British Journal of Anaesthesia, xxx (xxx): xxx (xxxx)

doi: 10.1016/j.bja.2020.03.005
Advance Access Publication Date: xxx
Editorial

EDITORIAL

Atelectasis during general anaesthesia for surgery: should we treat

atelectasis or the patient?
Marcelo Gama de Abreu1,*, Marcus J. Schultz2 and Paolo Pelosi3,4
1
Department of Anaesthesiology and Intensive Care Medicine, Pulmonary Engineering Group, University Hospital Carl
€ t Dresden, Dresden, Germany, 2Department of Intensive Care Medicine and
Gustav Carus, Technische Universita
Laboratory of Experimental Intensive Care and Anaesthesiology, Academic Medical Center, University of Amsterdam,
Amsterdam, the Netherlands, 3Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, Genoa,
Italy and 4San Martino Policlinico Hospital, IRCCS for Oncology and Neurosciences, Genoa, Italy

*Corresponding author. E-mail: mgabreu@ukdd.de

Keywords: age; atelectasis; computed tomography; general anaesthesia; obesity; positive end-expiratory pressure;
postoperative pulmonary complications

During general anaesthesia, several conditions that occur can
promote atelectasis. Induction of anaesthesia is usually con-
ducted with inspired oxygen fraction (FIO2) as high as 100%.
The main goal of this approach is to provide a safety margin
for apnoea whilst the anaesthetist places an artificial airway.
The increase in available oxygen reserves makes haemoglobin
oxygen saturation less likely to decrease to dangerous levels if
multiple attempts and longer times are required, or if intu-
bation fails. However, washout of lung nitrogen promotes
instability of perfused but poorly ventilated lung zones, which
will ultimately collapse. In addition, neuromuscular blocking
agents are usually required to enhance conditions for laryn-
goscopy and facilitate tracheal intubation. Paralysis of the
diaphragm leads to increased intra-pleural pressure in the
dorsalecaudal lung regions, further decreasing the
mechanical stability of those zones, which can also result in
alveolar collapse. Patients kept immobilised during surgery,
usually in supine position and for certain surgical
procedures in Trendelenburg position, expose the dependent
parts of lungs to prolonged higher pressure transmitted from
mediastinal and intra-abdominal structures. Such changes
are intensified with laparoscopic surgery. Thus, patients
undergoing surgery with general anaesthesia develop
atelectasis, and anaesthetists are particularly concerned
about older1 and obese2 patients.
In this issue of the British Journal of Anaesthesia, Heden-
stierna and colleagues3 report on the results of an analysis of
pooled CT data from patients undergoing general anaesthesia
with tracheal intubation and mechanical ventilation. Data
from 243 adult patients aged up to 78 yr with BMI in the range
of 18e52 kg m 2 were included. A single CT scan was per-
formed above the dome of the right hemidiaphragm at end-
expiration before and after induction of anaesthesia with
different post-intubation FIO2, all at zero PEEP. The key findings
were that atelectasis was seen in 90% of patients, with a peak
at age 50 yr (inverse U-shaped relationship), and increased up
to a BMI of 30 kg m 2, but not significantly beyond this in-
flection point. The authors concluded that high age and severe
obesity might limit atelectasis formation during general
anaesthesia. Notably, formation of atelectasis was heteroge-
neous across BMI categories, and hardly predictable by this
variable.
These results are intriguing, but not completely surprising,
and anaesthetists should be aware. A previous study by the
same group identified age-dependent deterioration of arterial
oxygenation during general anaesthesia.4 This deterioration
was explained primarily by increased intrapulmonary shunt,
but in older patients, also by ventilation/perfusion mis-
matching, whereas atelectasis was not significantly associated
with increased age.
It is possible that increased small airway closure at expi-
ration, but not inspiration, as typically seen in patients older
than 50 yr, might lead to delayed nitrogen washout and
explain why those patients are less prone to develop atelec-
tasis in the presence of higher FIO2.5 This phenomenon might
also explain the lack of increase in atelectasis in patients with
BMI over 30 kg m 2.
An important methodological limitation of the study by
Hedenstierna and colleagues3 is that atelectasis was assessed
in single CT scans and that results could be presented only as

