Crit Care Nurs Q

Vol. 39, No. 2, pp. 176–189

Copyright c 2016 Wolters Kluwer Health, Inc. All rights reserved.

Acute Pneumothorax
Hammad Arshad, MD; Meilin Young, MD; Rajashekar Adurty, MD;
Anil C. Singh, MD, MPH, FCCP

Pneumothorax is defined as the abnormal presence of air within the pleural space (cavity) that
results in the partial or complete collapse of a lung. It can occur spontaneously or due to a
traumatic event. Symptoms can vary from a nondescriptive complaint of shortness of breath or
chest pain to complete cardiopulmonary collapse. Diagnosis is based on a combination of clinical
suspicion along with supporting imaging studies. Treatment often involves surgical or nonsurgi-
cal approaches with goal to alleviate symptoms and prevent recurrence. Key words: primary
spontaneous pneumothorax, secondary spontaneous pneumothorax, tension pneumothorax,
traumatic iatrogenic and noniatrogenic pneumothorax, tube thoracostomy

T HE TERM “pneumothorax” originally de-

scribed in the early 19th century refers
to the abnormal presence of air in the space
between the lung and the chest wall, the pleu-
ral cavity. The air subsequently produces an
external force, causing the lung to either par-
tially or completely collapse. It was first dis-
covered as a complication to tuberculosis in-
fection but then also found to be present in
healthy individuals. In the modern era, pneu-
mothoraces still remain a significant global
health problem with an annual incidence of
18 to 28/100 000 males and 1.2 to 6/100 000
women and have been a growing cause of
morbidity in the United States.1
Pneumothorax has been categorized on the
basis of its etiology. The causes of a pneumoth-
orax or “air leak” include spontaneous oc-
currence (primary or secondary), traumatic:
noniatrogenic with blunt or penetrating force
to the chest or iatrogenic from medical proce-
dures and catamenial. Despite the differences
in underlying etiology, the general symptoms,
diagnosis, and the decision-making process
of intervention remain relatively similar.
However, definitive surgical treatment is con-
sidered in selected individuals who may have
a high recurrence rate. With the improve-
ments and increased use of medical devices
for imaging and treatment, the detection and
management of pneumothorax continues to
become simpler. The incidence of pneumoth-
orax, though, continues to rise, either due to
the growing awareness of the condition as a
complication of known medical diseases or
as a result of medical treatment.
This article will discuss the pathophysiol-
ogy, etiology, epidemiology, signs and symp-
toms, diagnosis, management, and treatment
of a pneumothorax. Given the rarity of cata-
menial pneumothorax, it will only be briefly
discussed.

Author Affiliation: Department of Pulmonary and PATHOPHYSIOLOGY

Critical Care, Allegheny Health Network/Allegheny
General Hospital, Pittsburgh, Pennsylvania.
The pleural cavity is a negative pressure sys-
The authors have disclosed that they have no signif-
icant relationships with, or financial interest in, any
tem, where the pressure within the space
commercial companies pertaining to this article. is less than the normal atmospheric pres-
sure within the alveoli. Inspiration is consid-
Correspondence: Hammad Arshad, MD, Department
of Pulmonary and Critical Care, Allegheny Health Net- ered an active process, involving the contrac-
work/Allegheny General Hospital, 320 East North Ave, tion of the diaphragm, the expansion of the
Pittsburgh, PA 15212 (harshad@wpahs.org).
chest wall, and downward shift of the abdom-
DOI: 10.1097/CNQ.0000000000000110 inal contents. This creates a larger thoracic
176

Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.

