Atelectasis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

The pathophysiology of obstructive and non-obstructive atelectasis can be better explained by understading underlying pathology. Obstructive atelectasis, the most common type of atelectasis, occurs due to obstruction at any level from the trachea to the alveoli. Foreign bodies, tumors, and mucus plugs are the most common causes of obstructive atelectasis. Non obstructive atelectasis occurs due to severe lung scarring caused by necrotizing pneumonias or granulomatous diseases leading to cicatrisation atelectasis. Lung infiltration by a tumor (bronchoalveolar carcinoma) may cause replacement atelectasis, thoracic space occupying lesions can cause compression atelectasis, diminished levels of surfactant can lead to adhesive atelectasis presenting as ARDS. Passive atelectasis occurs due to absence of contact between the parietal and visceral pleurae due to fluid (pleural effusion), air (pneumothorax), blood (hemothorax) etc. Patients undergoing upper abdominal and thoracic procedures may develop postoperative atelectasis which may arise as a complication of surgery or anaesthesia leading to decreased surfactant activity and dysfunction of the diaphragm.

• It is understood that atelectasis is the result of obstructive and non-obstructive etiologies.
• The pathophysiology of obstructive and non-obstructive atelectasis is determined by several factors.

• Obstructive atelectasis is the most common type of atelectasis
• Obstructive atelectasis occurs due to obstruction at any level from the trachea to the alveoli.
• Ventilation defect
  • Bronchial obstruction leads to resorption of alveolar gas by the blood circulating in the alveolar capillary membrane.
  • Alveolar gas reabsorption due to obstruction leads to diminished lung volume and subsequent atelectasis.^[1]

• Perfusion defect
  • Perfusion of under ventilated lung tissue leads to hypoxemia due to shunt formation. leading to obstruction
  • Following bronchial obstruction, complete collapse of the affected lung is prevented by secretions that fill up the spaces of the alveoli.
  • The adjacent lung distends to prevent collapse of the part of the lung undergoing atelectasis.
  • The mediastinum shifts towards the affected side.
  • Diaphragmatic elevation of the diaphragm leads to flattening of the chest wall.
• The extent of atelectasis depends upon the level of obstruction.
  • Lobar atelectasis occurs due to lobar bronchus obstruction.
  • Segmental atelectasis arises from segmental bronchus obstruction.

• The rate and pattern of development of atelectasis depends on collateral ventilation and gas composition of inspired air.

• Non obstructive atelectasis occurs due to severe lung scarring caused by necrotizing pneumonias or granulomatous diseases leading to cicatrisation atelectasis.
• Lung infiltration by a tumor (bronchoalveolar carcinoma) may cause replacement atelectasis, thoracic space occupying lesions can cause compression atelectasis, diminished levels of surfactant can lead to adhesive atelectasis presenting as ARDS.
• Passive atelectasis occurs due to absence of contact between the parietal and visceral pleurae due to fluid (pleural effusion), air (pneumothorax), blood (hemothorax) etc.
• Atelectasis of the upper lobe commonly occurs due to pneumothorax, whereas atelectasis of the middle and lower lobes occurs due to pleural effusion.
• Rounded atelectasis, which presents at a mean age of 60 years, arises due to formation of fibrous bands which adhere the lung to the pleura.
  • There is a high association of rounded atelectasis in asbestosis due to the formation of fibrous pleural plaques.

• Middle lobe syndrome (Fixed or recurrent atelectasis of the lingula/right middle lobe) occurs due to Sjogren’s syndrome.
• Intraluminal or extraluminal obstruction (compression of the bronchi by adjacent structures) results in middle lobe syndrome.^[2][3]
• Patients with lower respiratory tract infections, PE and hypoventilation may develop obstruction of the small bronchus, leading to formation of small atelectatic areas within the lung.
• This may be due to respiratory stressors such as toxins, hyperoxia, hypoxia, ischemia leading to impaired surfactant production and impaired regional ventilation. Intrapulomary shunt formation and ventilation perfusion mismatch may arise to due to development of this platelike atelectasis.
• Patients undergoing upper abdominal and thoracic procedures may develop postoperative atelectasis which may arise as a complication of surgery or anaesthesia leading to decreased surfactant activity and dysfunction of the diaphragm.
• Postoperative atelectasis is segmental and basilar in distribution.

Common conditions associated with atelectasis include:

• Lower respiratory tract infections
• Pneumonia
• Bronchiectasis
• Chronic obstructive pulmonary disease (COPD)
• Cystic Fibrosis
• ARDS

• On gross pathology, pleural folds with deep invaginations are characteristic findings of atelectasis.^[4]

• On microscopic histopathological analysis, fibrosis and pleural invaginations are characteristic findings of atelectasis.^[4]
• If there is an existing pathology leading to atelectasis, characteristic features of the underlying disease may also be seen on microscopic pathology.

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