Pneumothorax in Patients With Acute

Respiratory Distress Syndrome:

Pathophysiology, Detection, and Treatment
Kenneth J. Woodside, MD*
Eric vanSonnenberg, MD†
Kenneth S. Chon, MD, ME†
David B. Loran, MD*
Irena M. Tocino, MD‡
Joseph B. Zwischenberger, MD*

The incidence of pneumothorax in patients on

Pneumothorax is a frequent and potentially fatal compli-
cation of mechanical ventilation in patients with acute res-
piratory distress syndrome (ARDS). Prompt recognition
and treatment of pneumothoraces is necessary to mini-
mize morbidity and mortality. The radiologic and clinical
signs of pneumothoraces in ARDS patients may have
unusual and subtle features. Furthermore, small pneu-
mothoraces in these patients can cause severe hemody-
namic or pulmonary compromise. Sparse clinical litera-
ture exists on when or how to treat pneumothoraces once
they develop in patients with ARDS. In this article, the
authors review the pathogenesis, radiologic signs, clinical
significance, and treatment of pneumothoraces in ARDS
patients. Treatment options include traditional tube thora-
costomy, open thoracotomy, and image-guided percuta-
neous catheters.
Key words: pneumothorax, adult respiratory distress syndrome,
thoracostomy, interventional radiology, radiologic catheters,
pneumothorax drainage
In mechanically ventilated patients with acute res-
piratory distress syndrome (ARDS), pneumothorax
is a frequent and life-threatening complication [1].
From the *Division of Cardiothoracic Surgery, Department of
Surgery, University of Texas Medical Branch, Galveston, TX; the
†
Department of Radiology, Dana-Farber Cancer Institute and
Brigham and Women's Hospital, Harvard Medical School,
Boston, MA; and the ‡Department of Radiology, Yale University
School of Medicine, New Haven, CT.
Received Jul 10, 1999, and in revised form Jul 29, 2002.
Accepted for publication Aug 1, 2002.
Address correspondence to Dr vanSonnenberg, Dana-Farber
Cancer Institute, Department of Radiology, 44 Binney Street,
Boston, MA 02115, or e-mail: evansonnenberg@partners.org.
Woodside KJ, vanSonnenberg E, Chon KS, Loran DB, Tocino IM,
Zwischenberger JB. Pneumothorax in patients with acute respi-
ratory distress syndrome: pathophysiology, detection, and treat-
ment. J Intensive Care Med 2003;18:9-20.
DOI: 10.1177/0885066602239120
mechanical ventilation is variable, ranging from 4%
to 15% [2]. In patients with underlying ARDS, the
incidence of pneumothorax is significantly higher
and is the most commonly encountered manifesta-
tion of pressure- (barotrauma) and volume-related
(volutrauma) lung trauma induced by mechanical
ventilation. Gammon et al [3] demonstrated an
overall incidence of pneumothorax of 14% in 139
mechanically ventilated patients, whereas a sub-
group of 29 ARDS patients had a 60% incidence of
pneumothorax. Other ARDS studies have reported
a 30% to 87% incidence of pneumothorax, depend-
ing on the severity and duration of ARDS, as well
as the mode of ventilator management [4].
Prompt recognition and treatment of pneumo-
thorax in mechanically ventilated patients with
ARDS is important, as there is a high risk of pro-
gression to tension pneumothorax [5,6]. Much of
the existing clinical literature on barotrauma
involves patients who are in the intensive care unit
(ICU) on mechanical ventilation for a variety of res-
piratory diseases, ranging from primary obstructive
lung disease (asthma or chronic obstructive pul-
monary disease) to various secondary lung diseases
such as aspiration pneumonia, necrotizing bacteri-
al pneumonia, and ARDS. Recent low-volume and
pressure-limited ventilator management strategies
have been advocated to minimize lung damage
and improve survival [7].
Pathophysiology
Many potential causes of pneumothorax exist in
patients on mechanical ventilation. For example,
attempts at central line placement or other invasive