volume and a negative pressure, allowing the
air to flow down the pressure gradient. The
lung tissue has intrinsic elastic recoil with a
tendency to collapse inward.2
In pneumothorax, air has entered the pleu-
ral cavity from either the lung or outside the
chest. The air then causes the pressure of the
pleural space to increase, creating the exter-
nal force that either partially or completely
collapses the lung. This results in regions of
low ventilation perfusion ratio and absent ven-
tilation (shunt) inside the lung. As a conse-
quence, the partial pressure of oxygen and
vital capacity decreases.3 The mechanism of
the air leak varies depending on the cause and
type of the pneumothorax, but many are at-
tributed to the formation and rupture of air
blebs and bullae in the lung.
ETIOLOGY
A pneumothorax can be classified as: spon-
taneous (either primary or secondary), trau-
matic (either noniatrogenic or iatrogenic),
and catamenial.
Spontaneous pneumothorax
A spontaneous pneumothorax affects
roughly 20 000 individuals a year in the
United States and account for an estimate of
$130 000 000 in health care expenses. It is fur-
ther categorized as primary and secondary.4,5
Primary spontaneous pneumothorax
Primary spontaneous pneumothorax (PSP)
occurs in the absence of lung disease and
could be seen in smokers without any struc-
tural lung disease. Anatomical abnormalities
such as apical blebs and bullae, however, have
been documented on computed tomographic
scans and during thoracoscopy even in the
absence of any underlying lung disorder in
90% of cases.6 Recent evidence has suggested
the concept of pleural porosity in which air
leaks from multiple pores on the visceral
surface. Histological biopsies of patient
with pneumothorax have shown an intense
inflammatory reaction in the small airways of
such individuals, indicating a potential role of
Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Acute Pneumothorax 177
small airway obstruction in the pathogenesis.
Pneumothorax is more common in tall men
as the gradient of negative pleural pressure
increases from lung base to the apex, and the
alveoli at lung apex are subject to significantly
greater distending pressure and development
of subpleural plebs. Smoking is another im-
portant risk factor with the risk of developing
pneumothorax being 12% in healthy smoking
men as compared with 0.1% in nonsmokers.7
Around 10% of individuals have a significant
family history. This has been linked to a
mutation in the FLCN gene (Birt-Hogg-Dube
syndrome) in addition to other hereditary dis-
orders (Marfan syndrome and Ehlers-Danlos
syndrome). Folliculin is thought to play a
pivotal role in repairing and reforming of lung
tissue after damage. The mutation results
in an abnormally short and nonfunctional
protein. An inflammatory response to this
protein results in the formation of small air
sacs (blebs) that can rupture and cause an air
leak into the pleural space.8,9 Other factors
that may predispose the development of PSP
include age, low body mass index and caloric
restriction, connective tissue abnormalities,
and anatomical irregularities of the bronchial
trees.
Secondary spontaneous pneumothorax
Secondary spontaneous pneumothoraces
occur as a complication of an underlying
pulmonary disease. Chronic obstructive pul-
monary disease (COPD) is the most common
underlying disorder in patients with sec-
ondary spontaneous pneumothorax (SSP) al-
though almost every lung disease has been
associated with SSP (Table 1). Among pa-
tients with COPD, the incidence of SSP
increases with the progressive increase in
the severity of the COPD. In the Veteran
Administrative Cooperative study, 27% of
229 patients had forced expiratory volume
in the first second of expiration/forced vi-
tal capacity (FEV1 /FVC) ratio below 0.40.10
The rate of recurrence of spontaneous sec-
ondary pneumothorax is also higher in pa-
tients with COPD/emphysema. Other im-
portant causes of secondary spontaneous
178 CRITICAL CARE NURSING QUARTERLY/APRIL–JUNE 2016
Table 1. Classification of Pneumothorax on the Basis of Etiology
Spontaneous Primary
Secondary
Traumatic Noniatrogenic
Iatrogenic
Catamenial
Abbreviations: CF, cystic fibrosis; COPD, chronic obstructive pulmonary disease; IPF, idiopathic pulmonary fibrosis;
PCP, pneumocystis pneumonia; RA, rheumatoid arthritis; TB, tuberculosis.
pneumothoraces include cystic fibrosis,11
Pneumocystis jirovecii infection in HIV,12
radiation and cystic lung diseases such as
Langerhans cell histiocytosis,13 and lymphan-
gioleiomyomatosis.
Traumatic pneumothorax
Noniatrogenic pneumothorax
A traumatic pneumothorax can result from
both blunt and a penetrating injury to the
chest. With penetrating chest trauma, the
wound allows air to enter the pleural space via
the chest wall or via the visceral pleura from
the tracheopleural tree. With blunt trauma,
the rib fracture is a common mechanism of vis-
ceral pleura laceration with subsequent pneu-
mothorax. However, in a significant number
of patients with pneumothorax due to non-
penetrating trauma, there is no associated rib
fracture. It is thought that the sudden chest
compression abruptly increases the alveolar
Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Anatomical abnormalities
Smoking
Increased height
Hereditary: Birt-Hogg-Dube syndrome
Marfan syndrome
Ehler-Danlos syndrome
Cutis laxa
Low body mass index and caloric restriction
Airway disease—COPD/emphysema, asthma, CF
Infectious—PCP (HIV), TB
Interstitial disease—IPF, sarcoidosis, histiocytosis X
Connective tissue disease—RA, scleroderma
Malignancy—lung cancer, sarcoma
Radiation and drug toxicity
Blunt force to the chest
Penetrating chest injury
Transthoracic or transbronchial biopsy
Central venous catheterization
Pleural biopsy
Thoracentesis
Feeding tube perforation
Mechanical ventilation
Women and within 48 h of menstrual period
pressure, causing alveolar rupture, and allow-
ing air to enter into the interstitial space.4
Iatrogenic pneumothorax
Iatrogenic pneumothoraces occur as a
complication of medical management and
invasive procedures. These procedures in-
clude transthoracic needle aspiration (most
common), transbronchial or pleural biopsy,
central venous catheterization of subclavian
or internal jugular vein, and thoracentesis.
Mechanical ventilation with high tidal vol-
umes and positive end-expiratory pressure
can cause barotrauma, which involves alve-
olar rupture from excessive pressure and
pneumothorax.14
Catamenial pneumothorax
Catamenial pneumothorax is unique to
women as it is a pneumothorax that occurs
1 day before and 3 days after menstruation.
The pathogenesis is not yet established but

