.
  • Anesthesia-induced atelectasis occurs in almost all anesthetized patients.
  • Bronchogenic carcinoma, which may present with atelectasis, must be excluded in all patients >35 years.
  • In complete atelectasis of an entire lung, the mediastinal ipsilateral shift separates atelectasis from massive pleural effusion.
  • Low serum albumin is a powerful predictor of postoperative pulmonary complications, including atelectasis.