The term atelectasis is derived from the Greek words ateles and ektasis, which mean incomplete expansion. Atelectasis is defined as diminished volume affecting all or part of a lung. Pulmonary atelectasis is one of the most commonly encountered abnormalities in chest radiographs. Recognizing an abnormality due to atelectasis on chest radiographs can be crucial to understanding the underlying pathology. Several types of atelectasis exist; each has a characteristic radiographic pattern and etiology. Atelectasis is divided physiologically into obstructive and nonobstructive causes.
Obstructive atelectasis is the most common type and results from reabsorption of gas from the alveoli when communication between the alveoli and the trachea is obstructed. The obstruction can occur at the level of the larger or smaller bronchus. Causes of obstructive atelectasis include foreign body, tumor, and mucous plugging. The rate at which atelectasis develops and the extent of atelectasis depend on several factors, including the extent of collateral ventilation that is present and the composition of inspired gas. Obstruction of a lobar bronchus is likely to produce lobar atelectasis; obstruction of a segmental bronchus is likely to produce segmental atelectasis. Because of the collateral ventilation within a lobe or between segments, the pattern of atelectasis often depends on collateral ventilation, which is provided by the pores of Kohn and the canals of Lambert.
Nonobstructive atelectasis can be caused by loss of contact between the parietal and visceral pleurae, compression, loss of surfactant, and replacement of parenchymal tissue by scarring or infiltrative disease. Examples of nonobstructive atelectasis are described below.
Relaxation or passive atelectasis results when a pleural effusion or a pneumothorax eliminates contact between the parietal and visceral pleurae. Generally, the uniform elasticity of a normal lung leads to preservation of shape even when volume is decreased. The different lobes also respond differently, eg, the middle and lower lobes collapse more than the upper lobe in the presence of pleural effusion, while the upper lobe is typically affected more by pneumothorax.
Compression atelectasis occurs from any space-occupying lesion of the thorax compresses the lung and forces air out of the alveoli. The mechanism is similar to relaxation atelectasis.
Adhesive atelectasis results from surfactant deficiency. Surfactant normally reduces the surface tension of the alveoli, thereby decreasing the tendency of these structures to collapse. Decreased production or inactivation of surfactant leads to alveolar instability and collapse. This is observed particularly in acute respiratory distress syndrome (ARDS) and similar disorders.
Cicatrization atelectasis results from diminution of volume as a sequela of severe parenchymal scarring and is usually caused by granulomatous disease or necrotizing pneumonia. Replacement atelectasis occurs when the alveoli of an entire lobe are filled by tumor (eg, bronchioalveolar cell carcinoma), resulting in loss of volume.
Middle lobe syndrome is a disorder of recurrent or fixed atelectasis involving the right middle lobe and/or lingula. It can result from either extraluminal (bronchial compression by surrounding lymph nodes) or by intraluminal bronchial obstruction. It may develop in the presence of a patent lobar bronchus without identifiable obstruction. Inflammatory processes and defects in the bronchial anatomy and collateral ventilation have been designated as the nonobstructive causes of middle lobe syndrome. Timely medical intervention with fiberoptic bronchoscopy with bronchoalveolar lavage in patients, particularly children, with middle lung syndrome may prevent the long-term consequence of bronchiectasis. Bronchiectasis in turn may be responsible for recurrent infections and, ultimately, the unfavorable outcome of chronic atelectasis.
Middle lobe syndrome has been reported as a pulmonary manifestation of primary Sjögren syndrome. Transbronchial biopsies performed in such patients revealed lymphocytic bronchiolitis in the atelectatic lobes. Atelectasis responds well to glucocorticoid treatment, suggesting that the peribronchiolar lymphocytic infiltrates may play an important role in the development of middle lobe syndrome in these patients.
Rounded atelectasis represents folded atelectatic lung tissue with fibrous bands and adhesions to the visceral pleura. Incidence is high in asbestos workers (65-70% of cases), most likely due to a high degree of pleural disease. Affected patients typically are asymptomatic, and the mean age at presentation is 60 years. Rounded atelectasis may mimic a neoplastic tumor. The comet tail sign or talon sign is its distinguishing radiographic characteristic.
The mechanism of obstructive and nonobstructive atelectasis is quite different and is determined by several factors.