Copyright © 2003
2002 Sage Publications 9
Woodside et al
procedures, such as bronchoscopy, may lead to
direct laceration of the visceral pleura. Necrotizing
bacterial pneumonias can cause air leaks into the
pleura, with development of pneumothorax. How-
ever, in ventilated patients, pressure and volume-
related alveolar rupture is the most frequent cause
of pneumothorax [8]. Any sudden increase in alve-
olar pressure may establish a gradient sufficient to
disrupt the alveolar walls [9,10].
Once mechanical ventilation establishes a suffi-
cient pressure gradient and the alveoli rupture, air
dissects along the loose connective tissues of the
bronchovascular bundle or the interlobular septa
medially toward the pulmonary hilum and periph-
erally toward the visceral pleura, where it accumu-
lates in the subpleural connective tissue and forms
subpleural air cysts. Rupture of the subpleural alve-
oli that cause pneumothorax often is preceded by
subpleural air cyst formation [11]. Because the
mediastinal pleura is not as thick and resistant as
the visceral pleura, air often dissects toward the
hilum. At the hilum, air can enter the mediastinum
and form a pneumomediastinum. The mediastinal
pleura subsequently can rupture, allowing air to
enter the pleural space and a pneumothorax to
form. This route is usually responsible for pneu-
mothoraces that accompany pulmonary interstitial
emphysema, rather than rupture of the peripheral
subpleural air cysts through the visceral pleura [9].
Gammon et al [3] found that mediastinal emphyse-
ma was the initial manifestation of barotrauma in
61% of ARDS patients, with subsequent pneumo-
thoraces developing in 42% of these patients with-
in 3 days. In addition, a continuum of fascial planes
connects the soft tissue compartments of the neck,
mediastinum, and retroperitoneum. Thus, mediasti-
nal air may decompress into the cervical soft tissue,
anterior chest wall, or other compartments, result-
ing in subcutaneous emphysema, pneumoretroperi-
toneum, or pneumoperitoneum [12].
Clinical studies of mechanically ventilated
patients have identified several risk factors for
baro- or volutrauma that are associated with the
development of a pneumothorax. These factors
include peak inspiratory pressures greater than 40
to 50 cm H2O [13], high positive end-expiratory
pressure (PEEP) values [3], high tidal volumes [14],
and high minute ventilations [3]. Several retrospec-
tive human studies demonstrated a correlation
between high peak airway pressures and the devel-
opment of pneumothoraces [2,15,16]. Human stud-
ies have not distinguished the effects of high peak
airway pressure versus lung overdistention, as
measuring lung volume directly in ventilated
patients is difficult [1,14].
10
In animal studies that have separated the effects
of pressure and volume, there is considerable evi-
dence to conclude that lung overdistention, rather
than high airway pressure, is the primary cause of
alveolar and interstitial injury [14,17,18]. High tidal
volumes cause lung injury even if obtained with
negative pressure ventilation [18]. Thus, volutrau-
ma, rather than barotrauma, is probably a more
appropriate label for this type of lung injury [19]. In
patients treated with positive pressure ventilation,
alveolar overdistention usually occurs during
increasing peak airway pressure. However, peak
airway pressures can be influenced by other factors
that do not affect or reflect alveolar volume [20].
Increased resistance in the ventilatory circuit or
bronchi or increased chest wall pressure can
increase peak airway pressure without increasing
transalveolar pressure or alveolar volume.
Alveolar rupture may be influenced by mechan-
ical ventilation, ventilation method, and underlying
lung pathology [8]. A wide range of preexisting
parenchymal diseases, ranging from primary lung
disease (asthma or chronic obstructive pulmonary
disease) to a variety of secondary lung diseases
(including aspiration pneumonia, necrotizing bac-
terial pneumonia, and ARDS), are known to
increase the risk of developing pneumothoraces
[1,21]. Pneumothoraces are rare in intubated
patients with normal lungs, but are common in
intubated patients with ARDS [8].
ARDS is a heterogeneous disease with a mixture
of both diseased and relatively normal alveoli [22].
The dependent lung regions (usually posterior and
basal) tend to be collapsed, and the nondependent
lung regions tend to be relatively open and may
have normal compliances [23]. The ARDS lung is
both stiff from interstitial edema and physiological-
ly small. During mechanical ventilation, PEEP
inflates and recruits some of the collapsed regions,
but also overinflates the more normal nondepen-
dent regions [24]. The lung regions most subject to
high-pressure overinflation and alveolar rupture
are the nondependent regions, with resulting air
tracking to the mediastinum and rupture through
the mediastinal parietal pleura [10,25]. Regional
pressure-related overdistention of healthy alveoli,
termed baro- or volutrauma, can result in a pattern
of diffuse alveolar damage that is histologically
indistinguishable from other causes of ARDS [26].
This volutrauma is a result of a tidal volume that
causes hyperexpansion of nonuniform lung dis-
ease. Nonuniform lung disease causes preferential
ventilation of normal alveoli that leads to overdis-
tention of normal alveoli, as they accommodate the
majority of the tidal volume.
Journal of Intensive Care Medicine 18(1); 2003

