Atelectasis

Kelly Grott; Julie D. Dunlap.

Author Information

Last Update: August 10, 2020.

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Introduction
The word "atelectasis" is Greek in origin; It is a combination of the Greek
words atelez (ateles) and ektasiz (ektasis) meaning "imperfect" and
"expansion" respectively. It results from the partial or complete, reversible
collapse of the small airways leading to an impaired exchange of CO2 and
O2 - i.e., intrapulmonary shunt. The incidence of atelectasis in patient's
undergoing general anesthesia is 90%.[1]
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Etiology
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.[2]
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 other words, there is a decreased transmural
pressure gradient (transmural pressure gradient = alveolar pressure -
intrapleural pressure) across the alveolus resulting in alveolar 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. Adhesive
atelectasis is often the result of a surfactant deficiency or dysfunction as
seen in ARDS or RDS in premature neonates. 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.e.,
intrathoracic tumor). The use of high inspiratory oxygen concentration
(high FiO2) during induction and maintenance of general anesthesia also
contributes to atelectasis via absorption atelectasis. Room air is 79%
nitrogen; nitrogen is slowly absorbed into the blood and therefore helps
maintain alveolar patency. 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.[3]
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.
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Epidemiology
Atelectasis does not preferentially affect either sex. There is also no
increased incidence of atelectasis in patients with COPD, asthma, or
increased age.[4] It is more common in patient's who recently underwent
general anesthesia, with the incidence being as high as 90% in this patient
population.[1] Research has shown that atelectasis appears in the
dependent regions of both lungs within five minutes of induction of
anesthesia.[5]  Atelectasis is more prominent after cardiac surgery with
cardio-pulmonary bypass than after other types of surgery, including
thoracotomies; however, patients undergoing abdominal and/or thoracic
procedures are at increased risk of developing atelectasis.[3] Obese and/or
pregnant patients are more likely to develop atelectasis due to cephalad
displacement of the diaphragm (see the section on epidemiology).  
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Pathophysiology
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.
The incidence of atelectasis in patient's undergoing general anesthesia is
90%.[1] Studies have demonstrated that up to 15 to 20% of the lung at its
base collapses during uneventful anesthesia before any surgical
intervention. 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.[6] The use of high inspiratory oxygen
concentration (high FiO2) during induction and maintenance of general
anesthesia also contributes to atelectasis via absorption 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.
Inadequate pain control can contribute to the development of atelectasis by
inducing shallow breathing ("splinting") and/or inhibiting coughing.
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History and Physical