Following obstruction of a bronchus, the blood circulating in the alveolar-capillary membrane absorbs the gas from alveoli. This process can lead to retraction of the lung and an airless state within those alveoli in a few hours. In the early stages, blood then perfuses the unventilated lung. This results in a shunt and, potentially, arterial hypoxemia. Subsequent to obstruction of a bronchus, filling of the alveolar spaces with secretions and cells may occur, thereby preventing complete collapse of the atelectatic lung. The uninvolved surrounding lung tissue distends, displacing the surrounding structures. The heart and mediastinum shift toward the atelectatic area, the diaphragm is elevated, and the chest wall flattens.
If the obstruction to the bronchus is removed, any complicating postobstructive infection subsides and the lung returns to its normal state. If the obstruction is persistent and infection continues to be present, fibrosis and/or bronchiectasis may develop.
The loss of contact between the visceral and parietal pleurae is the primary cause of nonobstructive atelectasis. A pleural effusion or pneumothorax causes relaxation or passive atelectasis. Pleural effusions affect the lower lobes more commonly than pneumothorax, which affects the upper lobes. A large pleural-based lung mass may cause compression atelectasis by decreasing lung volumes.
Adhesive atelectasis is caused by a lack of surfactant. The surfactant has phospholipid dipalmitoyl phosphatidylcholine, which prevents lung collapse by reducing the surface tension of the alveoli. Lack of production or inactivation of surfactant, which may occur in acute respiratory distress syndrome (ARDS), radiation pneumonitis, and blunt trauma to the lung, cause alveolar instability and collapse.
Middle lobe syndrome (recurrent atelectasis and/or bronchiectasis involving the right middle lobe and/or lingula) has recently been reported as the pulmonary manifestation of primary Sjögren syndrome.
Scarring of the lung parenchyma leads to cicatrization atelectasis.
Replacement atelectasis is caused by filling of the entire lobe by a tumor such as bronchoalveolar carcinoma.
Also called discoid or subsegmental atelectasis, this type is seen most commonly on chest radiographs. Platelike atelectasis probably occurs because of obstruction of a small bronchus and is observed in states of hypoventilation, pulmonary embolism, or lower respiratory tract infection. Small areas of atelectasis occur because of inadequate regional ventilation and abnormalities in surfactant formation from hypoxia, ischemia, hyperoxia, and exposure to various toxins. A mild-to-severe gas exchange abnormality may occur because of ventilation-perfusion mismatch and intrapulmonary shunt.
Atelectasis is a common pulmonary complication in patients following thoracic and upper abdominal procedures. General anesthesia and surgical manipulation lead to atelectasis by causing diaphragmatic dysfunction and diminished surfactant activity. The atelectasis is typically basilar and segmental in distribution. After induction of anesthesia, atelectasis increases from 1 to 11% of total lung volume. End-expiratory lung volume is also found to be decreased.
In 2009 study, a recruitment maneuver plus positive end-expiratory pressure (PEEP) reduced atelectasis to 3 ±4%, increased end-expiratory lung volume, and increased the PaO2/FiO2 ratio from 266 ±70 mm Hg to 412 ±99 mm Hg. It was found that the PEEP alone did not reduce the amount of atelectasis or improve oxygenation, but a recruitment maneuver followed by PEEP reduced atelectasis and improved oxygenation.
Postoperative atelectasis is extremely common. Lobar atelectasis is also common. The incidence and prevalence of this disorder are not well documented.
Atelectasis has no racial predilection.
Atelectasis has no sexual predilection.
The mean age at presentation for rounded atelectasis is 60 years.
Atelectasis may occur postoperatively following thoracic or upper abdominal procedures.
Although atelectasis is considered to be the most common cause of early postoperative fever, the existing evidence is contradictory. In a study by Mavros et al, they found no clinical evidence supporting the concept that atelectasis is associated with early postoperative fever.
Most symptoms and signs are determined by the rapidity with which the bronchial occlusion occurs, the size of the lung area affected, and the presence or absence of complicating infection.
Rapid bronchial occlusion with a large area of lung collapse causes pain on the affected side, sudden onset of dyspnea, and cyanosis. Hypotension, tachycardia, fever, and shock may also occur.
Slowly developing atelectasis may be asymptomatic or may cause only minor symptoms. Middle lobe syndrome often is asymptomatic, although irritation in the right middle and right lower lobe bronchi may cause a severe, hacking, nonproductive cough.
The physical examination findings may demonstrate dullness to percussion over the involved area and diminished or absent breath sounds. Chest excursion of the involved hemithorax may be reduced or absent. The trachea and the heart may be deviated toward the affected side.