Subpleural and intrapulmonary air cysts occur in
ARDS patients [4]. Although some authors have
reported rupture of these air cysts as a cause of
pneumothorax [27], many suggest that such air
cysts are markers of barotrauma, with pneumo-
thoraces occurring more commonly from air track-
ing along the bronchi to the mediastinum [13].
Hence, whether the pneumothoraces seen in ARDS
arise from overinflation of more normal lung regions
or from pathologic processes such as cyst rupture
in collapsed dependent regions of the lung has not
been established conclusively [4]. Pneumothoraces
in ARDS also appear to be related to structural lung
changes that occur over a few weeks. Gattinoni et
al [4] found that late ARDS (> 2 weeks of mechan-
ical ventilation) patients had an increased inci-
dence of pneumothoraces when compared to early
ARDS (less than 1 week of mechanical ventilation)
patients (87% vs 30%), an increased number of bul-
lae, and decreased lung compliance.
Mechanical Ventilation Strategies
to Manage ARDS
Patients treated with volume-cycled or controlled
mechanical ventilation have a higher incidence of
barotrauma compared to patients treated with
pressure-limited or intermittent mandatory ventila-
tion (IMV) [8,28-31]. Gattinoni et al [23] also
observed that ARDS is a heterogeneous injury, with
areas of relatively normal lung interspersed with
areas of alveolar and interstitial edema. Exposure
of relatively normal alveoli with near-normal com-
pliance characteristics to high distending pressures
results in a larger delivered volume per lung unit,
marked overdistension, and the possible increased
risk of further lung injury [8,23,28-31]. This scenario
occurs regardless of which mode of ventilation
generates the high inspiratory pressure.
A ventilator management strategy aimed directly
at reducing airway pressures during ARDS to avoid
exacerbating volutrauma and the resulting endoge-
nous inflammation is the use of low-pressure, low-
volume ventilation [32-35]. The American College
of Chest Physicians Consensus Conference recom-
mended that under conditions of lung overdisten-
tion, airway pressures should be limited to reduce
tidal volumes, while accepting the increase in arte-
rial PCO2 levels [36]. Allowing blood PCO2 levels to
rise, with or without control of arterial blood pH, is
termed “permissive hypercapnia” [37]. Lower tidal
volumes of 5 to 8 mL/kg are used to prevent exces-
sive alveolar distention [32], whereas low levels of
PEEP and supplemental oxygen can improve
Journal of Intensive Care Medicine 18(1); 2003
Pneumothorax in ARDS
hypoxemia. Thus, even in diseased lung, ventilation/
perfusion match and arterial oxygenation can be
improved, independent of the reduced level of ven-
tilation required to excrete CO2 during hypercapnia.
Amato et al [33] compared “protective ventila-
tion” at 6 mL/kg tidal volume with “conventional
ventilation” at 12 mL/kg tidal volume in patients
with ARDS. Protective ventilation allowed 66% of
patients to be weaned from ventilators, compared
to 29% with conventional ventilation. Furthermore,
clinical barotrauma was 7% versus 42%, respective-
ly, and hospital mortality was 38% versus 71%,
respectively. Brower et al [38] recently published a
randomized trial that compared 2 ventilatory strate-
gies and their impact on mortality in ARDS. Like
other recent trials [33,34], this study demonstrated
that a mean plateau pressure of < 35 cm H2O is
associated with a very low incidence of barotrau-
ma. The impact of protective ventilation on patient
outcome needs additional clarification. Although
some studies report an improved outcome [33],
several randomized controlled studies did not
demonstrate significant beneficial effects [34,38,39].
The recent “NIH/NHLBI ARDS Network on
Ventilator Management of ALI and ARDS” low-tidal
volume study, a multicenter randomized controlled
trial comparing 6 versus 12 mL/kg tidal volume,
was terminated after 861 patients, as the outcome
of patients in the low-tidal volume group was
improved by approximately 25% [7]. The trial com-
pared traditional ventilation treatment that used an
initial tidal volume of 12 mL/kg of predicted body
weight and an airway plateau pressure of 50 cm of
H2O or less, with ventilation with lower tidal vol-
umes; the latter initial tidal volume was set at 6
mL/kg of predicted body weight and plateau pres-
sure was less than 30 cm of H2O. The trial was
stopped because mortality was reduced in the
group treated with lower tidal volume compared to
the group treated with traditional tidal volume
(31.0% vs 39.8%, P = .007), and the number of days
without ventilator use during the first 28 days after
randomization was greater in the former group
(112 ± 11 days vs 10 ± 1, P = .007). Likewise, the
American Thoracic Society International Consensus
Conference on ventilator-associated lung injury in
ARDS confirmed that ventilator-induced lung injury
is an important determinant of mortality in patients
with ARDS [7,40].
These studies and others have prompted the
development of new ventilator techniques and
modes, including pressure-controlled and inverse
ratio ventilation [41], high-frequency jet ventilation