is believed to be due to pleural endometrio-
sis implant or a defect in the diaphragm.
Women often present with respiratory com-
plaints within the first 48 hours of the onset
of menstrual period. Treatment is aimed at
ovulatory suppression.15
EPIDEMIOLOGY
Spontaneous pneumothorax: Primary
and secondary
The incidence of primary pneumothorax
is 7.4 per 100 000 population per year in
the United States and 37 per 100 000 popu-
lation per year in the United Kingdom.1 This
incidence is likely an underestimate as 10%
of patients with a spontaneous pneumoth-
orax are asymptomatic and do not gener-
ally seek active medical attention. Two-thirds
of patients with spontaneous pneumothorax
are between 20 and 40 years of age, with
the male/female ratio approximately being
5:1. There is a slight predominance of right-
sided over left-sided pneumothorax due to
increased lung volume and rarely does bi-
lateral spontaneous pneumothorax simultane-
ously occur. The risk of recurrence is as high
as 54% within 4 years, with isolated risk fac-
tors including smoking,7 height, and age more
than 60 years.
The incidence of SSP is similar to PSP;
however, secondary spontaneous pneumoth-
oraces occur more frequently in the later
years, that is, in the 60 to 65 years range. The
rate is also higher in men at 3:1 but not as
great as in primary pneumothorax. At an inci-
dence of 26 cases per 100 000, COPD is the
most common cause of SSP.4
Traumatic pneumothorax: Iatrogenic
and noniatrogenic
The current rate of iatrogenic pneumoth-
orax and noniatrogenic pneumothorax is
greater than the rate of occurrence of sponta-
neous pneumothorax and is continuing to in-
crease. This is attributed to the increasing use
of mechanical ventilators, placement of cen-
tral venous catheters, and other procedures
Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Acute Pneumothorax 179
that could cause an iatrogenic pneumothorax.
The estimated incidence of unpredicted iatro-
genic pneumothorax is 5 to 7 for every 10 000
hospital admissions. This causes a significant
increase of morbidity and length of stay.4
Catamenial pneumothorax
Largely underrecognized, catamenial pneu-
mothorax occurs roughly in 3% to 6% of all
pneumothoraces in women. Most cases are
right sided (87%); however, left-sided and bi-
lateral pneumothoraces have been reported.
Catamenial pneumothoraces tend to be recur-
rent, with an average of 5 pneumothoraces
occurring before the diagnosis is made.15
SYMPTOMS
The initial presentation and complaints con-
sistent with pneumothorax are nondescrip-
tive. The two most common symptoms con-
sist of sudden chest tightness or pain and
shortness of breath characterized by increas-
ing difficulty breathing. The chest pain has
an acute onset and is localized to the side of
pneumothorax while the shortness of breath
is generally present at rest. Other complaints
may include rapid heart rate, cough, and fa-
tigue. In secondary spontaneous pneumotho-
races, clinical symptoms are more severe due
to an already compromised lung function. The
skin may also become cyanotic as a result
of decreased blood oxygen concentration. A
rare complication of PSP is Horner syndrome,
which is thought to result from the traction
on the sympathetic ganglion by the shift of
the mediastinum.
DIAGNOSIS
Clinical manifestations
On examination, following signs of pneu-
mothorax are routinely noted (Table 2):
Tension pneumothorax is an acute condi-
tion that may cause cardiopulmonary collapse
with development of hypoxic respiratory fail-
ure and hypotension.
Patients on mechanical ventilator are noted
to have a sudden decrease in pulmonary
180 CRITICAL CARE NURSING QUARTERLY/APRIL–JUNE 2016
Table 2. Clinical Manifestations of a
Spontaneous Pneumothorax

