• Atelectasis is defined as the incomplete expansion of lung tissue due to collapse or closure.
  • Broadly categorized as:
    • Obstructive: due to airway blockage
    • Nonobstructive: multiple etiologies including loss of contact between the parietal and visceral pleurae, replacement of lung tissue by scarring or infiltrative disease, surfactant dysfunction, and parenchymal compression
  • Often asymptomatic; symptoms depend on the rate of collapse, the amount of lung involved, and whether the patient has underlying lung disease and/or comorbidities.
  • Reduced respiratory gas exchange can cause hypoxemia.


  • Mean age is 60 years, but all ages are susceptible.
  • Male = female; no racial or socioeconomic predilection
  • Frequently occurs in patients on mechanical ventilation
  • Increased risk in postoperative patients and patients with lung or chest wall injury

Postoperative atelectasis, especially after major cardiovascular or gastrointestinal (GI) procedures; can be seen in up to 90% of patients

Rounded atelectasis can be seen in up to 65–70% of asbestos workers.

Etiology and Pathophysiology

  • Obstructive (resorptive) atelectasis is caused by intrinsic airway blockage and is the most common variety. It can be caused by luminal blockage (i.e., foreign body, mucus plug, asthma, cystic fibrosis, trauma, mass lesion) or airway wall abnormality (i.e., congenital malformation, emphysema).
    • Distal to the obstruction, alveolar air is rapidly reabsorbed into the deoxygenated venous system, causing complete collapse of the alveolar tissue.
    • The patency and function of the collateral ventilatory systems in each lobe (pores of Kohn, canals of Lambert, and fenestrations of Boren) depends on multiple patient factors including age, underlying lung disease, and fraction of inspired oxygen (FiO2).
    • In patients with emphysema, the fenestra of Boren become enlarged, which acts as a compensatory mechanism and can lead to a delay in atelectasis despite an obstructing lesion or mass.
  • Nonobstructive atelectasis
    • Passive atelectasis (i.e., during a pleural effusion, pneumothorax, or large emphysematous bulla) is due to pleural membrane separation of the visceral and parietal layers.
    • Compression atelectasis occurs with space-occupying lesions, cardiomegaly, abscess, or significant lymphadenopathy. The increased chest wall pressure compresses the alveoli.
    • Adhesive atelectasis occurs in the setting of acute respiratory distress syndrome (ARDS), radiation, smoke inhalation, posttraumatic lung contusion, or uremia. The underlying surfactant dysfunction causes increased surface tension and alveoli collapse.
    • Cicatrization atelectasis is common in granulomatous disease (i.e., sarcoidosis, TB), toxic or radiation exposure, and drug-induced fibrosis (i.e., amiodarone, cyclophosphamide). The scarring and fibrosis reduce lung expansion.
    • Replacement atelectasis: occurs when a tumor fills alveoli of a lobe causing complete lobar collapse
  • Rounded atelectasis is a distinct form of atelectasis seen in patients with asbestos exposure.
  • Muscular weakness: due to anesthesia side effect, or in neuromuscular diseases with respiratory muscle involvement

Pediatric Considerations
Children are at a higher risk of developing atelectasis due to their less developed collateral ventilation and compensatory mechanisms.

Risk Factors

  • Critical care, surgery, and prolonged immobilization
  • General anesthesia (including long-acting muscle relaxants, postoperative epidural anesthesia)
  • Positive fluid balance
  • Massive blood transfusion (≥4 units)
  • Nasogastric tube placement
  • Hypothermia
  • Mechanical ventilation with high tidal volume (Vt >10 mL/kg) and plateau pressure (>30 cm H2O)
  • Patient risk factors for postoperative atelectasis:
    • Age >60 years and <6 years
    • Chronic obstructive pulmonary disease (COPD), obstructive sleep apnea, congestive heart failure (CHF), pulmonary hypertension
    • Alcohol abuse, smoking
    • Poor cough effort
    • 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)

General Prevention

  • Early mobilization, deep breathing exercises, coughing, and frequent changes in body position
  • Preoperative physical therapy lowered rates of atelectasis, pneumonia, and length of stay (LOS) in patients undergoing elective cardiac surgery (1)[A].
  • Mechanical ventilation settings with high Vt (Vt >10 mL/kg) and plateau pressures (>30 cm H2O) and without positive end-expiratory pressure (PEEP) are associated with postoperative pulmonary complications (i.e., pneumonia, respiratory failure) (2):
    • Minimize ventilator-induced injury by employing low Vt and plateau pressures at sufficient PEEP (3)[C].
    • Ensure lower FiO2 during anesthetic induction and intraoperatively to prevent nitrogen washout (2)[A].

Commonly Associated Conditions

  • Obstructive lung diseases (COPD and asthma)
  • Trauma
  • ARDS, neonatal RDS, pulmonary edema, pulmonary embolism, pneumonia, pleural effusion, pneumothorax
  • Respiratory syncytial virus (RSV), bronchiolitis
  • Bronchial stenosis, pulmonic valve disease, and pulmonary hypertension
  • Neuromuscular disorders (muscular dystrophy, spinal muscular atrophy, spinal cord injury, and Guillain-Barré syndrome) and cystic fibrosis

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