The primary cause of acute or chronic atelectasis is bronchial obstruction by the following:
External pulmonary compression by pleural fluid or air (ie, pleural effusion, pneumothorax) may also cause atelectasis.
Abnormalities of surfactant production contribute to alveolar instability and may result in atelectasis. These abnormalities commonly occur with oxygen toxicity and ARDS.
Resorptive atelectasis is caused by the following:
Relaxation atelectasis is caused by the following:
Compression atelectasis is caused by the following:
Adhesive atelectasis is caused by the following:
Cicatrization atelectasis is caused by the following:
Replacement atelectasis is caused by alveoli filled by tumor or fluid.
Right middle lobe syndrome (also known as Brock syndrome) refers to recurrent right middle lobe collapse secondary to airway disease, infection, or a combination of the two. The right middle lobe bronchus is long and thin, has the poorest drainage or clearance of all the lobes of the lung, which can result in retained mucus, and is more prone to extrinsic compression by the lymphatic system. Individuals with middle lobe syndrome are often asymptomatic, although some present with recurrent productive cough and history of right-sided pneumonias.
Rounded atelectasis is caused primarily by asbestos-related pleural disease and uremic pleuritis.
Atelectasis of a significant size can result in hypoxemia as measured on arterial blood gas determinations. Arterial blood gas evaluation may demonstrate that despite a low PaO2. The PaCO2 level is usually normal but may be low as a result of the increased minute ventilation.
Chest radiographs and CT scans may demonstrate direct and indirect signs of lobar collapse. Direct signs include displacement of fissures and opacification of the collapsed lobe.
Indirect signs include displacement of the hilum, mediastinal shift toward the side of collapse, loss of volume on ipsilateral hemithorax, elevation of ipsilateral diaphragm, crowding of the ribs, compensatory hyperlucency of the remaining lobes, and silhouetting of the diaphragm or the heart border.
Complete atelectasis of an entire lung (see images below) is when (1) complete collapse of a lung leads to opacification of the entire hemithorax and an ipsilateral shift of the mediastinum and (2) the mediastinal shift separates atelectasis from massive pleural effusion.
Complete atelectasis of the left lung. Mediastinal displacement, opacification, and loss of volume are present in the left hemithorax.
Complete right lung atelectasis.
With right upper lobe (RUL) collapse, the collapsed RUL shifts medially and superiorly, resulting in elevation of the right hilum and the minor fissure. Rarely, the RUL may collapse laterally, producing a masslike opacity that may look like a loculated pleural effusion. The minor fissure in RUL collapse is usually convex superiorly but may appear concave because of an underlying mass lesion. This is called the sign of Golden S. Tenting of the diaphragmatic pleura juxtaphrenic peak is another helpful sign of RUL atelectasis. Upon CT scanning, RUL collapse appears as a right paratracheal opacity, and the minor fissure appears concave laterally. Note the images below
Atelectasis. Left upper lobe collapse showing opacity contiguous to the aortic knob, a smaller left hemithorax, and a mediastinal shift.
Atelectasis. Right upper lobe collapse demonstrating Golden sign of S.
Atelectasis. Right upper lobe collapse and consolidation.
Atelectasis. Right upper lobe collapse.
Atelectasis. Right upper lobe collapse.
Right middle lobe (RML) collapse (see images below) obscures the right heart border on a posteroanterior (PA) film. Occasionally, a triangular opacity may be observed. The lateral view demonstrates a triangular opacity overlying the heart because the major fissure shifts upward and the minor fissure shifts downward. Upon CT scanning, the atelectatic RML appears as a triangular opacity against the right heart border with the apex pointing laterally and is termed the "tilted ice cream cone sign."
Atelectasis. A lateral chest x-ray film confirms the diagnosis of right middle lobe collapse. The minor fissure moves down, and the major fissure move....
Atelectasis. Left lower lobe collapse.
Atelectasis. Right middle lobe collapse showing obliteration of the right heart border.
Atelectasis. Right middle lobe collapse on a lateral chest x-ray film.
In right lower lobe (RLL) collapse (see images below), the collapsed RLL shifts posteriorly and inferiorly. A triangular opacity obscuring the RLL pulmonary artery may be observed. The major fissure, which normally is not visible, is seen with RLL collapse. The superior mediastinal structure shifts to the right, causing a superior triangle sign. Laterally, the collapsed RLL blurs the posterior third of the right hemidiaphragm. Upon CT scanning, a paraspinal masslike appearance is observed. Concomitant RML and RLL atelectasis may appear as an elevated right hemidiaphragm or a subpulmonic effusion. An attempt to identify the fissures usually leads to the accurate diagnosis.
