Expert Review of Respiratory Medicine

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Current challenges in the recognition, prevention

and treatment of perioperative pulmonary
atelectasis

Ruben D Restrepo & Jane Braverman

To cite this article: Ruben D Restrepo & Jane Braverman (2015) Current challenges in the
recognition, prevention and treatment of perioperative pulmonary atelectasis, Expert Review of
Respiratory Medicine, 9:1, 97-107, DOI: 10.1586/17476348.2015.996134

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© 2014 The Author(s). Published by Taylor &

Francis

Published online: 26 Dec 2014.

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 Review

Current challenges in the

recognition, prevention and
treatment of perioperative
pulmonary atelectasis
Expert Rev. Respir. Med. 9(1), 97–107 (2015)

Ruben D Restrepo*1
and Jane Braverman2
1 group of patients previously deemed ineligible for surgery now undergo high-complexity
Department of Respiratory Care,
The University of Texas Health Science
Center at San Antonio, MSC 6248,
San Antonio, TX 78229, USA
2
187 Malcolm Avenue SE, Minneapolis,
MN 55414, USA
*Author for correspondence:
restrepor@uthscsa.edu
Innovations in surgery have significantly increased the number of procedures performed every
year. While more individuals benefit from better surgical techniques and technology, a larger
surgical procedures. Despite continuous improvements in the operating room and
post-operative care, post-operative pulmonary complications (PPCs) continue to pose a serious
threat to successful outcomes. PPCs are common, serious and costly. Growing awareness of
the impact of PPCs has led to intensified efforts to understand the underlying causes. Current
evidence demonstrates that a high proportion of PPCs are directly traceable to the
pre-operative risk for and perioperative development of atelectasis. The substantial costs and
losses associated with PPCs demand strategies to reduce their prevalence and impact.
Effective interventions will almost certainly produce cost savings that significantly offset
current economic and human resource expenditures. The purpose of this review is to describe
the most common challenges encountered in the recognition, prevention and management
of perioperative atelectasis. Expanding awareness and understanding of the role of atelectasis
as a cause of PPCs can reduce their prevalence, impact important clinical outcomes and
reduce the financial burden associated with treating these complications.

KEYWORDS: atelectasis . hyperinflation therapy . perioperative . pulmonary complication . pulmonary hygiene

that is clinically significant and adversely affects

The Problem
Atelectasis is a clinically important condition
that is often a precursor, contributor, or simply
part of other important, and often more severe,
post-operative pulmonary complications
(PPCs). These complications include, but are
not limited to, bronchial obstruction, aspiration
pneumonitis, interstitial and/or alveolar edema,
gas exchange abnormalities, pneumonia, acute
lung injury/respiratory failure, need for re-
intubation within 48 h, weaning failure, pleural
effusion, bronchospasm and pneumothorax [1–3].
Very simply defined, a post-operative pulmo-
nary complication is a pulmonary abnormality
that produces identifiable disease or dysfunction
the clinical course [4,5].
PPCs account for a substantial proportion of
prolonged hospitalizations, admissions to the
intensive care unit (ICU) and hospital re-admis-
sions, and are associated with increased morbid-
ity, mortality and healthcare expenditure [6–10].
They are considered the leading cause of death
and of hospital costs in both cardiothoracic and
non-cardiothoracic surgical procedures [11,12].
Reporting the prevalence of PPCs is compli-
cated because reporting decisions are influenced
by patient population, institutional criteria, sur-
gical site and the clinical treatment setting. For
example, milder abnormalities may resolve
quickly and tend not to be counted.