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1
 2 - Editorial
surface area. In fact, surface and volume are poor surrogates of
atelectasis, as atelectatic tissue has higher tissue density than
non-atelectatic tissue. Data from the study suggest that all
patients developed a substantial degree of atelectasis, even if
not accompanied by hypoxaemia. Another limitation of this
study is that intraoperative ventilation was conducted with
relatively high tidal volumes and ventilatory frequencies. It is
worth noting that tidal volumes as high as 10.6 ml kg 1 of ideal
body weight were used, and ventilatory frequency showed a
weak association with atelectasis. High tidal volumes might
have contributed to a decrease in atelectasis formation, and
possibly an underestimation in patients with higher BMI.
Importantly, because of the retrospective nature of the study
and the fact that most of the data were collected before pro-
tective ventilation was adopted into the operating theatre, the
study could not give insight into the impact of atelectasis
formation on driving pressure, which has been associated
with the development of postoperative pulmonary
complications.6
The findings that the formation of atelectasis is heteroge-
neous and not easily predicted in older and obese patients are
relevant from a pathophysiological perspective. They suggest
that intraoperative ventilation settings to prevent or reverse
atelectasis might differ importantly between individual pa-
tients. The implications of the findings remain uncertain, and
additional factors must be considered before clinical practice
is changed. First, atelectasis is not necessarily associated with
intra- and postoperative hypoxaemia; it is well tolerated in
most patients, and settings may not need to be adjusted at all.
Second, loss of lung volume as a result of atelectasis might not
lead to increased plateau or driving pressure at lower levels of
PEEP if low tidal volumes are used. Third, more atelectasis
does not invariably require more PEEP than lower amounts of
atelectasis after opening the lungs. Lastly, PEEP always results
in a compromise between over-distension and atelectasis,
especially when titrated according to the mechanical proper-
ties of the respiratory system, for example compliance or
driving pressure. As volutrauma may be more injurious than
atelectrauma,7,8 optimal PEEP based on physiological end-
points is not necessarily optimal PEEP for lung damage.
When it comes to individualisation of PEEP settings,
anaesthetists must keep in mind that both the circulation and
the lungs play a role. Accordingly, the optimal PEEP for lung
stabilisation is possibly not the optimal PEEP haemodynami-
cally, and could lead to circulatory compromise in a given
patient. Thus, the choice of PEEP should not be based solely on
its potential to avoid atelectasis, but also on its impact on
cardiac preload.
Current evidence from large-scale international multi-
centre RCTs does not support the use of higher levels of PEEP
combined with recruitment manoeuvres to protect against
postoperative pulmonary complications in high-risk pop-
ulations,9 including obese patients.10 Moreover, individualised
titration of PEEP has not been shown to be effective in avoiding
postoperative atelectasis11 or clinical complications.12
In summary, the study by Hedenstierna and colleagues3
adds to the body of knowledge regarding the effects of gen-
eral anaesthesia on formation of intraoperative atelectasis in
populations at increased risk. This knowledge is relevant for
anaesthetists from a pathophysiological perspective, but
whether it will have implications for guiding intraoperative
ventilation management aimed at improving clinical out-
comes remains uncertain. In the end, we are treating the pa-
tient, not the atelectasis.
Authors’ contributions
Writing the paper: all authors.
Approval of final version: all authors.
Declarations of interest
MGA has received payments and travel funding of about V10
000 from GE Healthcare, Ambu, and Dra € ger Medical for
consultation and lectures in the field of mechanical ventila-
tion. MJS and PP declare no conflicts of interest.
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 Editorial - 3

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