Atelectasis is the partial or complete collapse of lung tissue, and it is one of the most common respiratory complications people encounter in hospitals, particularly after surgery. The condition occurs when tiny air sacs in the lung deflate or fill with fluid, reducing the lung’s ability to exchange oxygen and carbon dioxide. While the word sounds alarming, atelectasis ranges from a small patch of deflated tissue that resolves on its own to a fully collapsed lobe that requires urgent intervention. What makes atelectasis worth understanding is how often it happens without people realizing it, and how much the treatment landscape depends on knowing exactly what caused it.
What Actually Happens Inside the Lung
Your lungs contain hundreds of millions of tiny air sacs called alveoli. These stay open thanks to a balance of forces: air pressure inside the sacs pushes outward, while the tissue connecting neighboring sacs helps tether them open. Working against that are the natural elastic recoil of the lung, the pressure from the chest wall, and surface tension within the sacs themselves. When the collapsing forces win, alveoli deflate, and the affected area of lung stops participating in gas exchange.
The consequences go beyond just losing some breathing capacity. Collapsed lung tissue triggers local inflammation, weakens immune defenses in the affected area, and can damage the thin barrier between the air sacs and the blood vessels that surround them. That damage can lead to fluid leaking into the lung, increased vulnerability to infection, and a cascade that worsens lung injury if left unchecked.1PubMed Central. Perioperative Pulmonary Atelectasis: Part I. Biology and Mechanisms This is why doctors treat even moderate atelectasis seriously, especially in patients who are already critically ill.
The Different Ways Lungs Collapse
Not all atelectasis is the same. The underlying mechanism matters because it determines both how the condition behaves and what treatment will work. There are four main types, each with a distinct trigger.2PubMed Central. Treatment of atelectasis: where is the evidence?
- Resorption: An airway gets blocked, often by a mucus plug, a tumor, or an inhaled foreign object. The air trapped beyond the blockage gradually gets absorbed into the bloodstream, and without fresh air replacing it, the downstream lung tissue collapses. This is the type most commonly associated with something physically obstructing a bronchus.
- Passive (relaxation): When someone breathes too shallowly for too long, the alveoli do not inflate fully and eventually deflate. This is the classic post-surgical scenario, especially after abdominal operations where pain limits deep breathing.
- Compressive: Something outside the lung pushes on it hard enough to squeeze out air. A large pleural effusion, abdominal distension, or even a massively enlarged heart can do this.
- Adhesive: The air sacs lose the substance that normally keeps them from sticking shut. This substance, called surfactant, reduces surface tension inside the alveoli. When surfactant is deficient or dysfunctional, surface tension rises and the sacs collapse on themselves.3Osmosis. Atelectasis · What Is It, Causes, Diagnosis, and More Premature infants are especially vulnerable to this type because their lungs have not yet produced enough surfactant.
In practice, patients often have more than one mechanism at work simultaneously. A person recovering from abdominal surgery might be breathing shallowly (passive atelectasis) while also developing mucus plugs (resorption atelectasis) because pain prevents effective coughing.
Why Surgery Is the Most Common Trigger
If you have ever been told to take deep breaths after an operation, this is the reason. Atelectasis after anesthesia is strikingly common. Imaging studies have shown collapsed lung tissue in roughly nine out of ten people under general anesthesia, regardless of whether they were breathing on their own or paralyzed, and regardless of which type of anesthetic was used.4PubMed. Atelectasis formation during anesthesia: causes and measures to prevent it The collapse typically develops in the parts of the lung closest to the back and the diaphragm, often within minutes of induction.
Several factors pile up during surgery. The diaphragm relaxes and shifts upward when muscles are paralyzed. High concentrations of oxygen used during anesthesia are absorbed faster than room air, accelerating the collapse of poorly ventilated regions. And lying flat for hours eliminates the gravitational help that normally keeps the lower lung expanded. Most post-surgical atelectasis resolves within hours to days as patients wake up, start moving, and begin breathing deeply again, but in patients with underlying lung disease, obesity, or prolonged operations, it can persist and set the stage for pneumonia.
