What causes atelectasis of the lung postoperatively?

What Causes Postoperative Atelectasis

Postoperative atelectasis develops primarily through three mechanisms: compression of lung tissue from supine positioning and diaphragmatic dysfunction, absorption atelectasis from high oxygen concentrations, and loss of functional residual capacity from anesthetic-induced muscle relaxation. 1, 2

Primary Mechanisms

1. Compression Atelectasis

• Supine positioning during anesthesia induction causes cephalad displacement of abdominal contents, forcing the diaphragm upward and compressing dependent lung regions 1
• This compression effect is particularly pronounced in obese patients 1, 2
• Diaphragm dysfunction may persist for up to 7 days after surgery, leading to significant deterioration in arterial oxygenation 2
• Surgical factors that worsen compression include laparoscopic procedures, thoracic surgery, upper abdominal surgery, pneumoperitoneum insufflation, and prone or Trendelenburg positioning 1

2. Absorption Atelectasis

• High oxygen concentrations (FiO₂ >0.8) during induction and emergence from anesthesia cause rapid absorption of gas behind closed airways, leading to alveolar collapse 3, 4
• The use of 100% oxygen during induction or post-oxygenation maneuvers accelerates atelectasis formation 4
• Ventilation with pure oxygen after lung recruitment causes rapid reappearance of atelectasis, while 40% oxygen in nitrogen results in slower collapse 4

3. Loss of Functional Residual Capacity (FRC)

• Anesthetic agents cause loss of muscle tone and reduction in FRC, which is a common action of almost all anesthetics 4
• This reduction in FRC, combined with airway closure, creates conditions for rapid alveolar collapse 5
• Up to 15-20% of the lung base regularly collapses during uneventful anesthesia before any surgery begins 4

Contributing Factors

Ventilator Settings

• Zero end-expiratory pressure (ZEEP) during mechanical ventilation fails to maintain alveolar patency and promotes collapse 1, 3
• High tidal volumes (>10 ml/kg) with high plateau pressures (>30 cmH₂O) without PEEP are associated with lung injury in partially collapsed lungs 6

Postoperative Factors

• Pain limits deep breathing and effective cough, impairing secretion clearance 2, 7
• Thoracic muscle injury, chest wall instability, and ongoing diaphragmatic dysfunction further impair respiratory mechanics 7
• Mucus plugging can cause obstructive atelectasis, particularly in patients with underlying lung disease 7

Patient-Related Risk Factors

• Advanced age (>50 years), BMI >40 kg/m², ASA class >2 are significant risk factors 1
• Emergency or urgent surgery increases risk substantially 1
• Prolonged surgery (>3 hours), particularly abdominal, thoracic, neurosurgery, head and neck, or vascular procedures 1
• Low serum albumin (<35 g/L) is a powerful marker of increased risk 1

Clinical Significance

Atelectasis occurs in approximately 90% of all anesthetized patients and is the main cause of perioperative hypoxemia 8, 4. The formation of perioperative clinically significant atelectasis is an important risk factor for development of postoperative pulmonary complications including pneumonia, respiratory failure, and exacerbation of chronic lung disease 1. These complications contribute equally to cardiac complications in terms of morbidity, mortality, and length of stay 1.

Common Pitfalls

• Using high FiO₂ (>0.8) during emergence significantly increases atelectasis formation 3
• Turning off the ventilator to allow CO₂ accumulation before extubation causes alveolar collapse 3
• Routine suctioning of the tracheal tube just before extubation reduces lung volume 3
• Applying PEEP without first performing recruitment maneuvers—PEEP maintains FRC but does not restore it 3