Pulmonary findings
Respiratory distress
Tachypnea
Decreased or absent breath sounds
Hyperresonance to percussion
Decreased tactile fremitus
Asymmetric chest expansion (if severe and
causing tension pneumothorax)
Shift of trachea to the contralateral side
Cardiovascular findings
Tachycardia
Pulsus paradoxus
Hypotension Figure 1. Displacement of the pleural line (white
Jugular venous distention arrows) Lung margins are absent peripheral to the
Displacement of cardiac apex margin of pleural line.

a supine position, which makes the detection

compliance as noted by elevation in both
peak and plateau pressures on volume control
ventilation, or decreased tidal volume on pres-
sure control ventilation.
Imaging modalities
Chest radiography
The mainstay of imaging for the detection
of pneumothorax is an upright posteroan-
terior chest radiograph captured on inspira-
tion. The size of the pneumothorax is often
underestimated on a plain chest radiograph
because of its 2-dimensional imaging for a
3-dimensional structure. The displacement of
the pleural line is the diagnostic characteris-
tic of an image used to diagnose a pneumoth-
orax (Figure 1). This may be mistaken for a
skin fold when the patient is elderly and has
loose skin. The distinguishing factor is the
absence of lung markings consistent with a
pneumothorax, peripheral to the linear edge.
Radiographs obtained in expiration may make
the line easier to detect; however, evidence
shows that expiratory film does not improve
the detectability of a pneumothorax.16 Alter-
natively, a lateral decubitus chest radiograph
obtained with the suspected side upper can
prove to be helpful.17 Frequently in a hospital-
ized patient, chest radiograph is obtained in
of pneumothorax even more challenging. Rel-
ative hyperlucency overlying the diaphragm,
a deep and sometime lateral costophrenic sul-
cus (deep sulcus sign), increase in sharpness
of the cardiac borders, and visualization of the
inferior edge of the collapsed lung above the
diaphragm are all useful clues that can aid in
the diagnosis of a pneumothorax in patient
with supine chest radiograph.
Chest computed tomography
Computed tomographic (CT) scan is
regarded as the gold standard in the detec-
tion of pneumothoraces for uncertain or
complex cases (Figures 2A and B). Given
the 3-dimensional imaging capability, in
comparison with a standard radiograph, the
size of the pneumothorax can be more accu-
rately estimated by a CT scan and has been
widely incorporated in clinical trials.18 The
presence of underlying lung pathology, that
is, lung bullae, apical blebs, and cystic lung
disease can also be very accurately assessed.
In a review of pneumothoraces detected
incidentally on abdominal CT scan obtained
from trauma patient, Neff et al19 found that
a pneumothorax was present in 230 of 312
patients (74%) and 126 (55%) had not been
detected by plain radiography. However,

Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
 Acute Pneumothorax 181

published and reviewed to determine the ben-

efit of ultrasonography being the preferred
imaging to diagnose pneumothorax in com-
parison with chest radiography. Ultrasonogra-
phy has not only been proven to have a greater
sensitivity and equal specificity to chest ra-
diography in detecting pneumothorax, it has
been found,20 when readily available, to be
quicker with an average user time from setup
to detection being 2 to 7minutes.
On ultrasonography, the absence of 2 differ-
ent signs, the lung sliding sign and the comet-
tail sign, has a higher sensitivity and specificity
than radiography when combined. The inter-
face between the visceral and parietal pleura
produces a hyperechoic line termed the pleu-
ral line. In “the lung sliding sign,”21 the pleural
line produces a sliding motion during respira-
tion. In pneumothorax, the air obstructs the
visualization of the visceral pleura, thus the
lung sliding sign is absent on ultrasonography.
Artifacts from the pleural line with radiation
to the edge of the screen produce a “comet
tail artifact.”22 The absence of these artifacts
has been shown to be consistent with a pneu-
mothorax. For optimal detection, the pleural
interfaces should be evaluated at the second
to sixth intercostal space anteriorly and sixth
to eighth space in midaxillary line for the de-
tection of lung point (the point where lung
sliding becomes absent). Figure 3 shows the
Figure 2. (A) Decubitus position showing free air
in the pleural cavity at the apex. Incidental finding
of significant pleural effusion causing compression.
(B) Lateral imaging redemonstrating the free air in
the pleural cavity.