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informahealthcare.com 10.1586/17476348.2015.996134 Ó 2014 The Author(s). Published by Taylor & Francis ISSN 1747-6348 97
 Review Restrepo & Braverman
Figure 1. AP view of the chest of a patient scheduled for
an elective surgical procedure. The image shows no obvious
signs of parenchymal lung disease.
Figure courtesy of Carlos S Restrepo MD, Professor of Radiology
and Director, Cardio-Thoracic Radiology, The University of Texas
Health Science Center, San Antonio, TX, USA.
Interpretation of clinical studies yielding prevalence data is like-
wise complicated by lack of a uniform definition of qualifying
events. A combination of these factors may explain why preva-
lence statistics differ dramatically, ranging from 2 to 40% [2,6].
Imprecise data, notwithstanding, the impact of PPCs on patient
outcomes is sobering. Hospital length of stay has been consis-
tently reported to be increased by as much as 8 days together
with a 2- to 12-fold increase in associated healthcare expendi-
tures [13]. Among those adults who experience respiratory failure,
more than 26% die within 30 days [14]. Total expenditures
attributable to PPCs, including ICU care, pneumonia manage-
ment, respiratory therapy, intubation and mechanical ventilation
(MV), greatly exceed those of uncomplicated patients. A well-
powered study based upon 2002 data from a single private-sector
center comparing the hospital costs of post-surgical patients with
and without PPCs found that median charges for those with
such complications were US$62,704 (range US$27,959–
US$135,463) versus US$5015 (range US$4498–US$5686) for
those without any problems [6]. These figures do not include
therapeutic services and equipment. Dollar amounts have, of
course, increased substantially over the past decade, but have
likely remained relatively proportional. The cost of providing
MV for patients who need 24-h therapy was estimated in
2003 as US$1500/day [15]. Compelling data from a prospective
study of more than 100,000 Veterans Administration patients
underscores the importance of predicting and preventing
PPCs [16]. An analysis of survival following eight common surgi-
cal procedures found that the occurrence of a PPC (or other seri-
ous complications) within the first 30 post-operative days was
98
the single most important determinant of survival. Independent
of pre-operative patient risk and intraoperative factors, mortality
rates related to respiratory complications including pneumonia
and failure to wean from MV at 30 days, 1 year and 5 years
were 22, 45.9 and 71.4%, respectively. In sharp contrast, death
rates for cohorts without complications were 2, 8.7 and 41.1%
for the same intervals. These figures demonstrate dramatically
decreased longer-term survival among patients following dis-
charge after a PPC event. With understanding of the causes of
PPC, most are potentially preventable. It is impossible to over-
state the urgency of developing process improvement, best-
practice models and/or guidelines to maximize prevention of
these complications.
A preponderance of evidence implicates the occurrence of
perioperative atelectasis as a key element in the progression to
PPCs. Indeed, its presence appears to be a universal finding in
PPCs arising from a diverse array of intrinsic and extrinsic con-
tributing factors. Understanding atelectasis, recognizing its risk
factors and clinical consequences, and selecting the best therapeu-
tic approaches may significantly reduce prevalence and mitigate
the devastating human and economic costs of preventable PPCs.
Historical perspectives: focus on atelectasis
In the simplest terms, atelectasis is defined as a reversible alveolar
collapse typically resulting from obstruction of the airway serving
the affected alveoli. As a consequence, respiratory exchange of
carbon dioxide and oxygen is impaired [17–19]. For many decades,
surgeons have recognized that patients with previously healthy
lungs experience measurable respiratory compromise when
exposed to general anesthesia [20]. Routine observations include
reduced respiratory system compliance and impaired oxygen-
ation. In 1963, it was first suspected by Bendixen et al. that pro-
gressive alveolar collapse, or atelectasis, was the principle
cause [21]. Those investigators found that in anesthetized patients,
both lung compliance and the partial pressure of arterial oxygen
decreased in succession but could be quickly restored with lung
expansion maneuvers. However, owing to the limitations of con-
ventional radiology, it has been difficult to verify this concept
until the emergence of improved imaging techniques. Appropri-
ate technologies now include computed tomography, MRI, elec-
tric impedance tomography, ultrasonography and, most recently,
intravital microscopy [22,23]. With the implementation of these
methods, it has been shown that 90% of patients undergoing
general anesthesia demonstrate atelectasis in the most dependent
parts of the lung (FIGURES 1–3) [20,23,24]. It has been further shown
that anesthesia-induced atelectasis triggers a cascade of patho-
physiological events that may culminate in diffuse alveolar dam-
age, respiratory failure and, in extreme cases, death [5,20,24].
Etiology & pathogenesis of atelectasis
Atelectasis is a critical factor in the pathophysiology of a broad
range of PPCs. Virtually all patients undergoing major surgical
procedures develop some degree of atelectasis along with mea-
surable alterations in lung function and compromises in pul-
monary defense. As a rule, those changes are transitory and
Expert Rev. Respir. Med. 9(1), (2015)
 Current challenges in the recognition, prevention & treatment of perioperative pulmonary atelectasis
recovery is uneventful. However, subpopulations of patients are
significantly more likely to experience problems.
Although the etiology of atelectasis in the perioperative set-
ting has not been fully explained, three important ‘physiologic’
mechanisms have been found to cause or contribute to
its development. These include compression, alveolar gas
resorption and surfactant impairment [18,20,25]. These mecha-
nisms have been found to interact simultaneously in vivo and
are explained in detail below [20].
Compression
Mechanical compression of the alveoli is a characteristic effect of
general anesthesia that results when the forces that cause the
alveoli to collapse are exceeded by the transmural pressure that
maintains them in the open state [19,20,26]. In anaesthetized
patients, muscle relaxation displaces the diaphragm cephalad.
Pleural pressure is then increased in the dependent parts of the
lung, resulting in compression of adjacent lung tissue. Other fac-
tors that influence development of compression atelectasis
include chest geometry, regional diaphragmatic and respiratory
muscle changes, altered diaphragmatic dynamics and any condi-
tion with the potential to increase intra-abdominal pressures such
as a shift of central vascular blood into the abdomen [19,20,25,27].