[42], permissive hypercapnia [43], and more
advanced techniques that involve complete car-
11
Woodside et al
diopulmonary support such as extracorporeal
membrane oxygenation (ECMO) [44] and extracor-
poreal carbon dioxide removal with low-frequency
positive-pressure ventilation [45-47].
Presentation of Pneumothoraces in ARDS
Approximately 30% of pneumothoraces that occur
in critically ill ICU patients are missed either clini-
cally or on portable chest radiograph at initial pre-
sentation. The classic physical signs of a pneumo-
thorax, such as diminished breath sounds, decreased
chest wall excursion, and increased percussive res-
onance, can be difficult to detect in an ARDS
patient. The background noise of the ICU and the
ventilator may mask some of these clinical signs of
pneumothorax. Radiologically, the underlying lung
disease and the often compromised position of the
patient lead to atypical locations and appearances
of pneumothoraces [48,49]. One third to one half of
these pneumothoraces that are undiagnosed
progress to tension pneumothoraces [50]. Clinically
subtle pneumothoraces in mechanically ventilated
patients may present on chest radiograph or by an
unexplained deterioration in pulmonary function.
Worsening oxygenation, an increased peak inspira-
tory airway pressure, or a fall in lung compliance
may signal the development of a pneumothorax
that has affected pulmonary function but has not
yet become hemodynamically significant. Elevated
or altered tracings of pulmonary artery pressures
may be early indicators of pneumothoraces [51].
Tension pneumothorax can be rapidly fatal and
does not always have radiographic signs [52]. Most
commonly, the patient with tension pneumothorax
has a dramatic clinical presentation, with agitation,
respiratory distress, hypotension, tachycardia, and
hypoxia [5]. Changes in pulmonary mechanics, such
as increased airway resistance, decreased pulmonary
compliance, or auto-PEEPing, may occur [31]. Also,
ARDS patients may be hypoxic prior to pneumo-
thorax development; thus, hypoxia itself is not con-
sidered a pathognomonic manifestation [53]. Any
acute clinical deterioration in a ventilated patient
should prompt consideration of pneumothorax [5].
Pneumothoraces in neonates who require
mechanical ventilation can have significant effects
on mortality [54,55]. Because 5% to 22% of
neonates with respiratory distress syndrome have
air leaks, a high clinical suspicion must be main-
tained [56,57]. Advanced management techniques
such as inhaled nitric oxide or high-frequency
oscillatory ventilation have similar air leak rates
[58]. Neonates who require ECMO often present
12
only with the clinical triad of increased arterial oxy-
gen tension, decreased peripheral perfusion as evi-
denced by lower arterial pulse pressures and lower
mixed venous oxygen saturations, and decreased
ECMO flow with progressive hemodynamic deteri-
oration [59]. Because tension pneumothorax in
these patients can be rapidly fatal [60], immediate
intervention and high clinical suspicion are
required.
ARDS patients have a mortality rate between
16% and 91% [61]. In comparison, the development
of a pneumothorax in a critically ill patient is asso-
ciated with mortality rates between 66% and 77%
[4,6]. This overlap in mortality has resulted in some
authors reporting increased mortality [4] and some
authors reporting no change in mortality [61] in
ARDS patients with a concurrent pneumothorax.
Although the independent effect on mortality of a
pneumothorax in an ARDS patient may be nearly
impossible to address as an isolated variable,
untreated pneumothoraces in this patient popula-
tion have a high risk of progression to tension and
should be drained promptly [49].
Radiologic Presentation of
Pneumothoraces in ARDS
In intubated and critically ill patients, chest radi-
ographs frequently can be obtained only in the
supine or semirecumbent position [48,52]. Thus,
the more familiar radiographic signs of pneumo-
thoraces seen in erect films, such as visualization of
a thin, white visceral pleural line with no peripher-
al lung markings and a radiolucent space juxta-
posed to the chest wall, may be absent [52]. The
majority of pneumothoraces in supine ICU and
ARDS patients occur in anteromedial (paracardiac)
and subpulmonic locations (Figs 1, 2) [48]. In the
supine position, the anteromedial pleura is the least
dependent site, and air in this location often is the
earliest and most subtle radiographic sign of pneu-
mothorax. As the volume of air increases, radi-
ographic evidence of the pneumothorax is found in
the subpulmonic space and, eventually, in the
remainder of the pleural space [62]. In a study of
112 pneumothoraces in 88 supine ICU patients,
including 9 ARDS patients, the location and fre-
quencies of the pneumothoraces were as follows:
38% anteromedial, 26% subpulmonic, 22% apico-
lateral, 11% posteromedial, 2% inferior pulmonary
ligament, and 2% within pleural fissures [48]. In
several studies of ARDS patients, pneumothoraces
most commonly occurred in anteromedial or sub-
pulmonic locations [63,64].
Journal of Intensive Care Medicine 18(1); 2003
 Pneumothorax in ARDS