obtaining a CT scan for the initial diagnosis of

pneumothorax may not be practical, nor
efficient in a hemodynamically compromised
patient.

Ultrasonography: A better and more con-

venient alternative
The first document use of ultrasonography
to detect a pneumothorax was described in Figure 3. Lung ultrasonogram showing lung sliding
1986. Since then, multiple studies have been with a lung point (arrow).

Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
182 CRITICAL CARE NURSING QUARTERLY/APRIL–JUNE 2016
most accurate ultrasonographic sign for diag-
nosis of pneumothorax.
TREATMENT
There are 2 goals of managing a patient with
a pneumothorax:
r Evacuate the pleural space of the accumu-
lated air
r Decrease the likelihood of a recurrence
1. The treatment options for evacuation
of pneumothorax vary from observation
and supplemental oxygen to simple as-
piration or tube thoracostomy.
2. Recurrence prevention requires tube
thoracostomy with pleurodesis or tho-
racoscopy/thoracotomy for over sewing
of blebs plus pleurodesis.
While selecting treatment of any given pa-
tient, it should be remembered that PSP is
rarely a life-threatening event and a conserva-
tive approach is most often required. How-
ever, there are specific exceptions that need
to be applied if and when required. We shall
now discuss the management of PSP in de-
tail. Management of secondary pneumothorax
shall be referred to as necessary in the context
of this article.
EVACUATION OF PNEUMOTHORAX
Observation
Patients with no clinical manifestations of
shortness of breath or hypoxia and with small
pneumothoraces can be safely managed as an
outpatient provided they seek medical atten-
tion with clinical deterioration. In defining a
treatment strategy, the size of pneumothorax
is less important than the clinical symptoms
and hemodynamic stability as it does not cor-
relate well with the clinical manifestations.
Up to 80% of pneumothoraces estimated to
be smaller than 15% will have no persistent
air leak and recurrence when managed with
observation alone.23 Marked breathlessness
in a small PSP, however, may herald tension
pneumothorax. The symptoms are severe in
secondary pneumothorax as compared with
Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
their primary counterpart due to the under-
lying lung dysfunction. Hence, their clinical
evaluation takes further precedence in mak-
ing the decision.
Kircher and Swartzel24 estimated that 1.25%
of the volume of hemithorax is absorbed ev-
ery 24 hours. For a patient with a pneumoth-
orax that occupies 20% of the hemithorax, it
will take 16 days for the pleural air to be ab-
sorbed spontaneously. Using the cube func-
tion of the interpleural distance at the level
of the hilum, 2-cm radiographic pneumoth-
orax approximates 50% of lung collapse (as
per the equation of Light Index). The choice
of 2 cm to aspirate a pneumothorax is a com-
promise between the theoretical risk of nee-
dle trauma with a more shallow pneumoth-
orax and the significant volume and length
of time required for spontaneous resolution
of a greater depth of pneumothorax and has
been recommended by most guidelines.25,26
Recently, CT scan has shown to be more accu-
rate in calculating the degree of lung compro-
mise and is increasingly used to decide about
the management of pneumothorax.
Selected asymptomatic patients with large
PSP may be managed with observation in hos-
pital alone. They should be followed up as an
outpatient at the earliest opportunity (within
1 week) to ensure satisfactory resolution with
advise on smoking cessation and pertinent
lifestyle avoidance such as air travel, deep sea
diving, and strenuous exercise.
Oxygenation use
In pneumothorax, gases move in and out of
the pleural space from the capillaries in the
visceral and parietal pleura. The movement
of each gas depends on the gradient between
its parietal pressure in the capillaries and the
pleural space, the blood flow per unit surface
area available for gas exchange, and the sol-
ubility of the gas in the surrounding tissue.
If a patient is placed on 100% oxygen, the
partial pressure of all the gases in the capil-
laries falls precipitously (due to displacement
of nitrogen by O2 ), with increase in the gra-
dient of the gas absorbed and 4-fold increase
in the rate of pneumothorax resolved.27 This
 Acute Pneumothorax 183