Alveolar gas resorption
Alveolar gas resorption can occur in two ways. The first mecha-
nism involves the physics of oxygen tension in the presence of
supplemental oxygen. In the normal state, lung regions that have
low ventilation compared with perfusion have low alveolar oxy-
gen tension when the fraction of inspired oxygen is low. During
general anesthesia, when the fraction of inspired oxygen is
increased with the addition of supplemental oxygen, alveolar oxy-
gen tension (partial pressure of arterial oxygen) also rises. Accord-
ingly, the rate of gas transfer from the alveolus to the capillary is
increased and alveolar nitrogen tension decreases. With the loss
of inert nitrogen, corresponding increases in oxygen absorption
result in diminished alveolar volume [20,28]. The second mechanism
is activated in the presence of complete collapse of small airways.
In this circumstance, a pocket of gas is trapped in alveoli distal to
the obstruction. This pocket gradually collapses because oxygen
gas uptake by the mixed venous blood passing through the lung
capillaries continues as a result of the diffusion gradient [19,20,25].
Surfactant impairment
Pulmonary surfactant is a phospholipid that reduces alveolar sur-
face tension, thereby increasing alveolar stability and preventing
collapse. Anesthesia has been shown to depress the stabilizing
properties of surfactant. Repetitive opening and closing of the
alveoli during general anesthesia with MV leads to deactivation
and reduced availability of the surface active agent, producing an
increase in surface tension at the local level and an overall reduc-
tion in functional residual capacity (FRC) [20,29,30].
Other factors contributing to development of atelectasis
among surgical patients include disruption of normal respira-
tory muscle activity and loss of lung volumes.
informahealthcare.com
Review
Figure 2. AP view of the chest obtained on the second
post-operative day. The image shows effaced left hemidiaph-
ragm and dense left retrocardiac opacity consistent with left
lower lobe post-op atelectasis.
Radiograph courtesy of Carlos S Restrepo MD, Professor of Radiol-
ogy and Director, Cardio-Thoracic Radiology, The University of
Texas Health Science Center, San Antonio, TX, USA.
Diaphragmatic dysfunction
Diaphragmatic dysfunction plays a critical role in progression
to PPC. This is especially true in patients undergoing upper
abdominal and thoracic surgeries. For reasons unclear, signifi-
cant post-anesthesia impairment of diaphragmatic contraction
often persists for up to a week after surgery in some
patients [31]. Increased expiratory muscle activity also occurs
commonly both during anesthesia and post-operatively. Such
an activity produces a rapid decrease in end-expiratory lung
volume. Combined with reduced FRC, these mechanisms
intensify the severity of atelectasis [25,32].
Lung volume reduction
Lung volume reduction occurs in any surgical procedure involv-
ing general anesthesia. Placing the patient in a supine position
leads to a modest reduction of resting lung volume that signifi-
cantly worsens during induction of general anesthesia due to its
effect over FRC [5,33]. A single agent, ketamine, is an exception to
this rule since even the deeper level of anesthesia induced by this
agent does not affect FRC, ventilation distribution or minute
ventilation [34]. Post-surgical deficits in FRC and vital capacity
indicate the presence of a restrictive process. In some procedures,
these effects are considerable. Abdominal surgery patients lose a
great deal of inspiratory and expiratory reserve volume during
the first post-operative days, with a 40% reduction in FRC, total
lung capacity and forced expired volume in 1 s persisting for at
least 1 week post-operatively [31]. Results for coronary bypass
patients are similar [35]. Decreases in FRC lead to V/Q mismatch
and promote development of atelectasis and hypoxemia.
99
 Review Restrepo & Braverman
Figure 3. Chest tomographic axial image at the lung base
showing air space opacity in the left lower lobe consistent
with atelectasis.
Chest tomography courtesy of Carlos S Restrepo MD, Professor of
Radiology and Director, Cardio-Thoracic Radiology, The University
of Texas Health Science Center, San Antonio, TX, USA.
Recognition of patients at risk
Numerous risk-stratification and prediction models have been
developed to identify patients with increased risk for perioperative
atelectasis and PPCs. Several of these tools yield a numerical PPC
prediction score based upon multivariable logistic analysis of eval-
uated patient-specific intrinsic and extrinsic risk fac-
tors [1,2,11,12,36–42]. These variables are categorized broadly as
procedure and treatment-related factors and patient-related factors
(BOX 1). Among these systems, the Lawrence Risk Index, published
in 1996, offers the advantage of requiring neither spirometry nor
arterial blood gases [42]. With this tool, based upon a nested case
control study of 2291 patients undergoing elective abdominal sur-
gery between 1982 and 1991, highest-scoring patients are shown
Box 1. Risk factors for atelectasis.
. General anesthesia – type and duration
. Surgery – type and duration
. Underlying lung disease
. Underlying neuromuscular disease
. Chronic systemic disease or debility
. Obesity
. Age
. Airway mucus retention or mucus plugging
. Pleural effusion
. Prolonged bed rest (especially with limited position changes)
. Shallow breathing (result of pain and splinting)
100
to be at 5.8-times greater risk for PPCs than low-scoring individ-
uals [43]. However, in the Lawrence analysis of PPC events,
patients whose only pulmonary abnormality was microatelectasis
were excluded because it was considered clinically unimportant.
Occurrences of macroatelectasis were likewise excluded because at
that time, its clinical significance was unclear. Although assess-
ments of absolute and relative risk vary significantly depending
upon criteria particular to individual evaluation instruments, they
all seek to rank patients on the basis of a growing body of data
with the goal of implementing appropriate preventive and/or
therapeutic interventions [1,4]. To date, no definitive, widely appli-
cable instrument provides a simple and useful score for quantify-
ing risk for PPC. Currently, a large international multicenter
observational study addressing this problem is in progress. Desig-
nated by the acronym PERISCOPE, the study goals include
refining tools to predict PPCs and to more accurately track their
incidence among the general surgical population in Europe [44,45].
Outcome measures are a composite of in-hospital fatal and non-
fatal adverse respiratory events that include atelectasis.
Procedure/treatment-related risk factors
Procedure-related variables known to increase the risk for atel-
ectasis and PPCs include type of surgery, duration of operative
time, and type and duration of anesthesia [1,2,4]. The incidence
of PPCs after thoracic surgery is higher than that after abdomi-