The Fever Myth
Ask almost any medical professional trained before about 2010 and they will tell you that atelectasis causes fever after surgery. It has been taught in textbooks and passed along in clinical training for decades. The logic seemed intuitive: collapsed lung tissue becomes inflamed, inflammation causes fever, therefore atelectasis causes postoperative fever.
The evidence does not support this. A systematic review looking specifically for clinical data linking atelectasis to early postoperative fever found none. The authors concluded that there is no clear evidence atelectasis causes fever at all.5PubMed. Atelectasis as a cause of postoperative fever: where is the clinical evidence? Fever after surgery is far more likely to come from the surgical wound itself, medications, blood transfusions, or an early infection. Blaming atelectasis for a fever can actually delay the search for the real cause. This is one of those medical myths that persists through repetition rather than evidence, and it is worth knowing about if you are a patient being told your postoperative fever is “just atelectasis.”
How Doctors Spot It
A standard chest X-ray remains the first-line tool. Atelectasis shows up as increased density in the affected area, with the surrounding structures shifting toward the collapsed region. The fissures between lobes may move, the diaphragm on the affected side may ride higher, and the trachea or heart may shift. Recognizing these signs correctly is important because atelectasis from an obstructed airway can signal a tumor or other serious underlying problem.6PubMed. Manifestations of lobar atelectasis on chest x-rays and correlation with computed tomography findings A CT scan provides more detail and can reveal the cause of the obstruction, but it means transporting the patient to a scanner, which is not always practical in critical care.
Bedside lung ultrasound has become increasingly useful, particularly in intensive care units where moving patients is risky. In trauma patients on mechanical ventilation, ultrasound achieved roughly 82% sensitivity and 100% specificity for detecting atelectasis and consolidation when compared to CT scans, with very high agreement between the two methods.7Critical Ultrasound Journal. Detection of lung atelectasis/consolidation by ultrasound in multiple trauma patients with mechanical ventilation A modified ultrasound protocol tested in critically ill patients reported even higher sensitivity, around 96%, with diagnostic accuracy better than CT in that particular study.8PubMed. The value of bedside lung ultrasound in emergency-plus protocol for the assessment of lung consolidation and atelectasis in critical patients
One tricky diagnostic challenge is telling atelectasis apart from pneumonia, since both can look similar on imaging. Researchers have explored using specific ultrasound signs to distinguish them. A dynamic air bronchogram sign (where you can see air moving in the bronchi during breathing) was highly specific for pneumonia, correctly ruling it out about 99% of the time, though it missed many cases. Combining it with color Doppler imaging improved the overall picture, achieving around 86% accuracy for both sensitivity and specificity.9PubMed. Extended Lung Ultrasound to Differentiate Between Pneumonia and Atelectasis in Critically Ill Patients: A Diagnostic Accuracy Study
Preventing and Treating Post-Surgical Atelectasis
The incentive spirometer is the device most people associate with post-surgical lung care. It is a simple plastic gadget that encourages you to take slow, deep breaths by giving visual feedback as you inhale. Hospitals hand them out routinely, but the evidence for their effectiveness is more mixed than you might expect.
A randomized trial after abdominal surgery found that simply handing patients an incentive spirometer without structured supervision did not produce a meaningful improvement in lung function compared to standard care alone.10JAMA Surgery. The Effect of Incentive Spirometry on Postoperative Pulmonary Function Following Laparotomy: A Randomized Clinical Trial On the other hand, when incentive spirometry was integrated into an intensive physiotherapy program with active coaching, one study of over 260 patients reported that lung complications dropped from 17% to 6%, and time spent in the high-dependency unit shortened.11PubMed. Incentive spirometry decreases respiratory complications following major abdominal surgery A meta-analysis focusing on patients after lung surgery found that spirometry reduced complications by about a third and shortened hospital stays by nearly two days.12Asian Journal of Surgery. Incentive spirometry is an effective strategy to improve the quality of postoperative care in patients
The takeaway: the spirometer itself is not magic. What matters is the deep breathing, the coughing, and the supervision that goes along with it. Walking early after surgery, changing positions in bed, and working with a physiotherapist are at least as important as any device. When patients are in too much pain to breathe deeply, adequate pain management becomes the real intervention against atelectasis.