has proved to be accurate in both clinical and
experimental trials.28 It is recommended that
hospitalized patients with any type of pneu-
mothorax who are not subject to aspiration
or tube thoracostomy be treated with supple-
mental oxygen at highest concentrations.
Needle aspiration versus chest drain
The initial treatment of patient with more
than 2-cm size of pneumothorax or breathless-
ness is simple aspiration (Figure 4). If success-
ful, simple aspiration avoids hospitalization
and there is far less pain from the smaller tube.
The recurrence rates appear to be similar
with large bore chest tube. Several small-sized
meta-analyses and randomized trials have con-
firmed the equivalence between the 2 meth-
ods and a reduction in the length of hospital
stay.29,30
In needle aspiration, a relatively small nee-
dle with internal polyethylene catheter is
inserted in the anterior midclavicular line.
An alternative site is selected if pneumotho-
rax is loculated or if adhesions are present.
The catheter (after needle removal) is sub-
sequently connected to a 3-way stop cock
catheter and air is manually withdrawn with a
60-mL syringe (Figure 5A). The process is re-
peated until no more can be aspirated. The
evacuation should cease after 2.5 L of air
has been aspirated, as further re-expansion is

Figure 4. General management of patient with spontaneous pneumothorax (exceptions to this: Patients
with minimal symptoms and remaining hemodynamic stable may be managed conservatively with close
monitoring).

Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
184 CRITICAL CARE NURSING QUARTERLY/APRIL–JUNE 2016
Figure 5. Thoracentesis needle with internal
polyethylene catheter attached to 3-way stop
catheter (yellow arrows). Eight and 10 French
chest drain catheters are indicated by the double
arrows.
unlikely, except if a persistence air leak is
suspected. If the chest radiograph confirms
that there is no recurrence, the catheter is re-
moved and the patient is discharged. Alterna-
tively, the patient can be observed overnight
or discharged with a Heimlich 1-way valve at-
tached to the catheter. There is no consensus
on clamping the catheter for 24 hours before
its evacuation.26
Small bore less than 14 F Seldinger chest
drains (Figure 5B) have become increasingly
common in clinical practice in present day.
Their effectiveness has been documented in
several clinical studies and has shown to have
similar success rate to larger drains.31 There
are no randomized clinical trials comparing
needle aspiration with small bore chest drains;
however, failure in approximately one-third
of patients with needle aspiration requires a
second procedure usually in the form of chest
tube placement. The attachment of Heimlich
valve facilitates mobilization and outpatient
care. British Thoracic Guidelines recommend
needle aspiration to be the first procedure of
choice whereas American College of Chest
Physicians has given more weightage to chest
tube drainage. In actual clinical practice, the
choice depends on the patient choice and op-
erator experience.25,26
Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
A persistent leak (after 48 hours) with-
out complete re-expansion of the lung is
the usual reason for the consideration of
the use of suction, although there is no ev-
idence for its routine use. A retrospective
review of 142 cases of spontaneous pneu-
mothorax found a median time to resolu-
tion of 8 days, which was not related to the
initial size of pneumothorax.32 A persistent
leak was observed in 43 cases, 30 of which
were treated with suction. Using this mech-
anism, the air removed from the pleural cav-
ity is at a higher rate than its accumulation,
which subsequently promotes healing by ap-
position of the visceral and parietal pleural lay-
ers. High-volume low pressure systems such
as wall suction with low pressure adaptors are
recommended and should be avoided during
the first 24 hours to prevent re-expansion pul-
monary edema. The incidence of re-expansion
pulmonary edema can be up to 14% (higher in
young patient with large PSP, which has been
present for more than few days) and proved
fatal in 20% of patient in 1 case series.33
Secondary spontaneous pneumothorax
Secondary spontaneous pneumothorax is
less likely to be tolerated by patients than
PSP with the air leak less likely to be settled
spontaneously. Although most of the manage-
ment algorithms (Figure 4) follow the same
sequence, there are few important modifica-
tions that need to be considered.
r Aspiration is less likely to be successful but
can be considered in very small pneumoth-
oraces in symptomatic patients.
r A small bore chest drain is indicated most of
the time (which is found to be as effective
as a large drain).34
r Every patient should be admitted for
24 hours with the use of O2 as indicated.
r Persistent air leak with non re-expansion
after 48 hours should be considered for sur-
gical intervention with pleurodesis.25
PREVENTION OF RECURRENCE
There is no evidence to indicate the ideal
timing for thoracic surgical intervention in