nal or peripheral surgery [4]. Procedures associated with signifi-
cant risk include thoracic resections, coronary artery bypass
grafting, upper abdominal operations, head and neck proce-
dures, certain orthopedic procedures including joint replace-
ment and surgery for trauma. Treatment-related factors include
type and duration of anesthesia, use of certain medications
including immunosuppressive drugs and use of MV [4]. Physio-
logical and psychogenic influences, including treatment-related
altered breathing patterns, diaphragmatic weakness, splinting
and fear of pain may also contribute to PPCs [4,46].
Patient-related risk factors
Patient-related factors that influence PPCs risk include presence
of cardiovascular disease, chronic obstructive pulmonary disease
(COPD), neuromuscular/neuromotor disorders, renal failure,
malignancy and autoimmune disease [1,2,4,12,47,48]. Additional
factors include recent respiratory illness, traumatic injury, a his-
tory of tobacco smoking, obesity and age [4,41,49]. Among these,
COPD is the single most important risk factor for PPCs [50].
Likelihood of PPCs increases when high-complexity procedures
are performed in patients with pre-existing risk for complica-
tions [3,4,12]. These factors include symptomatic respiratory dis-
ease (abnormal chest examination, wheezing, coughing, sputum
production), current smoking, obesity and age. The effects of
smoking as a discrete variable independent of COPD are also
considerable. Smoking affects the lung at various loci including
the bronchi, bronchioles and the lung parenchyma [49]. The
effect of tobacco smoke in the larger airways (i.e., the bronchi)
alters both the structure and function of the bronchial mucus
glands. Exposure to smoke increases both the number and size
Expert Rev. Respir. Med. 9(1), (2015)
 Current challenges in the recognition, prevention & treatment of perioperative pulmonary atelectasis
of these mucus-secreting glands, resulting in the production
and deposition of excess mucus within the lumen of the airway.
In response to enlarged, hyperactive mucus glands, as well as to
the influx of inflammatory cells, the airway walls become thick-
ened. Correspondingly, the diameter of the airway lumen is
reduced and may more easily become congested or plugged
with mucus [51]. Atelectasis ensues.
Clinical implications of perioperative atelectasis
It is important to understand the harmful effects of atelectasis in
order to appreciate its impact on the post-operative clinical course.
Such knowledge is critical for identifying and implementing peri-
operative strategies to minimize PPC events. Even mild atelectasis
in surgical patients is associated with a variety of adverse effects
and, with progression, may trigger a cascade of serious, often fatal
complications. The consequences of atelectasis include, but are not
limited to, reduction in lung compliance, hypoxemia, increased
pulmonary vascular resistance (PVR), post-operative infection/
pneumonia and acute respiratory failure (ARF) [5,18,20,25,27].
Reduced lung compliance
The reduction in lung volume concomitant with exposure to
general anesthesia, surgical positioning and operative maneuvers
necessarily leads to an impairment of respiratory mechanics.
Respiratory cycles begin with a lower FRC and the energy con-
sumption is increased. The additive effects of atelectasis occur
in proportion to severity [20,25].
Hypoxemia
Under anesthesia, alveolar collapse leads to an intrapulmonary
shunt, V/Q mismatch and hypoxia [25]. Deterioration of oxy-
genation correlates with the amount of atelectasis. Likewise, the
amount of lung surface affected by atelectasis and the degree of
shunt correlate closely with the severity of hypoxia. Atelectasis
in the surgical context also contributes to hypoventilation,
hypovolemia, low cardiac output, anemia and alterations in the
V/Q ratio [52]. Post-operative hypoxemia is the main cause of
ARF and subsequent need for re-intubation and MV [53].
Increase in PVR
In healthy individuals, PVR is lowest when the lung volume is
equal to FRC [54]. In surgical patients with atelectasis, hypoxia
associated with the affected lung regions produces an increase
in local PVR. This increase in the vascular resistance is trig-
gered by the hypoxic pulmonary vasoconstriction activated
when partial pressure of arterial oxygen and venous mixed
blood are reduced and by the physical compression or kinking
of large pulmonary vessels. Deleterious effects include increased
pulmonary vascular pressure, right ventricular failure and
extravasation of fluid at the microvascular level [17,19,20,25].
Post-operative pneumonia
Atelectasis and infectious complications account for most
PPCs [13,24]. This combination of events is important since pneu-
monia and atelectasis are associated with a 30–50% increase in
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Review
risk for progression to ARF requiring MV [16]. Perioperative
changes in lung mechanics and breathing patterns weaken the
lung defense system, impairing both cough and mucociliary clear-
ance [4,55]. As a consequence, particulate matter, including patho-
gens, is retained, increasing the risk for pulmonary infection.
Although atelectasis is an established predisposing factor in the
development of PPCs, it has been difficult to demonstrate a
direct link between atelectasis and pneumonia per se in the clinical
setting. Experimental evidence, however, supports a significant
role in aggravating the course of such infections [20,25,29,30]. van
Kaam et al. showed in an animal model that creating surfactant
deficiency by whole lung lavage followed by intratracheal instilla-
tion of bacteria induced severe pneumonia with bacterial translo-
cation into the blood stream [56]. Control group animals had a
mortality rate of almost 80%. In contrast, in one of two experi-
mental groups, pre-treatment with exogenous surfactant before
instillation of streptococci attenuated both bacterial growth and
translocation and prevented clinical deterioration. A similar out-
come was achieved in a second group by reversing atelectasis in
lavaged animals via open lung ventilation. Results suggest that
minimizing the alveolar collapse by exogenous surfactant and
open lung ventilation may reduce the risk of pneumonia and sub-
sequent sepsis in post-surgical and/or ventilated patients.
Impaired penetration of antibiotics into lung tissue
The goal of antibiotic therapy in treating lung infections is to
achieve therapeutic levels of tissue penetration. Since the peri-
operative V/Q mismatch associated with atelectasis impedes the
distribution of antibiotics into the lung tissue, prophylactic
and/or therapeutic antibiotic therapy may not be as effective
for the treatment of respiratory infections and/or pneumo-
nia [57]. Therefore, strategies to reverse atelectasis and enhance
delivery of drugs to target lung regions are critically needed.
Atelectrauma due to acute respiratory distress syndrome
