Atelectasis

Etiology

Atelectasis, the collapse of lung tissue, generally falls into 2 broad types: obstructive (resorptive) or nonobstructive. Both obstructive and nonobstructive atelectasis occur by any single or combination of 3 different pathophysiologic mechanisms: increased pleural pressure, low alveolar pressure, and surfactant impairment.[2][3]

Obstructive (resorptive) atelectasis: results from airway obstructions that prevent air from reaching the alveoli, and air distal to the obstruction is reabsorbed from the nonventilated alveoli, leading to the collapse of the airways.

• Intrathoracic tumors, mucous plugs, and foreign bodies can partially or completely block airways. Children are particularly susceptible due to their less-developed collateral ventilation pathways. Conversely, adults with chronic obstructive pulmonary disease (COPD), who have extensive collateral airways, are less likely to develop obstructive atelectasis.
• A high fraction of inspired oxygen (FiO₂) can lead to absorption atelectasis, as oxygen is more rapidly absorbed into the blood than nitrogen, reducing alveolar patency.

Nonobstructive atelectasis: includes types of atelectasis not directly caused by airway obstruction.

• Compression atelectasis is caused by increased external pressure on the lung. Pleural effusions, pneumothorax, abdominal distension, or tumors may cause compression atelectasis. In these cases, the transmural pressure gradient (alveolar pressure minus intrapleural pressure) across the alveolus decreases, leading to alveolar collapse.
• Surfactant-related atelectasis (adhesive atelectasis) occurs due to surfactant impairment. Surfactant reduces alveolar surface tension, and its impairment leads to increased tension and alveolar collapse, as seen in conditions like acute respiratory distress syndrome (ARDS) or neonatal respiratory distress syndrome (RDS). 
• Other Subtypes include cicatrization atelectasis from lung scarring (eg, tuberculosis, fibrosis), relaxation atelectasis from loss of lung-to-chest wall contact (eg, pneumothorax), and replacement atelectasis where tumors replace alveoli, typically seen in bronchioalveolar carcinoma.

Special cases

• Postoperative atelectasis occurs within 72 hours of surgery under general anesthesia. This type of atelectasis is often a mix of obstructive and nonobstructive mechanisms.[4]
• Rounded atelectasis is less common, often associated with asbestosis, and involves the folding of atelectatic lung tissue onto the pleura.
• Middle lobe syndrome involves recurrent or fixed atelectasis of the right middle lobe and lingula caused by extraluminal and intraluminal bronchial obstruction, nonobstructive inflammatory processes, or anatomical defects. 

Epidemiology

Atelectasis does not preferentially affect either sex. There is also no increased incidence of atelectasis in people with COPD, asthma, or advanced age.[5]

Atelectasis is more common in patients who are immobilized and mechanically ventilated, such as patients undergoing general anesthesia or in the intensive care unit. Atelectasis is more prominent after cardiac surgery with cardiopulmonary bypass than after other types of surgery, including thoracotomies; however, patients undergoing abdominal and thoracic procedures are at increased risk of developing atelectasis.[4] Additionally, patients with obesity and those who are pregnant are more likely to develop atelectasis due to a decreased functional residual capacity (FRC). 

Pathophysiology

Administration of general anesthesia, use of muscle relaxants, obesity, pregnancy, inadequate pain control, and thoracic or cardiopulmonary procedures increase the risk of developing atelectasis in the perioperative period.

The incidence of atelectasis in patients undergoing general anesthesia is 90%.[1] Research has shown that atelectasis appears in the dependent regions of both lungs within five minutes of induction of anesthesia, and up to 15% to 20% of the lung at its base collapses during uneventful anesthesia before any surgical intervention.[6]  Atelectasis is seen with general anesthesia regardless of whether or not muscle paralysis is used. Ketamine, when used as a sole agent, is the only anesthetic agent that does not increase the risk of developing atelectasis.[6] High FiO₂ during induction and maintenance of general anesthesia also contributes to atelectasis via absorption atelectasis. 

FRC is reduced in all patients under general anesthesia and in those in the supine position. This reduction leads to compressive atelectasis in dependent areas of the lungs. 

Inadequate pain control can contribute to the development of atelectasis by inducing shallow breathing or splinting. On the other hand, the use of opioids for pain control leads to respiratory depression and inhibition of coughing, also leading to atelectasis.[7]

History and Physical

Typically, atelectasis is asymptomatic if only a few alveoli are affected. As more alveoli become involved, however, the individual may report dyspnea, cough with or without sputum production, and pleuritic chest pain. The physical examination of a patient with atelectasis may reveal tachypnea, increased work of breathing, diminished or absent breath sounds, crackles, and decreased chest expansion.