case of persistent air leak. Although a cutoff
of 5 to 7 days has been widely advocated in
the past, some experts recommend surgical
intervention as early as 3 days while other
evidence has showed 100% resolution of
primary pneumothorax by 14 days if managed
by tube drainage even for persistent air leak
of more than 7 days.35 Also, 79% of secondary
pneumothoraces and persistent air leak re-
solved by 14 days with no mortality in either
group.36 Although surgical procedure carries
low morbidity and lower recurrence rate,
each case should be assessed on an individual
basis and should take patient wishes into
consideration.37
Following are the indications of surgical re-
pair that have a general census:
1. Second ipsilateral pneumothorax
2. First contralateral pneumothorax
3. Synchronous bilateral spontaneous
pneumothorax
4. Spontaneous hemothorax
5. Persistent air leak (despite 5-7 days of
chest tube drainage) or failure of lung
re-expansion
6. Secondary spontaneous pneumothorax
with high risk of recurrence such as
COPD and cystic fibrosis
7. Professions at risk (pilots, divers), preg-
nancy
VATS versus Open thoracotomy
The 2 main objectives of the surgical re-
pair are (1) repair of a persistent air leak
from a pneumothorax and (2) prevention of a
recurrence.
The first objective is achieved by the resec-
tion of any visible bullae or bleb on the vis-
ceral pleura surface and by obliteration of any
emphysematous changes or pleural porosities
under the surface of the pleura through which
the air is leaking. The prevention of recur-
rence is attained by creating an opposition
between the 2 pleural surfaces. This can be
achieved by pleural abrasion or simply by per-
forming a pleurectomy and forming adhesion
between visceral pleura and chest wall. In
clinical practice, a combination of both pro-
cedures, that is, parietal pleurectomy with ex-
Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Acute Pneumothorax 185
cision of visible bullae and pleural abrasion is
performed via open or minithoracotomy ap-
proach with single lung ventilation. Although
the open surgical approach has the least risk
of recurrence, that is, 1% recent clinical trials
have shown VATS pleurectomy to be compa-
rable with open pleurecotomy for recurrence
in both PSP and SSP, with a shorter hospital
stay, analgesic requirement and postoperative
pulmonary dysfunction.38 The videoscopic
approach is more cost-effective and has a
slight increase in the risk of recurrence.37
Chemical pleurodesis via surgery versus
chest tube
A systemic review of nonrandomized trials
showed that 5 g of intrapleural talc via VATS
achieves a success rate of 87%.39 The advent
of well-tolerated VATS has led to less use of
surgical chemical pleurodesis with talc. In pa-
tients too unwell to undergo surgery or are
unwilling for a procedure, medical pleurode-
sis with a chest tube should be considered.
The instillation of a pleurodesis substance
into the pleural space leads to an aseptic in-
flammation with dense adhesions, leading to
pleural symphysis. Various substances used
in the management of malignant pleural effu-
sion have been tried in pneumothorax. Tetra-
cycline (doxycycline, minocycline) is rec-
ommended as the first-line sclerosing agent
for both primary and secondary pneumoth-
oraces, as it proved to be most effective in
animal model. Recently, it has fallen out of fa-
vor because of high rate of recurrence, that is,
10% to 20% and the availability of better surgi-
cal options40 ; however, higher doses of tetra-
cycline, that is, 1500 mg, with higher anal-
gesic dose of lidocaine (250 mg [25 mL] of 1%
lidocaine), have been recommended when-
ever used.10 Pleurodesis with graded talc is
an effective alternative to tetracycline and is
much preferred secondary to its effectiveness
in achieving a pleurodesis especially when
used with thoracoscopic procedure.39 Acute
respiratory distress syndrome and empyema
are well-known complications of talc that can
be avoided with the use of graded talc.
186 CRITICAL CARE NURSING QUARTERLY/APRIL–JUNE 2016