Acute respiratory distress syndrome is characterized by rapid-
onset bilateral pulmonary infiltrates and hypoxemia of non-
cardiac origin. Several pathophysiologic phenomena that
include volutrauma, barotrauma, biotrauma and atelectrauma
explain the complexity of acute respiratory distress syndrome.
In the post-surgical setting, the term atelectrauma is used to
characterize lung injury mechanisms triggered by atelectasis [58].
In both healthy and atelectatic lung regions, varying degrees of
pulmonary damage occur when there is repetitive opening and
closing of alveoli [26]. In the presence of atelectasis, damage is
proportional to the degree of involvement. The greater the
amount of tissue affected by atelectasis, the smaller the portion
of lung that must adapt to the tidal volume administered. As a
consequence, hyperinflation develops in healthy areas of the
lung [26]. Simultaneously, the protective effects of surfactant are
diminished by activation of the inflammatory response [59].
Acute respiratory failure
Among PPCs, ARF is the most life-threatening event and is
defined as a condition in which the gas exchange fails and
101
 Review Restrepo & Braverman
oxygen and carbon dioxide cannot be maintained within their
normal ranges due to worsening of the V/Q ratio. The degree of
deterioration of alveolar compliance and gas exchange is strongly
correlated to number of collapsed alveoli when atelectasis is pres-
ent. Atelectasis causes V/Q mismatch, which ultimately results in
compromise of gas exchange and may lead to respiratory fail-
ure [24]. In the post-surgical setting, when these patients require
positive pressure ventilation and develop ARF, the mortality is
high. One study showed that fatal outcomes in patients with
ARF after major abdominal surgery may range from 40 to 65%.
Survivors experienced 5- and 10-year mortality rates of 50 and
70%, respectively [60]. Another study found that median long-
term survival is reduced by 87% when ARF develops in the first
30 post-operative days [13]. As expected, ARF is associated with
prolonged ICU and hospital stays and high rates of ventilator-
associated pneumonia [11,24]
Pre- & peri-surgical risk management
On the basis of current understanding of factors that predispose
to PPCs, including those factors discussed in this paper that are
associated with an increased likelihood of developing atelectasis,
most surgical facilities implement strategies to reduce complica-
tions. Although a number of tests may be available to confirm
the diagnosis and severity of atelectasis, the clinical impression
and a plain radiograph are the only parameters used in most
cases. They also help to determine the therapeutic strategy and
the response to therapy. Additional tests that could be considered
for the diagnosis of atelectasis include high-resolution computed
tomography, MRI, lung ultrasound and pulmonary function
testing. Making use of the accumulated knowledge, several pro-
tocols and guidelines have been created to promote modification
of risk and to suggest rational interventions aimed at reducing
the prevalence of PPCs [2,7,12,36,39,41,42,61–63].
Pre-operative management
Using validated assessment tools, the medical history of surgical
candidates is evaluated for factors including pre-existing respira-
tory and/or systemic disease, smoking history, medication use
and other factors identified above. Testing for cough and deep
breathing is recommended since poor cough effort is a strong
predictor for atelectasis and other PPCs.
Preventive interventions
Active tobacco smokers have a significantly heightened risk for
PPCs. Smoking cessation 6–8 weeks before surgery has been
shown to be beneficial and is strongly encouraged [4,49]. Patients
with a chronic pulmonary disease may be prescribed increased
doses of bronchodilator therapy to reduce bronchial hyper-
reactivity and increased airway clearance therapy (ACT) to reduce
secretion retention and improve the airway patency [4,55,64,65].
Intraoperative management
Attention to anesthetic technique, ventilator management, fluid
monitoring, and surgical technique and duration is fundamental
to reduce the risk for atelectasis. The role of anesthesia in
102
development of atelectasis and subsequent PPCs is well-
recognized and an extensive body of literature is focused on sur-
veillance and management procedures [4,33,53]. Intraoperative secre-
tion management is critical in MV patients. This is achieved by
various methods that include adequate humidification of medical
gases and the physical removal of airway secretions via a suction
catheter [4]. Non-invasive, individually tailored respiratory support
may be an important adjunct in the intraoperative setting.
A recent meta-analysis of eight trials that included 1669 patients
testing the effect of lung-protective intraoperative ventilator set-
tings on the incidence of PPCs found statistically significant
reduction in the incidence of lung injury, pulmonary infection
and atelectasis in patients receiving intraoperative MV at lower
tidal volumes [66]. These findings are of high importance in light
of results of the largest multicenter, international randomized con-
trolled trial (RCT) to date investigating the effects of MV during
general anesthesia for open abdominal surgery [67]. In this study,
designated by the acronym ‘PROVHILO’, investigators hypothe-
sized that a high level of positive-end expiratory pressure (PEEP)
with recruitment maneuvers protects against PPCs in at-risk open
abdominal surgery patients receiving MV with low tidal volumes
during general anesthesia. The hypothesis was not confirmed.
Outcomes revealed high rates of PPCs among patients receiving
either higher or lesser amounts of PEEP. PPCs, which included
atelectasis as a discrete entity, were reported in 40% of
445 patients in the higher PEEP group versus 39% in the lower
PEEP group. Patients in the higher PEEP group developed intrao-
perative hypotension and required more vasoactive drugs. The
current recommended intraoperative protective strategy, consis-
tent with the results of the meta-analysis cited above, should
include a low tidal volume and low PEEP without
recruitment maneuvers.
Post-operative risk management: general
Post-surgical interventions to promote optimal recovery vary
significantly depending upon the type of surgery and individual
patient needs. Among these, adequate pain control and judi-
cious use of nasogastric tubes directly reduce the risk for devel-
opment of atelectasis and PPCs [62].
Pain control
Post-operative pain control is critical to PPC prevention. Pain
contributes to diminishing the lung volumes and restricts the
expansion of the lung by impairing the ability to perform deep
inspirations and cough effectively [5,43]. Patients in pain have
difficulty with mobilization and cooperating with lung expan-
sion maneuvers. Several studies have shown that patients receiv-
ing post-operative epidural anesthesia show reduced rates of
atelectasis and other PPCs [68,69]. In a recent meta-analysis,
