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- Atelectasis is defined as the incomplete expansion of lung tissue due to collapse or closure. The loss of lung volume and function leads to impaired airway mucus clearance.
- Broadly categorized as:
- Obstructive: airway blockage
- 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 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
- Rounded atelectasis can be seen in up to 65–70% of asbestos workers.
- Lobar atelectasis is variable based on the collateral ventilation and number of lobes involved.
Postoperative atelectasis, especially after major cardiovascular or gastrointestinal (GI) procedures; can be seen in up to 90% of patients
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 and emphysema).
- Distal to the obstruction, alveolar air is rapidly reabsorbed into the deoxygenated venous system, causing complete collapse of the alveolar tissue.
- Fraction of inspired oxygen (FiO2): Compared to the rapid dissociation of O2 distal to the obstruction, the 79% atmospheric nitrogen in atmospheric dissociates more slowly from the alveoli. This prevents collapse by maintaining positive pressure inside the alveoli. However, with increased FiO2, the concentration of nitrogen is decreased, allowing rapid development of atelectasis at the onset of obstruction.
- 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 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 or pneumothorax) is due to pleural membrane separation of the visceral and parietal layers.
- Compression atelectasis occurs with space-occupying lesions, cardiomegaly, abscess, or significant lymphadenopathy.
- Increased chest wall pressure compresses the alveoli, leading to diminished functional residual capacity (FRC) or resting lung volume.
- Adhesive atelectasis in the setting of acute respiratory distress syndrome (ARDS), radiation, smoke inhalation, or uremia. The underlying surfactant dysfunction causes increased surface tension and alveoli collapse.
- Cicatrization represents pleural or parenchymal scarring and is common in granulomatous disease (i.e., sarcoidosis), toxic or radiation exposure, and drug-induced fibrosis (i.e., amiodarone, cyclophosphamide).
- Replacement atelectasis: diffuse tumor (i.e., bronchioalveolar cell carcinoma) manifestation resulting in complete lobar collapse
- Rounded atelectasis is a distinct form of atelectasis seen in patients with asbestos exposure as a result of their significant pleural disease.
- Hypoxemia from a pulmonary embolus.
- Muscular weakness: due to anesthesia side-effect, or in neuromuscular diseases with respiratory muscle involvement.
Children are at a higher risk of developing atelectasis due to their less developed collateral ventilation and compensatory mechanisms.
- Critical care and prolonged immobilization
- General anesthesia (including long-acting muscle relaxants, postoperative epidural anesthesia)
- Positive fluid balance
- Massive blood transfusion (≥4 units)
- Nasogastric tube placement
- 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)
- Alcohol abuse, smoking
- 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)
- Surgical procedures: cardiothoracic, vascular, upper GI, neurosurgical, oromaxillofacial, and ENT.
- Often a precursor to more serious pulmonary complications postoperatively (1)
- Right middle lobe syndrome (Brock syndrome): wedge-shaped density extending inferiorly and anteriorly from the hilum. Best seen on lateral chest radiography; no consistent clinical definition
- 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. However, there was no change in other postoperative pulmonary complications or mortality (2)[A]. Furthermore, large RCTs are needed before conclusions can be drawn regarding the efficacy of chest physiotherapy and incentive spirometry (IS).
- 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):
- Minimize ventilator-induced injury by employing low Vt and plateau pressures at sufficient PEEP.
- Ensure lower FiO2 during anesthetic induction and intraoperatively to prevent nitrogen washout.
- 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
- Obstructive lung diseases (COPD and asthma)
- 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