A B

C D

Fig 1. Large right anterobasilar pneumothorax in a trauma

E patient complicated by acute respiratory distress syndrome
(ARDS). Surgical chest tubes were unsuccessful; pneumothorax
was relieved by computed tomography-guided (CT-guided)
percutaneous catheter. (A) Chest radiograph demonstrates
large right basilar and medial left pneumothorax (open
arrow) in a patient with ARDS. Arrows on the right denote 2
surgical chest tubes in the right pleural space that were not
successful in relieving the pneumothorax. Closed arrows
point to the left surgical chest tubes as well. (B) CT scan:
open arrows point to the large right basilar pneumothorax.
The large arrowhead on the right points to a surgical chest
tube. Small arrows on the left denote left-sided pneumothorax.
The curved arrow on the left denotes another surgical chest
tube. Two smaller arrowheads on the right point to a 22-
gauge guide needle for percutaneous CT-guided needle
catheter placement. (C) CT-guided insertion site for 12 Fr
radiologic catheter. The small arrowhead points to the nee-
dle, whereas the 2 larger arrowheads note the catheter. (D)
The radiologic pigtail catheter is noted by the arrowhead.
The pneumothorax has been almost totally evacuated. (E)
The pigtail catheter is at the right base (arrowheads), with
resolution of the pneumothorax. The 4 surgical chest tubes
are still in place.

Journal of Intensive Care Medicine 18(1); 2003 13

Woodside et al

A B

Fig 2. Focal pneumothorax in a patient with postpneumonic acute respiratory distress syndrome treated by guided
catheter drainage. (A) Tracheostomy and nasogastric tubes are in place. A chest X-ray demonstrates lateral pneumothorax.
(B) A laterally and superiorly placed 7 Fr radiologic pigtail catheter has evacuated the pneumothorax. The catheter was
removed 4 days later.

An anteromedial pneumothorax can be recog-
nized by the abnormally sharp delineation of the
mediastinal structures, such as the great vessels or
heart, and by the lucency of the pneumothorax
[65]. If the anteromedial pneumothorax is large, the
affected hemithorax may be hyperlucent compared
to the opposite side. The most common radi-
ographic manifestation of subpulmonic pneumo-
thoraces is hyperlucency of the basilar lung or of the
upper quadrant of the abdomen [66]. Other signs
include the following: a deep costophrenic sulcus
outlined by a lucency that extends deep into the
costophrenic sulcus known as the deep sulcus sign,
a sharp diaphragmatic outline despite lower lung
parenchymal disease, visualization of both anterior
and posterior diaphragmatic sulci secondary to
depression of the anterior aspect of the hemidi-
aphragm that gives rise to the double diaphragm
sign, and visualization of the inferior vena cava or
an unusually distinct cardiac apex [65,66].
On a supine radiograph, visualization of an api-
colateral pneumothorax requires larger collections
of pleural air, and frequently is noted by the
appearance of pleural air in the anteromedial or
subpulmonic location [52]. In ARDS patients with
parenchymal and pleural disease, an apicolateral
pneumothorax may be an isolated loculated collec-
tion that does not result in the classic collapse of
the lung (Fig 2). Pleural lines may be obscured by
adjacent parenchymal disease. Pleural adhesions
and differences in compliance in ARDS lungs may
cause some segments of the lung to collapse,
whereas other segments appear normal or overin-
flated [64,67,68]. Hence, the presence of lung mark-
ings beyond the pleural line does not exclude
pneumothoraces in ARDS patients. In ARDS, a
pneumothorax can remain localized and loculated
from pleural adhesions or noncompliant lung
parenchyma that cannot collapse enough for air to
open the pleural space adequately for radiologic
detection [63].
The classic radiographic description of tension
pneumothorax includes near total lung collapse
with pleural air surrounding its edges, contralateral
shift of the heart and mediastinum, and inversion
of the hemidiaphragm. This triad seldom occurs in
ARDS patients with clinically evident tension pneu-
mothoraces. In tension pneumothorax, the degree
of collapse in the ipsilateral lung depends on its
stiffness and compressibility, and the mediastinal
shift depends on the ability of the contralateral lung
to decrease in volume. If the contralateral lung is
severely diseased and allows little mediastinal shift,
cardiac contour change alone will result. If the
lungs are sufficiently stiff or the tension is suffi-
ciently great, contour change or depression of the
diaphragm will result. There is often little volume
loss of the ipsilateral lung [49].
Loculated pneumothoraces may occur in the
presence of functioning ipsilateral chest tubes and
cause clinical tension pneumothorax that may lead
to hemodynamic instability and death. These pneu-