Popping et al. evaluated 125 trials (9044 patients, 4525 received
epidural analgesia) [70]. The investigators found improvement
in a number of respiratory endpoints including a statistically
significant reduction in atelectasis in patients treated with epi-
dural analgesia compared to controls. In an RCT, patients
receiving epidural anesthesia after major elective surgery were
Expert Rev. Respir. Med. 9(1), (2015)
 Current challenges in the recognition, prevention & treatment of perioperative pulmonary atelectasis
compared to cohorts who received systemic analgesia (opioids).
The epidural anesthesia group experienced a significantly lower
rate of respiratory failure [71]. A recent meta-analysis of studies
comparing the use of epidural versus systemic anesthesia 24 h
or longer post-operatively found that epidural users demon-
strated reduced need for prolonged MV or re-intubation, better
pulmonary function and decreased rates of pneumonia [72]. Evi-
dence suggests that despite the critical importance of adequate
pain control, monitoring for opioid-induced respiratory depres-
sion with continuous pulse oximetry and capnography/or/
transcutaneous CO2 should be recommended in all individuals
under the effect of potent analgesics, particularly in those using
patient-controlled analgesia [72].
Nasogastric decompression
Nasogastric tube placement, previously used routinely after cer-
tain surgical procedures, is currently recommended only for
patients demonstrating the need for intestinal decompression.
Nasogastric tubes increase the risk for respiratory infection by
impairing cough reflex and providing a more direct pathway for
oro-pharyngeal bacteria to reach the lungs [3,62,73]. Selective use
has been shown to significantly reduce the rates of atelectasis and
pneumonia without increasing the risk for aspiration [2,73,74].
Post-operative risk management: respiratory care
Prophylactic respiratory care is provided routinely after major
surgery to minimize the adverse effects of surgical trauma and
anesthesia on the pulmonary system. As discussed above,
decreased lung volumes, atelectasis, altered breathing patterns,
diaphragmatic dysfunction and impaired mucociliary clearance
contribute significantly to the development of PPCs. A group
of therapeutic modalities known as ACTs have been developed
to promote lung expansion and secretion mobilization [4,55,65].
They are administered to improve lung volumes, strengthen
respiratory muscles, mobilize retained pulmonary secretions and
resolve atelectasis. ACT techniques/modalities include incentive
spirometry (IS), deep breathing exercises, chest physiotherapy
techniques, continuous positive pressure breathing, positive
expiratory pressure and airway oscillation therapies including
intrapulmonary percussive ventilation and oral high-frequency
oscillation techniques.
Lung expansion therapy
Lawrence et al. evaluated qualifying RCTs that focused upon
strategies to reduce atelectasis, pneumonia and respiratory fail-
ure after non-cardiothoracic surgery [62]. Their team then syn-
thesized outcomes data and ranked the ‘strength of evidence’
on a graduated scale. Among the modalities evaluated, lung
expansion techniques only received ‘A’ level grade. Data did
not permit preference of one technique over another and led
only to the conclusion that all lung expansion therapies reduced
PPCs by >50% compared with no treatment and that any
treatment was superior to no treatment. The Lawrence/Smetana
reviews currently serve as the basis for the most recent practice
guideline by the American College of Physicians [47].
informahealthcare.com
Review
A recent literature review of the scientific basis of post-
operative respiratory care modalities addresses the considerable
variation found in treatment protocols from institution to insti-
tution [4]. In addition, the review discusses the therapeutic
modalities in current use, appraises supporting evidence and
calls for multicenter studies to develop evidence-based standards
to optimize reduction of preventable PPCs. The generally poor
quality of clinical studies of chest physiotherapy, IS, continuous
positive pressure breathing and positive expiratory pressure
yield unreliable data, thus precluding definitive judgment. Con-
tinuous positive pressure breathing alone was associated with
comparatively strong evidence, particularly when used in high-
risk patients with hypoxemia. It cannot be overstated that
recruitment/expansion of atelectatic lungs is more easily accom-
plished when acute lung injury has not occurred [23].
Post-operative risk management: a multidisciplinary
approach
In a recent study, Cassidy et al. designed, implemented and
evaluated a multidisciplinary program. Designated by the acro-
nym ICOUGH (Incentive spirometry, Coughing and deep
breathing, Oral care – brushing teeth and using mouthwash
twice daily, Understanding – patient and family education,
Getting out of bed frequently – at least three-times daily and
Head-of-bed elevation), this multidisciplinary approach resulted
in a 38.5% reduction of post-operative pneumonia [75]. More
consistent lung expansion therapy encouraged by the use of IS
may have contributed to the overall reduction in PPCs, as a
25% increase in the use of IS was achieved during their study.
This result should be viewed with caution, however, as it has
been shown in other studies that IS as monotherapy has limited
impact on the reduction of post-operative atelectasis and its
routine use should be questioned [76]. It may be that coughing
and deep breathing and getting patients out of bed three-times
daily were equal or greater contributors to the reduction in
PPCs, particularly in light of the growing body of evidence
underscoring the importance of early mobilization. Findings in
the Cassidy study showed the ICOUGH intervention resulted
in an increase in the frequency that patients were out of bed
from 19% pre-treatment to 61% with treatment [76,77].
Makhabah et al. recently summarized the positive effects of peri-
operative physiotherapy to reduce PPCs [65]. These physiotherapy
techniques included early mobilization, respiratory muscle train-
ing, neuromuscular electrical stimulation, breathing exercises and
fast-track rehabilitation [65]. Early mobilization has been a focus of
nursing practice and has been associated with an overall reduction
in the length of stay and improved clinical outcomes, regardless of
the clinical area where the patient is managed [78]. Use of lung
expansion therapy is an intuitive approach to treatment with a
base of support in the literature. A meta-analysis by Lawrence et al.
reported that five RCTs support the use of IS, deep breathing exer-
cises and continuous positive airway pressure to reduce the overall
risk of PPCs [62]. Though the quality of the evidence is rated only
as fair, positive outcomes provide a rationale to consider lung
recruitment therapies to prevent or treat atelectasis [20,33,59,79].
103
 Review Restrepo & Braverman