Atelectasis. Right lower lobe collapse.
Atelectasis. Both right lower lobe and right middle lobe collapse. The left lung is hyperexpanded.
Atelectasis. The right lower lobe collapses inferiorly and posteriorly.
Atelectasis. Right lower lobe collapse without middle lobe collapse, the right major fissure is shifted downward and is now visible.
In left upper lobe (LUL) collapse (see images below), an atelectatic LUL shifts anteriorly and superiorly. In half the cases, a hyperexpanded superior segment of the left lower lobe (LLL) is positioned between the atelectatic upper lobe and the aortic arch. This gives the appearance of a crescent of the aerated lung, called the Luft Sichel sign. On lateral views, the major fissure is displaced anteriorly and the hyperexpanded RUL may herniate across the midline. On PA views, an atelectatic LUL produces a faint opacity in the left upper hemithorax, obliterating the left heart border. A CT scan demonstrates the inferior location of the collapsed lobe and the shift of the RUL across the midline.
Atelectasis. Left upper lobe collapse showing opacity contiguous to the aortic knob, a smaller left hemithorax, and a mediastinal shift.
Atelectasis. CT scan of a left upper lobe collapse with a small pleural effusion.
Atelectasis. The left upper lobe collapses anteriorly on a lateral chest x-ray film.
Atelectasis. Left upper lobe collapse. The top of the aortic knob sign is demonstrated.
Atelectasis. Left upper lobe collapse. The Luft Sichel sign is demonstrated clearly in this radiograph.
Atelectasis. Chest CT scan showing left upper lobe collapse.
In left lower lobe (LLL) collapse (see images below), increased retrocardiac opacity silhouettes the LLL pulmonary artery and the left hemidiaphragm on frontal views. The hilum shifts downward, and the rotation of the heart produces flattening of the cardiac waist, which is known as the flat-waist sign. The superior mediastinum may shift and obliterate the aortic arch, the top of the aortic-knob sign. On lateral radiographs, opacity makes the posterior third of the left diaphragm indistinct. A CT scan shows the atelectatic LLL in the inferior posterior location.
Atelectasis. Loss of volume on the left side; an elevated and silhouetted left diaphragm; and an opacity behind the heart, called a sail sign, are pre....
Atelectasis. Left lower lobe collapse.
Atelectasis. Left lower lobe collapse. The sail sign is obvious.
Atelectasis. Left lower lobe collapse on posteroanterior view.
Rounded atelectasis is a segmental or subsegmental atelectasis that occurs secondary to visceral pleural thickening and entrapment of lung tissue. Rounded atelectasis is usually located in the lower lobes, the lingula, or the RML. On chest radiographs, rounded atelectasis manifests as a subpleural mass, with bronchovascular structures projecting out of the mass toward the hilum. An associated parietal pleural plaque may be present. The swirl appearance of bronchovascular shadows is called the comet-tail sign.
Flexible fiberoptic bronchoscopy can be a useful diagnostic and therapeutic procedure. Bronchoscopy helps evaluate the cause of bronchial obstruction. In addition, bronchoscopy helps clear mucous plugs when they cause bronchial obstruction. Bronchoscopy has limitations. Because only the subsegmental bronchi are visualized, a distal endobronchial lesion is not accessible through bronchoscopy.
In an evaluation of middle lobe syndrome, bronchoscopy may show an endobronchial etiology (mucus plugging/broncholithiasis/tumor), although inflammatory processes and defects in the bronchial anatomy and collateral ventilation have been designated as the nonobstructive causes of the syndrome.
During fiberoptic bronchoscopy, the washing, brushing, and biopsy specimens of any obstructing mass should be examined for evidence of malignancy or Aspergillus mucous plugging (ie, allergic bronchopulmonary aspergillosis).
Lobar atelectasis is a common problem caused by a variety of mechanisms including resorption atelectasis due to airway obstruction, passive atelectasis from hypoventilation, compressive atelectasis from abdominal distension, and adhesive atelectasis due to increased surface tension. Evidence-based studies on the management of lobar atelectasis are lacking. Assessment of air bronchograms on a chest radiograph may be helpful to determine whether the airway obstruction is proximal or distal. Chest physiotherapy, nebulized dornase alfa (DNase), and, possibly, fiberoptic bronchoscopy might be helpful in patients with mucous plugging of the airways. In passive and adhesive atelectasis, positive end-expiratory pressure might be a useful adjunct to treatment.