14 Journal of Intensive Care Medicine 18(1); 2003


A B
Fig 3. Pneumomediastinum in a patient with severe acute
respiratory distress syndrome. (A) Chest X-ray demon-
strates large lucencies accentuating the cardiomediastinal
silhouette (arrowheads). The superior arrows point later-
ally to surgical chest tubes in the pleural space. (B)
Supine computed tomography (CT) scan denotes the
pneumomediastinum collections bilaterally (arrowheads).
Note the severe parenchymal lung abnormalities. (C)
Chest X-ray demonstrates the bilateral CT-guided radio-
logic catheters (arrowheads) that have relieved the pneu-
momediastinum. There is a 10-Fr catheter on the left and
an 18-Fr catheter on the right.
mothoraces present with subtle shift of the medi-
astinum or flattening of the cardiac contour, along
with subtle flattening of the hemidiaphragm on
radiographs [49]. Mediastinal shift may be limited to
anterior structures, such as the anterior junction
line, or posterior ones, such as the azygoe-
sophageal recess, whereas the remainder of the
mediastinum remains unchanged [52]. Perhaps the
most specific sign of tension pneumothorax is the
flattening of the heart border and other vascular
structures, including the superior and inferior vena
cava [49,52].
Heffner et al [69] found that 16 of 47 pneumo-
thoraces (34%) in ventilated patients recurred
despite ipsilateral chest tubes. Recurrent pneu-
mothoraces occurred more commonly in patients
with ARDS (14 of 21 pneumothoraces) than in
patients without ARDS (2 of 26 pneumothoraces).
Pneumothorax recurrence appears to be related to
Journal of Intensive Care Medicine 18(1); 2003
Pneumothorax in ARDS
chest tube malpositioning into the interlobar fissure
or the posterior hemithorax visualized on chest
radiograph as horizontal chest tube placement. A
horizontally positioned chest tube on chest radi-
ograph has a high positive predictive value (86%)
for pneumothorax recurrence in ARDS patients.
Computed tomography (CT) scans can reveal
pneumothoraces not readily apparent on plain
chest films. Tagliabue et al [63] reported a series of
74 ARDS patients who underwent CT scans. Of
these scans, 66% yielded information that was not
available on chest radiographs. These scans detect-
ed ineffective positioning of thoracostomy tubes
that were attempting to drain loculated pneumo-
thoraces in 13 of 20 patients. Although one study
has reported no adverse effects from transportation
of ARDS or ICU patients to the CT scanner [63], there
is still a significant risk of moving a hemodynami-
cally compromised patient or a patient with poor
15
Woodside et al
oxygenation distant to immediate ICU care [53].
However, the potential diagnostic yield may war-
rant this risk. Studies to correlate risk, treatment
effects, and impact on outcomes are necessary to
address the issue of routine or frequent CT scans
for ICU patients. The reality of portable CT scan-
ners now offers a new option for these patients.
Treatment
Pneumothorax and some cases of pneumoperi-
cardium are life threatening and require prompt
treatment [61]. All other forms of extra-alveolar air,
such as intraparenchymal air cysts (parenchymal
cysts, bullae, pneumatoceles, or subpleural cysts),
pulmonary interstitial emphysema, subcutaneous
emphysema, and pneumomediastinum, rarely direct-
ly cause hemodynamic compromise. However,
these conditions are indicators of overdistension
and possible impending pneumothorax [51], as
extra-alveolar air in the pulmonary parenchyma
[27] or mediastinum [3] may track along the fascial
planes into the pleural space and lead to a hemo-
dynamically significant pneumothorax [51].
Virtually all authors agree that mechanically ven-
tilated patients with a pneumothorax require tube
thoracostomy placement, because of the high risk
of tension pneumothorax [70]. In critically ill
patients with minimal pulmonary reserve, even a
small pneumothorax can have adverse cardiopul-
monary effects [71]. Positive pressure ventilation
can exacerbate air leaks and prevent pleural heal-
ing, potentially causing a rapid increase in the size
and severity of existing pneumothoraces. Some
have suggested prophylactic chest tube placement
in mechanically ventilated patients for pneumome-
diastinum or subpleural air cysts in anticipation of
possible pneumothorax development [13]. Many
patients with nonpleural extra-alveolar air do not
develop pneumothoraces [3], so most authors pre-
fer careful monitoring and preparation for emer-
gent decompression [51]. Furthermore, pneumo-
thorax may occur or worsen despite the presence
of an ipsilateral chest tube [49].
Emergent Needle Decompression
Tension pneumothorax is a medical emergency. If
the diagnosis is made on a clinical basis, treatment
is initiated without delaying for radiographic
confirmation. Any tension pneumothorax should
have immediate large-bore needle decompression.
Although any hollow-bore device may be used, a
16
readily available large-bore angiocatheter is prefer-
entially inserted in the second intercostal space at
the midclavicular line. A rush of pleural air under
pressure confirms the diagnosis and location. After
decompression, the catheter is left in until a tube
thoracostomy has been placed [70].
Tube Thoracostomy
The traditional treatment for pneumothorax in
mechanically ventilated patients has been tube tho-
racostomy [70]. Chest tubes range in size from 6 to
40 Fr. Smaller chest tubes (6 to 24 Fr) are often
used in the pediatric population, although they are
also used for simple pneumothoraces in adults.
Larger chest tubes are used for fluid drainage, as in
patients with pleural effusions or empyemas. The
largest tubes (36 to 40 Fr) typically are used for
hemothoraces or empyemas. The most common
insertion site is the sixth intercostal space at the
anterior axillary line, which avoids the pectoralis
major and latissimus dorsi muscles, as well as the
breast tissue. In these locations, the tubes may be
easy to insert, as there is a relatively small amount
of subcutaneous fat. However, nonstandard place-
ment locations may be required if the lung is exten-
sively adhered to the pleura. Blind surgical chest
tube thoracostomy may traverse normal lung and
cause further injury or may miss the loculated
pneumothorax [64]. Furthermore, these patients are
poor candidates for video-assisted thoracostomy
for thoracostomy tube placement, since the need
for single-lung ventilation and general anesthesia
makes operative intervention more risky [72].
For the procedure, a sterile field is prepared and
local anesthesia is injected. A 2-cm incision is made
over the sixth rib. Using a hemostat, blunt dissec-
tion directly over the rib to the pleura is performed
and the parietal pleura is punctured by 1 cm only,
with extreme care taken not to puncture the lung.
A finger is inserted and swept in a gentle circular
motion along the inside of the chest wall to check
for adherent lung or entry into the parenchyma. The
chest tube is inserted and guided anteriorly and
apically, although posterior placement can be used
to drain associated pleural effusion. Because ARDS
patients often have pleural loculations, care must
be taken to avoid further lung damage. The chest
tube is sutured in place and anchored by tape, then
connected to a 3-chambered drainage device [70].
Alternate placement techniques have been used.
Bedside chest tube placement with a trocar has
been performed in the past, but there is a signifi-
cant risk of damage to the lungs, bronchi, or great
Journal of Intensive Care Medicine 18(1); 2003

