It results from the partial or complete, reversible collapse of the small airways leading to an impaired exchange of CO2 and O2 - i. The mechanism by which atelectasis occurs is due to one of three processes: compression of lung tissue compressive atelectasis , absorption of alveolar air resorptive atelectasis , or impaired pulmonary surfactant production or function.
Atelectasis can categorize into obstructive, non-obstructive, postoperative, and rounded atelectasis. Nonobstructive atelectasis can further classify into compression, adhesive, cicatrization, relaxation, and replacement atelectasis. Compression atelectasis is secondary to increased pressure exerted on the lung causing the alveoli to collapse. In an awake, spontaneously-ventilating patient, caudad excursion of the diaphragm during contraction causes a subsequent decrease in intrapleural pressure and alveolar pressure.
The decrease in pressure allows for passive movement of air into the lungs. This process is inhibited by general anesthesia due to diaphragm relaxation. Patients lying supine have cephalad displacement of the diaphragm further decreasing the transmural pressure gradient and increasing the likelihood of atelectasis.
Surfactant functions to decrease alveolar surface tension and prevent alveolar collapse; therefore, any alterations to surfactant production and function often manifest as an increase in the surface tension of the alveoli leading to instability and collapse.
Cicatrization atelectasis is often the result of parenchymal scarring of the lung, leading to contraction of the lung.
Processes that lead to cicatrization atelectasis include tuberculosis, fibrosis, and other chronic destructive lung processes. Relaxation atelectasis involves the loss of contact between parietal and visceral tissue as seen in pneumothoraces and pleural effusions.
Replacement atelectasis is one of the most severe forms and occurs when all of the alveoli in an entire lobe are replaced by tumor. This is typically seen in bronchioalveolar carcinoma and results in complete lung collapse. Obstructive atelectasis is often referred to as resorptive atelectasis and occurs when alveolar air gets absorbed distal to an obstructive lesion. The obstruction either partially or completely inhibits ventilation to the area.
Perfusion to the area is maintained; however, so gas uptake into the blood continues. Eventually, all of the gas in that segment will be absorbed and, without return of ventilation, the airway will collapse. Resorption atelectasis can be secondary to numerous pathologic processes, including intrathoracic tumors, mucous plugs, and foreign bodies in the airway.
Children are especially susceptible to resorption atelectasis in the presence of an aspirated foreign body because they have poorly developed collateral pathways for ventilation. In contrast, adults with COPD have extensive collateral ventilation secondary to airway destruction and thus are less likely to develop resorption atelectasis in the presence of an obstructing lesion i. The use of high inspiratory oxygen concentration high FiO2 during induction and maintenance of general anesthesia also contributes to atelectasis via absorption atelectasis.
In contrast, oxygen is rapidly absorbed into the blood. Postoperative atelectasis typically occurs within 72 hours of general anesthesia and is a well-known postoperative complication.
Rounded atelectasis is less common and often seen in asbestosis. The pathophysiology involves the folding of the atelectatic lung tissue to the pleura. While all of the mechanisms mentioned above may contribute to the formation of perioperative atelectasis, absorption and compression mechanisms are the two most commonly implicated.
Middle lobe syndrome involves recurrent or fixed atelectasis of the right middle lobe and lingula. Extraluminal and intraluminal bronchial obstruction can result in middle lobe syndrome.
Nonobstructive causes include inflammatory processes, defects in bronchial anatomy, and collateral ventilation. Fiberoptic bronchoscopy and bronchoalveolar lavage are the treatment of choice for this syndrome. Long term consequences of chronic atelectasis include bronchiectasis. Sjogren syndrome has associations with middle lobe syndrome and treatment with glucocorticoids has been favorable.
Atelectasis does not preferentially affect either sex. There is also no increased incidence of atelectasis in patients with COPD, asthma, or increased age. 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.
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 for developing atelectasis. Obese patients have an increased incidence of atelectasis due to decreased FRC functional residual capacity and compliance.
Atelectasis development in pregnant patients is by this same mechanism. Typically, atelectasis is asymptomatic. Atelectasis is usually a clinical diagnosis in a patient with known risk factors. A chest x-ray will reveal platelike, horizontal lines in the area of atelectatic lung tissue.
Atelectasis is not typically evident on convention chest radiographs until it is significant. Chest CT 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 i. An arterial blood gas may reveal arterial hypoxemia and respiratory alkalosis.
The PaCO2 is often normal; however, it may be lower secondary to increased minute ventilation, which often accompanies atelectasis.
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. Remove or relieve any blockage in the airways by bronchoscopy. Tilt the person so the head is lower than the chest.
This allows mucus to drain more easily. Symptoms includes Breathing difficulty, Chest pain, Cough. Prevention includes Encourage movement and deep breathing in anyone who is bedridden for long periods.
Keep small objects out of the reach of young children. Maintain deep breathing after anesthesia. Helmi M. Lubis Dr, Sp. Ridwan M. Daulay Dr, Sp. A Wisman Dr, Sp. Open navigation menu. Close suggestions Search Search. User Settings.
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