When a Mucus Plug Is the Problem
Sometimes atelectasis happens because thick mucus blocks an airway entirely. This is common in intubated patients, people with cystic fibrosis, and anyone recovering from surgery who cannot cough effectively. When chest physiotherapy and suctioning do not clear the blockage, bronchoscopy becomes the go-to procedure. A flexible scope is passed into the airways, and the mucus plug is either suctioned out directly or loosened with saline instilled in small batches.13PubMed Central. The Role of Bronchoscopy and Chest Physiotherapy in Postoperative Patients With Acute Lung Atelectasis Due to Airway Mucus Plugging: A Case Series and Review of Entity
For particularly stubborn plugs, clinicians have used an enzyme called recombinant human DNase, which breaks down the DNA strands that make mucus thick and sticky. In one pediatric case, direct instillation of this enzyme onto a large mucus plug through a bronchoscope softened the plug enough for easy removal, and the child’s atelectasis resolved immediately.14PubMed. Easy removal of a large mucus plug with a flexible paediatric bronchoscope after administration of rhDNase (Pulmozyme) This agent is better known as a daily inhaled treatment for cystic fibrosis, but using it directly inside the airways during bronchoscopy is a creative off-label application that appears safe and effective in selected cases.
Chest high-frequency oscillation devices offer another approach. These systems deliver rapid vibrations to the chest wall to loosen secretions and improve airway clearance. In at least one reported case involving a teenager with a severe skin condition who developed significant atelectasis after extubation, this type of therapy resolved the collapse completely and avoided the need for reintubation.15Journal of Burn Care & Research. Chest High-Frequency Oscillatory Treatment for Severe Atelectasis in a Patient With Toxic Epidermal Necrolysis
Atelectasis in the ICU and Mechanical Ventilation
In critically ill patients on ventilators, atelectasis is not just a nuisance: it can contribute to ventilator-associated lung injury. When collapsed and open regions sit side by side, the open areas get overdistended while the collapsed areas are subjected to repetitive opening and closing with each breath cycle. This process, sometimes called atelectrauma, generates shearing forces at the boundary between open and collapsed tissue. Microscopy imaging in animal models has shown that recruitment and derecruitment of airways happen simultaneously throughout the breathing cycle, even within the same lung region.16Scientific Reports. Imaging atelectrauma in Ventilator-Induced Lung Injury using 4D X-ray microscopy
Recruitment maneuvers are a standard countermeasure. These involve briefly applying high airway pressures to pop open collapsed alveoli. The technique is straightforward and can be performed at the bedside in patients with severe lung injury.17PubMed Central. Recruitment maneuvers in acute respiratory distress syndrome: The safe way is the best way But here is the catch: once you open those alveoli, you have to keep them open. An animal study demonstrated that alveoli recruited at high pressures remained stable only if followed by adequate positive end-expiratory pressure (PEEP). With lower PEEP, the newly opened alveoli became unstable and began collapsing and reopening with each breath, potentially worsening the very injury the maneuver was meant to prevent.18American Journal of Respiratory and Critical Care Medicine. Positive End-Expiratory Pressure after a Recruitment Maneuver Prevents Both Alveolar Collapse and Recruitment/Derecruitment
In children, the story is encouraging but nuanced. A trial comparing a lung-protective ventilation strategy (using PEEP and recruitment maneuvers) to standard zero-PEEP ventilation during pediatric surgery found that the protective strategy reduced atelectasis immediately after surgery and right after the breathing tube was removed. However, both groups looked the same by three hours after extubation, with lung aeration returning to normal in both.19PubMed Central. Effects of positive end-expiratory pressure/recruitment manoeuvres compared with zero end-expiratory pressure on atelectasis in children This suggests that in otherwise healthy children, the lungs recover quickly regardless, though preventing even a few hours of compromised oxygenation matters for sicker patients.
