Atelectasis

May have no signs and symptoms or they may include: • cough, but not prominent; • chest pain (not common); • breathing difficulty (fast and shallow); • low oxygen saturation; • pleural effusion (transudate type); • cyanosis (late sign); • Stridor • increased heart rate. Mild atelectasis is often asymptomatic and can only be found through X-Ray, though for larger collapsed specific clinical signs include tachypnea and diminished chest expansion on affected side. It is a common misconception and pure speculation that atelectasis causes postoperative fever. This claim has been perpetuated in medical textbooks as recently as 2021. Review articles published in 2011 and 2019 summarizing the available evidence on the association between atelectasis and post-operative fever concluded that there is no clinical evidence supporting this speculation. A recent article outlined the history of this myth and the true causes of postoperative fever. ==Causes==

The most common cause is post-surgical atelectasis, characterized by splinting, i.e. restricted breathing after abdominal surgery. Atelectasis develops in 75–90% of people undergoing general anesthesia for a surgical procedure. Common cause for Atelectasis is pulmonary tuberculosis. Smokers and the elderly are also at an increased risk. Outside of this context, atelectasis implies some blockage of a bronchiole or bronchus, which can be within the airway (foreign body, mucus plug), from the wall (tumor, usually squamous cell carcinoma) or compressing from the outside (tumor, lymph node, tubercle). Another cause is poor surfactant spreading during inspiration, causing the surface tension to be at its highest which tends to collapse smaller alveoli. Atelectasis may also occur during suction, as along with sputum, air is withdrawn from the lungs. There are several types of atelectasis according to their underlying mechanisms or the distribution of alveolar collapse; resorption, compression, microatelectasis and contraction atelectasis. Relaxation atelectasis (also called passive atelectasis) is when a pleural effusion or a pneumothorax disrupts the contact between the parietal and visceral pleurae. Risk factors associated with increased likelihood of the development of atelectasis include: the type of surgery (thoracic and cardiopulmonary surgeries), the use of muscle relaxants, obesity, high oxygen, the lower lung segments. Factors also associated with the development of atelectasis include: age, presence of chronic obstructive pulmonary disease or asthma, and type of anesthetic. In the early 1950s, in UK aviation medicine, the condition acceleration atelectasis was given the name "Hunter lung" due to its prevalence in pilots of the transonic fighter jet, the Hawker Hunter, which used a 100% oxygen supply. ==Diagnosis==

Clinically significant atelectasis is generally visible on chest X-ray; findings can include lung opacification and/or loss of lung volume. Post-surgical atelectasis will be bibasal in pattern. Chest CT or bronchoscopy may be necessary if the cause of atelectasis is not clinically apparent. Direct signs of atelectasis include displacement of interlobar fissures and mobile structures within the thorax, overinflation of the unaffected ipsilateral lobe or contralateral lung, and opacification of the collapsed lobe. Primarily, in a lung ultrasound the static air bronchogram is the what differentiates atelectasis from pneumonia. In addition to clinically significant findings on chest X-rays, patients may present with indirect signs and symptoms such as elevation of the diaphragm, shifting of the trachea, heart and mediastinum; displacement of the hilus and shifting granulomas. Classification Atelectasis is broadly categorized into obstructive (resorptive) and non-obstructive types. It may be further classified as an acute or chronic condition. In acute atelectasis, the lung has recently collapsed and is primarily notable only for airlessness. In chronic atelectasis, the affected area is often characterized by a complex mixture of airlessness, infection, widening of the bronchi (bronchiectasis), destruction, and scarring (fibrosis). The resulting absorption of air distal to the obstruction results in collapse of the alveoli. It is most commonly due to intrathoracic tumors, aspiration of a foreign body, or mucus plugs. Children are notably more susceptible to atelectasis due to poorly developed collateral airways, which protect against alveolar collapse by maintaining inflation. Adhesive atelectasis This type of atelectasis is due to lack or dysfunction of surfactant, which normally functions to reduce alveolar surface tension. The increased surface tension in the alveoli then results in alveolar instability and collapse. It is most commonly seen in infant respiratory distress syndrome and acute respiratory distress syndrome (ARDS). Compressive atelectasis This type occurs when the extra-alveolar pressure overcomes the intra-alveolar pressure, which results in collapse of the lung tissue. While the cause may vary, it is classically associated with the accumulation of blood, fluid, or air within the pleural cavity. These accumulations result in an increase in extra-alveolar pressure which leads to a pressure gradient favoring collapse of the alveoli. This is a frequent occurrence with pleural effusions secondary to congestive heart failure (CHF). Leakage of air into the pleural cavity (pneumothorax) may also lead to compressive atelectasis. Relaxation atelectasis This type of atelectasis occurs when there is loss of contact of the lung to the chest wall. It classically occurs as a result of a pleural effusion or pneumothorax. While relaxation and compressive atelectasis share a lot in common, compressive atelectasis tends to be more focal or localized. Special cases Right middle lobe syndrome In right middle lobe syndrome, the middle lobe of the right lung contracts due to pressure on the bronchus. This many be secondary to an enlarged lymph node or occasionally a tumor. The blocked, contracted lung may develop pneumonia that fails to resolve completely and leads to chronic inflammation, scarring, and bronchiectasis.) is often mistaken for lung cancer on imaging. The most common current theory for rounded atelectasis is that local pleural irritation leads to thickening and shrinkage of the pleura which causes the adjacent lung to shrink with it. The outer portion of the lung slowly collapses as a result of scarring and shrinkage of the membrane layers covering the lungs (pleura), which would show as visceral pleural thickening and entrapment of lung tissue. This produces a rounded appearance on X-ray that doctors may mistake for a tumor. Rounded atelectasis is usually a complication of asbestos-induced disease of the pleura, but it may also result from other types of chronic scarring and thickening of the pleura. ==Treatment==