Fiberoptic bronchoscopy may have a role management. In one study, bronchoscopy allowed diagnosing the degree of tracheobronchial tree obstruction and its causes in all cases. Single suction fiberoptic bronchoscopy led to normalization and encouraged positive dynamics in 76% of all cases (57 patients). Repeated endoscopic sanitation in the first two days was necessary for 25 patients (25.3%) with unresolved or reoccurring atelectasis. The effectiveness of second research was to 84%. Most patients with unresolved or recurring atelectasis had serious chest injury. In these cases, blood was mainly seen through the tracheobronchial tree lumen. Thus, when a mechanically obstructed bronchus is suggested and coughing or suctioning is not successful, bronchoscopy should be performed.
Nonpharmacologic therapies for improving cough and clearance of secretions from the airways include chest physiotherapy, including postural drainage, chest wall percussion and vibration, and a forced expiration technique (called huffing). Increased airway clearance as assessed by sputum characteristics (ie, volume, weight, viscosity) and clearance of the radioaerosol from the lung show that the long-term efficacy of these techniques compared with unassisted cough alone is unknown.
The treatment of atelectasis depends on the underlying etiology. Treatment of acute atelectasis, including postoperative lung collapse, requires removal of the underlying cause.
For postoperative atelectasis, prevention is the best approach. Anesthetic agents associated with postanesthesia narcosis should be avoided. Narcotics should be used sparingly because they depress the cough reflex. Early ambulation and use of incentive spirometry are important. Encourage the patient to cough and to breathe deeply. Nebulized bronchodilators and humidity may help liquefy secretions and promote their easy removal. In the case of lobar atelectasis, vigorous chest physiotherapy frequently helps re-expand the collapsed lung. When these efforts are not successful within 24 hours, flexible fiberoptic bronchoscopy could be performed.
Prevention of further atelectasis involves (1) placing the patient in such a position that the uninvolved side is dependent to promote increased drainage of the affected area, (2) giving vigorous chest physiotherapy, and (3) encouraging the patient to cough and to breathe deeply.
Patients may require nasotracheal suctioning if atelectasis recurs. This is particularly true in patients with neuromuscular disease and poor cough.
Therapy with a broad-spectrum antibiotic is started and modified appropriately if a specific pathogen is isolated from sputum samples or bronchial secretions.
Postoperative atelectasis is treated with adequate oxygenation and re-expansion of the lung segments. Supplemental oxygen should be titrated to achieve an arterial oxygen saturation of greater than 90%.
Severe hypoxemia associated with severe respiratory distress should lead to intubation and mechanical support. Intubation not only provides oxygenation and ventilatory support, but also provides access for suctioning of the airways and facilitates performing bronchoscopy, if needed. The positive pressure ventilation and larger tidal volumes may help to re-expand collapsed lung segments.
Continuous positive airway pressure delivered via a nasal cannula or facemask may also be effective in improving oxygenation and re-expanding the collapsed lung.
Broad-spectrum antibiotics should be prescribed if evidence of infection is present, such as fever, night sweats, or leukocytosis, because secondary atelectasis usually becomes infected regardless of the cause of obstruction. Obstruction of a major bronchus may cause severe hacking or coughing. Antitussive therapy reduces the cough reflex and may produce further obstruction. Thus, it should be avoided.
Fiberoptic bronchoscopy is commonly required for diagnosis, particularly if an endobronchial lesion is suggested. This procedure has a limited role in the management of postoperative atelectasis. Fiberoptic bronchoscopy is not more effective than standard chest physiotherapy, deep breathing, coughing, and suctioning of patients who are intubated. Therefore, simple and standard respiratory therapy techniques should be administered to patients who spontaneously ventilate or patients on mechanical ventilation. Fiberoptic bronchoscopy should be reserved for those situations in which chest physiotherapy is contraindicated (eg, chest trauma, immobilized patient), poorly tolerated, or unsuccessful.
Judicious use of perioperative analgesia is an essential adjunct, permitting patients to breathe deeply, cough forcefully, and participate in chest physiotherapy maneuvers. In patients with underlying pulmonary disease, use of epidural analgesia is a very effective pain control measure, thereby aiding aggressive chest physiotherapy.
N -acetylcysteine aerosols commonly are administered in an effort to promote clearance of tenacious secretions. However, their efficacy has not been documented. In addition, N -acetylcysteine may cause acute bronchoconstriction. Some clinicians recommend its use be limited to direct instillation at the time of fiberoptic bronchoscopy.