Typically, atelectasis is asymptomatic. However, a patient might also
present with decreased or absent breath sounds, crackles, cough, sputum
production, dyspnea, tachypnea, and/or diminished chest expansion.
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Evaluation
Atelectasis is usually a clinical diagnosis in a patient with known risk
factors. If imaging is warranted, a chest X-ray, chest CT, and/or thoracic
ultrasonography are useful in the diagnosis of atelectasis. 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. 
On chest X-ray, atelectasis will result in the displacement of interlobar
fissures, pulmonary opacification, and/or tracheal shift toward the affected
side.[7]
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.e.,
tumor, mucous plug, or foreign body).
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. 
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Treatment / Management
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. When general anesthesia use is unavoidable, the use of
continuous positive airway pressure, the lowest possible FiO2 during
induction and maintenance, PEEP (positive end-expiratory pressure), lung
recruitment maneuvers, and low tidal volumes will help prevent the
development of atelectasis.[8] One study showed that intraoperative
alveolar recruitment with a vital capacity maneuver followed by PEEP 10
cm H2O is effective at preventing lung atelectasis in morbidly obese
patients; this also correlated with better oxygenation, shorter PACU stay,
and fewer pulmonary complications in the postoperative period.[9]
Changing position from supine to upright increases FRC and decreases
atelectasis.[10] Encouraging patients to take deep breaths, early
ambulation, incentive spirometry, use of an acapella device, chest
physiotherapy, tracheal suctioning (in intubated patients), and/or positive
pressure ventilation has been shown to decrease atelectasis. The
mechanism behind all of these measures is a transient increase in
transmural pressure that allows for reexpansion of collapsed lung
segments. Prophylactic measures, such as incentive spirometry, should be
taught and instituted before surgery and continued on an hourly basis
following surgery until discharge to obtain the maximal benefit.
Additional pharmacologic treatment options include mucolytic agents
(acetylcysteine) and recombinant human DNase (dornase alpha) in patients
with cystic fibrosis. The aforementioned nebulized medications are
particularly beneficial in patients with atelectasis secondary to mucous
plugging of the airways. 
Fiberoptic bronchoscopy also has a role in the management of atelectasis.
In one study single-suction, fiberoptic bronchoscopy led to improved lung
function and reversal of atelectasis in 76% of cases.  Bronchoscopy should
always be the intervention when there is a high suspicion for a
mechanically obstructed bronchus and coughing/suctioning have not been
successful. Bronchoscopy is also indicated when less invasive efforts, such
as early ambulation, incentive spirometry, bronchodilators, and humidity,
have not been successful within 24 hours of their initiation. 
Employing early preventative strategies and valuing prompt
recognition/diagnosis will not only improve patient outcomes, but it will
also significantly decrease cost.[11]
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Differential Diagnosis
The differential diagnosis of atelectasis should include the following:
 Neoplasm
 Pneumonia
 Pleural effusion
 Pulmonary embolism
 Foreign body
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Prognosis
For patients with atelectasis, the prognosis varies greatly, and the primary
determination is the underlying etiology and patient co-morbidities. 
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Complications
Atelectasis is one of the most common respiratory complications in the
perioperative period, and it may contribute to significant morbidity and
mortality, including the development of pneumonia and acute respiratory
failure. 
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Postoperative and Rehabilitation Care
Postoperative fever has historically been attributed to atelectasis, but there
is no evidence supporting the finding that atelectasis is a causative
mechanism for fever.[12]
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Deterrence and Patient Education

The definition of atelectasis is a partial collapse of the lung. It can cause
people to feel short of breath. It can be a consequence of several different
processes, most commonly when there is a poor inspiratory effort, an
obstruction blocking airflow into the lung, extra pressure exerted on the
outside of the lung, or deficient production or function of a specific protein
in the lung. Treatment aims at the underlying cause of the condition, but
mainly involves supportive measures, such as deep breathing exercises,
incentive spirometry, and supplemental O2. 
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Enhancing Healthcare Team Outcomes

Prevention of atelectasis is vital to improving patient outcomes in the
postoperative period. Despite employing these strategies, atelectasis is not
always preventable and, therefore, early recognition and treatment
are equally important. Ultimately, this will decrease the length of hospital
stay, cost, and improve patient outcomes.
Both prevention and treatment of atelectasis need to be an
interprofessional team effort. Physicians, and especially surgeons and
anesthesiologists, need to be aware of the role of anesthesia in atelectasis.
Nursing will be monitoring the patient both during and after the procedure.
In the event of medical management, the pharmacist can provide
recommendations on opioids and mucolytics. The nursing staff will be
administering these and can report to the physicians on the effectiveness of
therapy as well as any adverse events, which may lead to dose or agent
changes, or other interventions. The nursing staff should assist the
clinicians in the education of the patient and family in incentive spirometry
and other techniques to minimize risk. In summary, atelectasis
management needs to be an interprofessional team collaboration to
optimize patient outcomes. [Level V]
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Continuing Education / Review Questions
 Earn continuing education credits (CME/CE) on this topic.
 Access board review questions for this topic.
 Comment on this article.

Figure

post op atelectasis chest x-ray. Image courtesy S Bhimji MD

Figure

Post surgical atelectasis. Image courtesy Dr Chaigasame

Figure

Chest computed tomography showing extensive emphysema in the right

middle lobe and compressive atelectasis of the right upper lobe. Courtesy:
Humberto C. Sasieta , Francis C. Nichols , Ronald S. Kuzo , Jennifer M.
Boland , and James P. Utz .
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