Expert commentary therapeutic interventions persists. The level of scientific evi-

Atelectasis plays a substantial role in the development of PPCs.
Recognition of the mechanisms that lead to atelectasis and of
its role in triggering a cascade of events resulting in serious
PPCs is of critical importance if the goal of preventing or
reducing this serious problem is to be realized. Awareness of
risk for atelectasis is especially critical in patients with charac-
teristics that are recognized as strong predictors for PPCs. Sig-
nificant factors include advanced age, abnormal cough,
presence of significant systemic and/or pulmonary comorbid-
ities including COPD and/or obstructive sleep apnea, higher
American Society of Anesthesologists class and abnormal find-
ings on the chest examination. The number of clinical manifes-
tations and their intensity depends on the severity of atelectasis.
Patients may present with dyspnea, cough, intercostal retrac-
tions, nasal flaring, tachypnea and diaphoresis. If severe, the
physical exam of the chest may reveal decreased chest excursion
and either decreased breath sounds or the presence of fine
crackles that can clear after deep breathing or cough. Shifting
of the trachea and cardiac point of maximum impulse occurs
in severe cases of unilateral atelectasis where the pulling forces
are strong enough to cause ipsilateral deviations of adjacent
intrathoracic structures. Likewise, risk evaluation must consider
the site and duration of certain surgical procedures that place
patients at higher risk for atelectasis and other PPCs. The type
and expected duration of anesthesia must also be factored in.
Because clinicians have little control over many of the risk fac-
tors that contribute to perioperative atelectasis and subsequent
PPCs, they are challenged to identify effective strategies to min-
imize atelectasis that include lung expansion maneuvers and
ACT techniques. Despite ever-increasing understanding of the
mechanisms that lead to perioperative atelectasis, robust evi-
dence demonstrating the efficacy of particular prophylactic and
dence derived from RCTs supporting the use of lung expansion
and ACT, either alone or in combination, is inadequate. Cur-
rent recommendations for the use of interventional approaches
rely more on clinicians’ judgment, preference and experience
than on guidelines resulting from well-conducted clinical trials.
Best evidence suggests implementation of a ‘bundle’ approach
based on individual patient needs. Increased awareness of the
impact of perioperative atelectasis, as well as of the potential
usefulness of an array of modalities to minimize complications,
is of critical importance in order to identify and test therapeu-
tic approaches that strengthen clinical, quality-of-life and
economic outcomes.
Five-year view
As the American population ages, and with expanded access to
health insurance, the frequency and complexity of surgical pro-
cedures performed on higher-risk individuals will increase sig-
nificantly. High rates of morbidity, hospital re-admission and
complication-related mortality must be moderated or societal
costs will become unsustainable. We anticipate significant effort
over the next five years to identify and implement interventions
to prevent or moderate these adverse outcomes. An understand-
ing of the role of atelectasis as an underlying cause of PPCs is
fundamental to accomplish this goal.
Financial & competing interests disclosure
RD Restrepo and J Braverman are independent consultants for Hill-Rom.
The authors have no other relevant affiliations or financial involvement
with any organization or entity with a financial interest in or financial
conflict with the subject matter or materials discussed in the manuscript
apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.