Atelectasis in ventilated patients also interacts with infection risk. Analysis of fluid from the lungs of patients with ventilator-associated pneumonia and those with atelectasis alone both showed severe surfactant abnormalities, increased permeability of the air-blood barrier, and local inflammation. These changes impair gas exchange, worsen lung mechanics, and could predispose already-injured lungs to further damage.20PubMed. Ventilator-associated pneumonia and atelectasis: evaluation through bronchoalveolar lavage fluid analysis
When the Heart Causes Lung Collapse
An enlarged heart can compress the airways or lung tissue directly, and this is an underappreciated cause of atelectasis, particularly in the left lower lobe. The left atrium sits right in front of the left lower lobe bronchus, so when it enlarges significantly, it can squeeze that bronchus shut. Imaging studies of patients with cardiomegaly have shown that reduced left lower lobe ventilation is common and depends on posture, worsening when patients lie flat.21PubMed. Impaired left lower lobe ventilation in patients with cardiomegaly. An isotope study of mechanisms The mechanism is essentially a regional loss of lung volume from external compression.
In severe cases, the compression can cause complete lobar collapse. One reported case described a patient with a massively dilated left atrium and ventricle whose CT showed complete left lower lobe collapse from extrinsic bronchial compression. Treating the underlying heart failure with aggressive fluid removal shrank the heart enough to relieve the compression, and the lobe fully re-expanded.22CHEST. Severe Left Atrial Enlargement Resulting in Complete Left Lower Lobe Collapse This is a reminder that treating atelectasis sometimes means treating a completely different organ system. Clinicians who focus only on the lung may miss the cause sitting right next to it.
Electrical Impedance Tomography and the Future of Monitoring
One of the persistent challenges with atelectasis in the ICU is knowing what is happening inside the lungs in real time. Chest X-rays give you a snapshot. CT gives you detail but requires a trip to the scanner. Ultrasound is portable but operator-dependent and provides a limited view. Electrical impedance tomography, or EIT, fills a gap by offering continuous, radiation-free monitoring of ventilation distribution at the bedside.23PubMed Central. Lung monitoring with electrical impedance tomography: technical considerations and clinical applications
EIT works by placing a belt of electrodes around the chest and measuring how electrical currents flow through the tissue. Air-filled lung has different electrical properties than collapsed or fluid-filled lung, so the system can map which regions are ventilating well and which are not. It can detect recruitment and derecruitment in real time, identify regions of overdistension, and help clinicians titrate ventilator settings to individual patients.24PubMed Central. Electrical impedance tomography The technology can also help evaluate whether a recruitment maneuver actually worked or whether it just inflated already-open areas while the collapsed ones stayed shut.
EIT is still considered an emerging technology and is not yet standard in most hospitals, but it is gaining traction in specialized ICUs. Consensus recommendations for standardized acquisition and clinical use have been published, suggesting the field is maturing toward broader adoption.25PubMed Central. Electrical impedance tomography monitoring in adult ICU patients: state-of-the-art, recommendations for standardized acquisition, processing, and clinical use, and future directions For patients with severe respiratory failure, where small changes in ventilator settings can mean the difference between lung protection and lung injury, having continuous feedback on what the lungs are actually doing is a meaningful advance over taking periodic pictures and hoping for the best.
Unusual Causes and Rare Presentations
Most atelectasis falls neatly into the categories already described, but unusual triggers turn up in clinical practice and are worth knowing about. Pregnancy combined with other anatomical factors can create unique problems. One case report describes a woman at 16 weeks of pregnancy with a pre-existing elevation of her left diaphragm who developed complete left lower lobe and partial upper lobe collapse. A large uterine fibroid measuring over 18 centimeters was pushing the already-elevated diaphragm even further upward, compressing the lung. She required noninvasive ventilatory support to maintain adequate breathing.26CHEST. Looking Deeper: Genetic and Autoimmune Disorder Critical Cases: A Rare Case of Dyspnea in a Pregnant Patient With Diaphragm Eventration Cases like this illustrate how atelectasis can result from a convergence of anatomical factors that individually might never cause trouble.
Prolonged bed rest, neuromuscular diseases that weaken the respiratory muscles, and even tight bandaging of the chest can contribute. In obese patients, the weight of the chest wall and abdomen on the lungs during sleep or anesthesia creates a baseline tendency toward collapse in the dependent (lowest) portions of the lung. This partly explains why obese patients have higher rates of postoperative pulmonary complications and may need more aggressive preventive strategies, including early mobilization and positioning upright rather than flat whenever possible.