Treatment is directed at correcting the underlying cause. In atelectasis manifestations that result from the mucus plugging of the airways as seen in patients with cystic fibrosis and pneumonia, mucolytic agents such as acetylcysteine (NAC) is used. This nebulized treatment works by reducing mucous viscosity and elasticity by breaking disulfide bonds in mucoproteins within the mucus complex, thus facilitating mucus clearance. Post-surgical atelectasis is treated by physiotherapy, focusing on deep breathing and encouraging coughing. An incentive spirometer is often used as part of the breathing exercises. Walking is also highly encouraged to improve lung inflation. People with chest deformities or neurologic conditions that cause shallow breathing for long periods may benefit from mechanical devices that assist their breathing. The primary treatment for acute massive atelectasis is correction of the underlying cause. A blockage that cannot be removed by coughing or by suctioning the airways often can be removed by bronchoscopy. Antibiotics are given for an infection. Chronic atelectasis is often treated with antibiotics because infection is almost inevitable. In certain cases, the affected part of the lung may be surgically removed when recurring or chronic infections become disabling or bleeding is significant. If a tumor is blocking the airway, relieving the obstruction by surgery, radiation therapy, chemotherapy, or laser therapy may prevent atelectasis from progressing and recurrent obstructive pneumonia from developing. == Prevention ==

• Post-Operative Movement. • Deep Breathing Exercises. • Avoid Smoking 6-8 Weeks Pre-Surgery. • Chest Physiotherapy (ie. Postural Drainage, Chest Percussion). == Prognosis ==

Prognosis for atelectasis is typically excellent when condition is treated early-on and effectively. Most cases occurring during general anesthesia are resolved spontaneously within the first 24 hours of surgery. If left untreated persistent atelectasis may lead to significant complications such as pneumonia, hypoxemia and in severe cases, respiratory failure. == Research ==

Recent clinical research has focused on new intraoperative ventilation strategies to reduce postoperative complications. A randomized controlled trial by Wei et al. in 2025 evaluated how individualized FiO2 filtration guided by SpO2 levels lowered the risk of postoperative atelectasis. The study suggests that avoiding too much oxygen during the surgery can help keep lungs open and lower risk of further damage. Clinical trials have also explored other more efficient strategies in preventing and/or treating atelectasis. Open-lung ventilation potentially reduces post-operative atelectasis. Comparative studies between PCV-VG and VCV ventilation modes, explored the different ventilation modes' affect development or prevention in patients being treated surgically. Mostly testing the pressure-controlled volume-guaranteed(PCV-VG) as opposed too volume-controlled ventilation(VCV). The trials have been completed. Additional research examined how ultra-sound guided lung recruitment may affect atelectasis outcomes. In this trial an ultrasound would be used to reopen collapsed areas in the lung and reduce postoperative atelectasis altogether. ==See also==