vessels, and the technique is now regarded as dan-
gerous. Placement of small-bore percutaneous
catheters using the trocar or the Seldinger tech-
nique is becoming more popular for simple pneu-
mothoraces [73,74]. Because ARDS patients often
have effusions and loculations, blind placement of
thoracostomy tubes or percutaneous catheters in
this patient population is more difficult.
Typically, the chest tube is left to suction (−10 to
−20 cm H2O) until the air leak resolves. The chest
tube is then placed to water seal for a brief period
(6 to 24 hours), and a repeat chest radiograph is
obtained. If the lung remains fully expanded, the
chest tube is removed. A postremoval chest radi-
ograph is obtained, again to assess lung expansion
[75]. Recent clinical data in postoperative pul-
monary resection patients suggest that the negative
intrathoracic pressure caused by continuous suc-
tion, often set at −20 cm H2O, can promote, rather
than stop, air leak. Lower suction (eg, −10 cm H2O)
and early water seal placement may shorten air
leak time [76,77].
Image-Guided Chest Catheters
Recently, the concept of an image-guided small
catheter has evolved from its first description in
1970 to become an effective therapeutic option for
both iatrogenic and spontaneous pneumothoraces
[64]. These catheters are small bore, usually ranging
from 7 to 10 Fr, with multiple sideholes [78], and are
placed percutaneously by the trocar or the Seldinger
technique. It is possible to place larger catheters, from
20 to 30 Fr, or to upsize smaller catheters under
image-guidance to treat pneumothoraces, although
this is usually unnecessary [79]. Until recently, the
majority of reports on pneumothorax drainage with
these catheters have been for treating pneumo-
thoraces complicating transthoracic needle biopsies
and other percutaneous transthoracic procedures in
patients who were not on mechanical ventilation.
Nonetheless, empyemas and hemothorax have
been treated by image-guided catheters, sometimes
aided by catalytic agents [68,80-82].
Loculated pneumothoraces often are located in
areas difficult to access by the traditional tube tho-
racostomy [64]. In such cases, recent studies have
shown that image-guided catheters are effective in
draining these loculated pneumothoraces and obvi-
ating the need for surgical chest tubes or operative
interventions (Fig 1) [53,68,83].
In general, drainage of loculated pneumothoraces
in ventilated patients with underlying lung disease
requires longer duration than in patients without
Journal of Intensive Care Medicine 18(1); 2003
Pneumothorax in ARDS
lung disease [64]. In 2 recent studies of image-
guided catheter drainage of loculated pneumo-
thoraces in ventilated patients, the mean duration of
drainage was 11 and 12 days [64,68]significantly
longer than the 1 to 3 days usually required when
image-guided catheters are used to treat pneumo-
thoraces occurring in patients who are not on
mechanical ventilation [70].
The choice of image guidance is mainly deter-
mined by the location of the loculated pneumoth-
orax. Although easily accessible pneumothoraces
may be drained under fluoroscopy, most abnor-
mally positioned air collections require CT guid-
ance [64,74,82]. For nonloculated pneumothoraces,
the anterior approach through the second inter-
costal space at the midclavicular line is used. The
lateral approach through the third through eighth
intercostal space in the midaxillary line for women
may be used to avoid traversing breast tissue [83].
The anterior approach theoretically allows for eas-
ier positioning of the catheter tip in the lung apex,
where nonloculated pneumothoraces collect when
the patient is upright. However, in patients with
ARDS and adhesions leading to loculated pneu-
mothoraces, flexibility in determining the insertion
site of these catheters is essential. If CT guidance is
used, the entry site is localized using a grid system.
The patient may need to be scanned in an oblique,
decubitus, or even prone position to access the
optimal entry site [79].
The catheter can be placed under CT guidance
using the standard tandem trocar technique [83].
After sterile preparation of the selected entry site,
local anesthesia is achieved over the superior mar-
gin of the rib. A localizing needle is inserted into
the pneumothorax, and its position is confirmed by
aspiration of air and repeat CT scanning. For
