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Atelectasis is a topic covered in the 5-Minute Clinical Consult.

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  • 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 how rapidly the 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.

Etiology and Pathophysiology

  • 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.
    • 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, drug-induced fibrosis (e.g., amiodarone, cyclophosphamide), 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)

Pediatric Considerations
The younger the child, the less developed the collateral ventilation, hence, the higher the risk of developing atelectasis.

Risk Factors

  • 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 (Vt) and plateau pressure
  • Surgical procedures: cardiothoracic, upper GI, neurosurgery, oromaxillofacial, ENT, vascular
    • Often a precursor to more serious pulmonary complications postoperatively (1)
  • 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 (ADLs), heart failure, smoking
  • Intensive care and prolonged immobilization
  • Right middle lobe syndrome (Brock syndrome): wedge-shaped density that extends inferiorly and anteriorly from the hilum of the lung. Best seen on lateral chest radiography; no consistent clinical definition

General Prevention

  • 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 (2)[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 Vt (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 (3)[C].

Commonly Associated Conditions

  • 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

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Stephens, Mark B., et al., editors. "Atelectasis." 5-Minute Clinical Consult, 27th ed., Wolters Kluwer, 2019. Medicine Central, im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/116059/all/Atelectasis.
Atelectasis. In: Stephens MB, Golding J, Baldor RA, et al, eds. 5-Minute Clinical Consult. 27th ed. Wolters Kluwer; 2019. https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/116059/all/Atelectasis. Accessed April 25, 2019.
Atelectasis. (2019). In Stephens, M. B., Golding, J., Baldor, R. A., & Domino, F. J. (Eds.), 5-Minute Clinical Consult. Available from https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/116059/all/Atelectasis
Atelectasis [Internet]. In: Stephens MB, Golding J, Baldor RA, Domino FJ, editors. 5-Minute Clinical Consult. Wolters Kluwer; 2019. [cited 2019 April 25]. Available from: https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/116059/all/Atelectasis.
* Article titles in AMA citation format should be in sentence-case
TY - ELEC T1 - Atelectasis ID - 116059 ED - Stephens,Mark B, ED - Golding,Jeremy, ED - Baldor,Robert A, ED - Domino,Frank J, BT - 5-Minute Clinical Consult, Updating UR - https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/116059/all/Atelectasis PB - Wolters Kluwer ET - 27 DB - Medicine Central DP - Unbound Medicine ER -