In a study of noncystic fibrosis in children who had atelectasis of infectious origin, treatment with DNase led to rapid clinical improvement observed within two hours and radiologic improvement documented within 24 hours. DNase may be an effective treatment for infectious atelectasis in pediatric patients with noncystic fibrosis. Such data does not exist for adult patients, but DNase could be used as a trial of therapy in adults as well.
Prophylactic maneuvers for reducing the incidence and magnitude of postoperative atelectasis in high-risk patients should be encouraged. These techniques are deep-breathing exercises, coughing exercises, and incentive spirometry. For maximal benefit, prophylactic measures should be taught and instituted before surgery and used regularly, on an hourly basis, after surgery. Early ambulation of patients after surgery is as effective as physical therapy.
Kato et al reported on the use of the RTX respirator for extensive atelectasis in elderly patients. Patients were placed in the lateral decubitus position. The RTX respirator was reported to be a useful tool to clear retained sputum in elderly patients.
Chronic atelectasis is treated with segmental resection or lobectomy.
Bronchodilators may be used to encourage sputum expectoration; if underlying airflow is present, these agents may also improve ventilation. Some patients may require broad-spectrum antibiotics to treat the underlying infections, which may occur because of bronchial obstruction. N -acetylcysteine aerosol is not routinely recommended because of the risk of bronchoconstriction and the lack of documented efficacy.
Clinical Context: Albuterol is a beta-agonist for bronchospasm refractory to epinephrine. It relaxes bronchial smooth muscle by action on beta-2 receptors, with little effect on cardiac muscle contractility. Most patients (even those with no measurable increase in expiratory flow) benefit from treatment. Inhaled beta-agonists initially are prescribed on an "as needed" basis. The frequency may be increased; institute a regular schedule in patients on anticholinergic drugs who are still symptomatic.
Albuterol is available as a liquid for nebulizer, metered-dose inhaler (MDI), and dry-powder inhaler.
Clinical Context: Metaproterenol relaxes bronchial smooth muscle by action on beta-2 receptors, with little effect on cardiac muscle contractility. Most patients (even those with no measurable increase in expiratory flow) benefit from treatment. Inhaled beta-agonists initially are prescribed on an as-needed basis. The frequency may be increased; institute a regular schedule in patients on anticholinergic drugs who are still symptomatic.
Metaproterenol is available as a liquid for nebulizer, MDI, and dry-powder inhaler.
Bronchodilators decrease muscle tone in both the small and large airways in the lungs, thereby increasing ventilation. They include subcutaneous medications, beta-adrenergic agents, methylxanthines, and anticholinergics.
Clinical Context: Cefuroxime is a second-generation cephalosporin that maintains gram-positive activity of first-generation cephalosporins; it adds activity against Proteus mirabilis, Haemophilus influenzae, Escherichia coli, Klebsiella pneumoniae, and Moraxella catarrhalis.
The condition of the patient, severity of the infection, and susceptibility of the microorganism determine proper dose and route of administration.
Clinical Context: Cefaclor is a second-generation cephalosporin indicated for infections caused by susceptible gram-positive cocci and gram-negative rods. Determine the proper dosage and route based on the condition of the patient, severity of the infection, and susceptibility of the causative organisms.
Antibiotics are used to treat underlying bronchitis or postobstructive infection.
Clinical Context: N-acetylcysteine inhalations may be tried to encourage sputum expectoration in patients with tenacious sputum and mucous plugging.
Clinical Context: Dornase alfa cleaves and depolymerizes extracellular DNA and separates DNA from proteins. This allows endogenous proteolytic enzymes to break down the proteins; thus, decreasing viscoelasticity and surface tension of purulent sputum.
N -acetylcysteine is only recommended for direct instillation via fiberoptic bronchoscopy or in an intubated patient. Therapy with mucolytics may promote sputum removal of thick mucous plugs and, therefore, helps treat atelectasis in many patients. Inhaled recombinant human deoxyribonuclease is a mucolytic agent successfully used in patients with cystic fibrosis.
Complications may include the following:
Patient mortality depends on the underlying cause of atelectasis. In postoperative atelectasis, the condition generally improves. The prognosis of lobar atelectasis secondary to endobronchial obstruction depends on treatment of the underlying malignancy.
For patient education information, see the Lung and Airway Center and Procedures Center, as well as Collapsed Lung and Bronchoscopy.