Evaluation

Atelectasis is usually a clinical diagnosis in a patient with known risk factors. If imaging is warranted, chest radiography, chest computed tomography, or thoracic ultrasonography are useful when diagnosing atelectasis. A chest x-ray will reveal platelike, horizontal lines in the area of atelectatic lung tissue and may result in the displacement of interlobar fissures, pulmonary opacification, or tracheal shift toward the affected side.[8]. Atelectasis is not typically evident on conventional chest radiographs until it is significant. 

Computed tomography of the chest performed in patients with atelectasis often reveals dependent lung densities and loss of volume in the affected side of the chest.   

Atelectasis may also be directly visible with fiberoptic bronchoscopy. Fiberoptic bronchoscopy can be both diagnostic and therapeutic, often revealing the cause of any obstruction contributing to the atelectasis, such as a tumor, mucous plug, or foreign body.

An arterial blood gas may reveal arterial hypoxemia and respiratory alkalosis. The PaCO₂ is often normal but may be decreased secondary to increased minute ventilation, which often accompanies atelectasis. 

Treatment / Management

Most atelectasis that appears during general anesthesia leads to transient lung dysfunction that resolves within 24 hours after surgery. Nevertheless, some patients develop significant perioperative respiratory complications that can lead to increased morbidity and mortality if not treated. Atelectasis is preventable through avoidance of general anesthesia, early mobilization, adequate pain control, and minimizing parenteral opioid administration. When general anesthesia is unavoidable, continuous positive airway pressure, the lowest possible FiO₂ during induction and maintenance, positive end-expiratory pressure (PEEP), lung recruitment maneuvers, and low tidal volumes of 6 to 10 mL/kg will help prevent the development of atelectasis.[7][9] One study showed that intraoperative alveolar recruitment with a vital capacity maneuver followed by PEEP 10 cm H₂O is effective at preventing lung atelectasis in patients with morbid obesity; this also correlated with better oxygenation, shorter postanesthesia care unit (PACU) stay, and fewer pulmonary complications in the postoperative period.[10](A1)

Changing position from supine to upright increases FRC and decreases atelectasis.[11] Encouraging patients to take deep breaths, early ambulation, incentive spirometry, use of an acapella device, chest physiotherapy, tracheal suctioning in intubated patients, and positive pressure ventilation have been shown to decrease atelectasis. The mechanism behind these measures is a transient increase in transmural pressure that allows for the reexpansion of collapsed lung segments. Prophylactic measures, such as incentive spirometry, should be taught and instituted before surgery and continued hourly following surgery until discharge to obtain the maximal benefit.[7]

Mucolytic agents, like N-acetylcysteine, have been tried with limited evidence that they prevent postoperative atelectasis. However, in certain populations, such as pediatric patients and those with cystic fibrosis, recombinant human dornase alpha may help alleviate atelectasis due to mucus plugging.[7][12] (B2)

Fiberoptic bronchoscopy also plays a role in the management of atelectasis. In one study, single-suction fiberoptic bronchoscopy improved lung function and reversed atelectasis in 76% of cases. Bronchoscopy should always be the intervention when there is a high suspicion of a mechanically obstructed bronchus and coughing and suctioning have not been successful. Bronchoscopy is also indicated when less invasive efforts, such as early ambulation, incentive spirometry, bronchodilators, and humidity, prove unsuccessful. Employing early preventative strategies and valuing prompt recognition of patients with atelectasis will improve patient outcomes and significantly decrease healthcare costs.[13]

Differential Diagnosis

The differential diagnosis of atelectasis should include:

• Neoplasm
• Pneumonia
• Pleural effusion
• Pulmonary embolism
• Foreign body.

Prognosis

For patients with atelectasis, the prognosis varies greatly, and the primary prognostic determinators are the underlying etiology and patient comorbidities. Untreated atelectasis can result in lung infections, including recurrent pneumonia. Atelectasis may result in impaired oxygen exchange, causing hypoxemia and respiratory distress. With time, recurrent instances of atelectasis may result in the formation of lung scarring or fibrosis and decrease overall lung reserve. Early detection and appropriate management are crucial to prevent these potentially serious complications.

Complications

Atelectasis is one of the most common respiratory complications in the perioperative period, and may contribute to significant morbidity and mortality, including the development of pneumonia and acute respiratory failure.