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Atelectasis Treatment & Management

  • Author: Tarun Madappa, MD, MPH; Chief Editor: Ryland P Byrd, Jr, MD  more...
 
Updated: Feb 11, 2016
 

Medical Care

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.[9]

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.[10]

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.[11]

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.[12]

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Surgical Care

Chronic atelectasis is treated with segmental resection or lobectomy.

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Contributor Information and Disclosures
Author

Tarun Madappa, MD, MPH Attending Physician, Department of Pulmonary and Critical Care Medicine, Christus Spohn-Shoreline Hospital

Tarun Madappa, MD, MPH is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, World Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University

Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Additional Contributors

Helen M Hollingsworth, MD Director, Adult Asthma and Allergy Services, Associate Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, Boston Medical Center

Helen M Hollingsworth, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American Thoracic Society, Massachusetts Medical Society

Disclosure: Nothing to disclose.

References
  1. Rosenbloom SA, Ravin CE, Putman CE, et al. Peripheral middle lobe syndrome. Radiology. 1983;. 149:17-21. [Medline]. [Full Text].

  2. Priftis KN, Mermiri D, Papadopoulou A, Anthracopoulos MB, Vaos G, Nicolaidou P. The role of timely intervention in middle lobe syndrome in children. Chest. 2005 Oct. 128(4):2504-10. [Medline].

  3. Chen HA, Lai SL, Kwang WK, Liu JC, Chen CH, Huang DF. Middle lobe syndrome as the pulmonary manifestation of primary Sjogren's syndrome. Med J Aust. 2006 Mar 20. 184(6):294-5. [Medline].

  4. Reinius H, Jonsson L, Gustafsson S, et al. Prevention of atelectasis in morbidly obese patients during general anesthesia and paralysis: a computerized tomography study. Anesthesiology. 2009 Nov. 111(5):979-87. [Medline].

  5. Mavros MN, Velmahos GC, Falagas ME. Atelectasis as a cause of postoperative fever: where is the clinical evidence?. Chest. 2011 Aug. 140(2):418-24. [Medline].

  6. Proto AV, Tocino I. Radiographic manifestations of lobar collapse. Semin Roentgenol. 1980 Apr. 15(2):117-73. [Medline].

  7. Kattan KR, Eyler WR, Felson B. The juxtaphrenic peak in upper lobe collapse. Semin Roentgenol. 1980 Apr. 15(2):187-93. [Medline].

  8. Partap VA. The comet tail sign. Radiology. 1999 Nov. 213(2):553-4. [Medline].

  9. [Urgent fiberoptic bronchoscopy for diagnostics and treatment of lung atelectasis]. Anesteziol Reanimatol. 2013 Nov-Dec. 51-4. [Medline].

  10. [Guideline] McCool FD, Rosen MJ. Nonpharmacologic airway clearance therapies: ACCP evidence-based clinical practice guidelines. Chest. 2006 Jan. 129(1 Suppl):250S-259S. [Medline].

  11. Hendriks T, de Hoog M, Lequin MH, Devos AS, Merkus PJ. DNase and atelectasis in non-cystic fibrosis pediatric patients. Crit Care. 2005 Aug. 9(4):R351-6. [Medline].

  12. Kato K, Sato N, Takeda S, et al. Marked improvement of extensive atelectasis by unilateral application of the RTX respirator in elderly patients. Intern Med. 2009. 48(16):1419-23. [Medline].

 
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Atelectasis. Left lower lobe collapse. The opacity is in the posterior inferior 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 present.
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.
Complete atelectasis of the left lung. Mediastinal displacement, opacification, and loss of volume are present in the left hemithorax.
Atelectasis. Right lower lobe collapse.
Atelectasis. Both right lower lobe and right middle lobe collapse. The left lung is hyperexpanded.
Complete right lung atelectasis.
Atelectasis. A lateral chest x-ray film confirms the diagnosis of right middle lobe collapse. The minor fissure moves down, and the major fissure moves up, leading to a wedge-shaped opacity.
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 lower lobe collapse.
Atelectasis. Right middle lobe collapse shows obliteration of the right heart border.
Atelectasis. The azygous lobe of the right lung may be mistaken for a collapsed right upper lobe.
Atelectasis. Left lower lobe collapse. The sail sign is obvious.
Atelectasis. Left upper lobe collapse. The Luft Sichel sign is demonstrated clearly in this radiograph.
Atelectasis. Chest CT scan showing left upper lobe collapse.
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.
Atelectasis. Right upper lobe collapse demonstrating Golden sign of S.
Atelectasis. Right middle lobe collapse showing obliteration of the right heart border.
Atelectasis. Right middle lobe collapse on a lateral chest x-ray film.
Atelectasis. Right upper lobe collapse and consolidation.
Atelectasis. Right upper lobe collapse.
Atelectasis. Right upper lobe collapse.
Atelectasis. Left lower lobe collapse on posteroanterior view.
The left lower lobe collapses toward the posterior and inferior aspects of the thoracic cavity; the atelectatic left lower lobe is present as a sail behind the cardiac shadow.
 
 
 
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