Key issues
. Significant excess morbidity, mortality and healthcare costs are directly associated with post-operative pulmonary complications (PPCs).
The incidence of PPCs is increasing sharply in proportion to aging, with more medically complex population eligible for higher-risk
surgical procedures.
. PPCs are a multifactorial syndrome in which atelectasis plays a significant role. Evidence demonstrates that development of atelectasis is
a nearly universal precursor and concomitant feature of PPCs.
. The etiology of atelectasis in the perioperative setting has not been fully explained. However, three major ‘physiologic’ mechanisms –
compression, alveolar gas resorption and surfactant impairment – have been identified and are shown to interact simultaneously in vivo.
Diaphragmatic dysfunction and lung volume reduction also play a role.
. Prevention or aggressive early management of atelectasis is vital to optimally minimize progression to serious/life-threatening PPCs and
unsustainable economic expenditure.
. Pulmonary hygiene measures are provided as Standard of Care for surgical patients. However, the evidence base for a diverse array of
largely empirical management strategies that include airway clearance therapy and lung expansion maneuvers remains weak.
. Currently, best evidence suggests that a multifaceted or ‘bundle’ approach to mitigate PPCs yields best results. Understanding the
cause/s of atelectasis and incorporating interventions that directly moderate the physiological risks for or consequences of this pathology
will likely lead to development of more dependable, scientifically sound therapeutic protocols.
. Expanding awareness and understanding of the role of atelectasis as a cause of PPCs is a fundamental step toward minimizing
prevalence, improving clinical outcomes and reducing the financial burden of this potentially preventable complication.

104 Expert Rev. Respir. Med. 9(1), (2015)

 Current challenges in the recognition, prevention & treatment of perioperative pulmonary atelectasis
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