catheters larger than 12 Fr, a tract through the sub-
cutaneous tissues should be made with serial dila-
tors or a hemostat to facilitate catheter passage over
the superior aspect of the rib. The catheter mount-
ed on the trocar is advanced toward the pleural
space, parallel to the localizing needle. Once
intrapleural position is confirmed by aspiration of
air or repeated imaging, the catheter is deployed
and positioned [84]. After insertion, management of
the image-guided catheter is similar to that of the
surgical chest tube. If the catheter kinks or mal-
functions, it can be manipulated under fluoroscopy
with guidewires, or the catheter can be replaced by
the exchange technique [83].
Pneumothorax, pneumomediastinum (Fig 3),
intraparenchyml cystic collections, or a combina-
tion may be treated by percutaneous radiologic
maneuvers. These procedures can be lifesaving.
17
Woodside et al
Operative Intervention
Surgical treatment of pneumothoraces in ARDS
patients is performed less often than in general tho-
racic surgery patients [72]. Although primary spon-
taneous pneumothorax usually resolves in 2 to 4
days of drainage, pneumothoraces in patients with
underlying lung disease often last substantially
longer [85,86]. Because chest tube drainage time
can be extended for pneumothoraces in ARDS
patients and the underlying lung disease may be
self-limited, adequate time for resolution must be
allowed [70]. Although data are limited, reports
examining the percutaneous drainage of pneu-
mothoraces in patients on positive-pressure venti-
lation and with ARDS [64,68] demonstrate a mean
of 11 to 14 days of drainage time. In addition, these
patients are often critically ill and unsuitable for
surgery [72].
Air leak etiology has some influence on the
need for operative intervention. Although an alve-
olar air leak may be allowed to seal on its own [87],
a high-output air leak from a bronchopleural fistu-
la is likely to require operative intervention,
through either traditional thoracotomy or a video-
assisted thoracoscopic approach. Although there
are few data on the operative mortality of ARDS
patients undergoing surgery, there is a study exam-
ining a relatively rare group of ARDS patients who
require extracorporeal carbon dioxide removal. In
this study, Wagner et al [72] found that a thoraco-
tomy performed for pneumothoraces increased
mortality. In this study, 19 patients underwent tho-
racotomy for a pneumothorax or pneumatocele,
with a 68% survival rate. Of the 50 patients who did
not require thoracotomy, there was a 44% survival
rate. Furthermore, they found that small, presum-
ably alveolar, air leaks closed as airway pressure
was reduced. Larger air leaks (> 2 L/min or > 26%
of the tidal volume) required intervention [72].
With either traditional thoracotomy or video-
assisted thoracic surgery, the goal is the sameto
identify and close the source of the air leak.
Pleurodesis can be performed with a sclerosing
agent such as tetracycline, fibrin glue, or even
autologous blood [88-90]. Talc has been effective in
the past, but it has been associated with increased
incidence of ARDS and is best avoided [91,92].
Although pleurodesis can be effective, air leaks
from ruptured bullae are best wedge resected or
stapled [93,94]. A chest tube typically is left in place
postoperatively and monitored for further air leaks
that may require intervention [87].
18
Conclusion
Prompt recognition and treatment of pneumo-
thorax in patients with ARDS is necessary to mini-
mize morbidity and mortality. Pneumothorax
detection requires a thorough familiarity with the
clinical signs and radiologic findings that can be
subtle or unusual. Patients on positive-pressure
ventilation with pneumothoraces require rapid
drainage, as there is a high risk of progression to
tension. Traditional treatment has been with tube
thoracostomy. Recent data suggest that there may
be a role for smaller, image-guided catheters for
draining loculated pneumothoraces located in sites
difficult to access with traditional chest tube place-
ment. Although there may be a prevailing notion
that these critically ill patients are poor operative
candidates, surgical thoracotomy should be consid-
ered when appropriate indications arise.
Acknowledgment
The authors thank Alexandra Friedman for assis-
tance with the manuscript.
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