Secondary spontaneous pneumothorax regional (epidural) anesthesia should

The recurrence rate for SSP (45%) is higher be performed in pregnant patient with
than that for PSP (30%) if measures are not pneumothorax to prevent its propagation.
taken to prevent recurrence.10 In addition, In addition, minimally invasive VATS
deaths have been reported before a chest tube procedure after convalescence should
can be inserted in 3 out of 57 (5%)41 patients be performed to prevent recurrence of
with COPD and in 3 out of 15 (20%) with cys- pneumothorax in subsequent pregnancies.
tic fibrosis.42 The threshold for a surgical eval-
uation in these patients should, therefore, be PNEUMOTHORAX IN INTENSIVE CARE
low especially in the presence of risk factors UNIT
that predispose them to a recurrence such as
age, smoking, and apical bullae, and the pres- The following 3 clinical conditions relating
ence of severe underlying cardiorespiratory to a pneumothorax are frequently encoun-
compromise. Thoracoscopy is the preferred tered in an intensive care unit:
method of choice for pleurodesis; however, 1. Tension pneumothorax
chemical pleurodesis and thoracotomy can be 2. Traumatic iatrogenic pneumothorax
performed on the basis of nontolerance or in 3. Traumatic noniatrogenic pneumothorax
availability of a thoracoscope. Tension pneumothorax develops because
r In patients with COPD, the median time of a 1-way valve at the site of breach in the
of lung expansion is 5 days. After 7 days pleural membrane, permitting air to enter the
of tube thoracostomy drainage, the lung pleural cavity during inspiration but prevent-
remains unexpanded or the air leak per- ing the egress during expiration (Figure 6).
sists in about 20% of patients.41 Such pa- The consequent increase in the intrapleural
tients should be considered for surgical pressure exceeds the atmospheric pressure
evaluation. for much of the respiratory cycle and leads
r Pneumocystis jiroveci pneumonia P to an impairment of venous return and de-
jirovecii has been considered the main crease in cardiac output, resulting in typi-
etiological agent of pneumothorax in cal features of hypoxemia and hemodynamic
HIV patients. The administration of pen-
tamidine is an independent risk factor.
Up to 40% of patients develop bilateral
pneumothorax,43 and treatment failure
with prolonged chest drainage is fairly
common. Prevention strategies should be
adopted in these patients after the first
pneumothorax, that is, thoracoscopy and
pleurodesis.
r The same principles of management apply
to patient with cystic fibrosis and tubercu-
losis, with pneumothorax portraying a poor
prognosis with high degrees of recurrence.
Patient should be treated for the under-
lying infection, with earlier consideration
of thoracoscopic prevention. Thoracotomy
should not be performed until the patient
has received antituberculous chemother-
apy for 6 weeks. Figure 6. Tension pneumothorax (with medi-
r Elected assisted delivery (forceps or ven- astinal shift) in patient receiving noninvasive
touse extraction) at or near term with ventilation.

Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.

compromise.44 Most patients who develop
tension pneumothorax are receiving positive
pressure to their airways during mechani-
cal (invasive and noninvasive) ventilation or
during resuscitation. Being a medical emer-
gency, the diagnosis should be made swiftly
using clinical examination and not wasting
valuable time obtaining a chest radiograph.
The availability of bedside ultrasonography
may also quickly help in confirming pneu-
mothorax. The patient should be given high-
concentration O2 with emergency needle de-
compression in the second intercostal space.
A formal chest tube should also be placed
subsequently.44
Traumatic pneumothorax results from
either penetrating or nonpenetrating trauma
and its incidence depends on the severity of
the trauma endured. The incidence of pneu-
mothorax has exceeded 35% in some series.45
Iatrogenic pneumothorax on the contrary has
been shown to be even more common than
spontaneous pneumothorax.46 The most
common procedures being transthoracic nee-
dle aspiration (24%), subclavian vein puncture
(22%), thoracentesis (22%), and mechanical
ventilation (7%), all of which are frequently
performed in the intensive care unit.46 The
diagnostic and management principals of
a traumatic pneumothorax are similar to
spontaneous pneumothorax. A chest tube
drainage, however, is required in all patients
on mechanical ventilation to decrease the risk
of tension pneumothorax. The risk of recur-
rence is low in both circumstances; however,
immediate thoracotomy is indicated for 2
uncommon traumatic pneumothoraces: (1)
tracheal or major bronchus tear47 (which
REFERENCES
1. Light RW. Pleural Diseases. 6th ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2013.
2. Nunn JF. Elastic Forces and Lung Volumes. In: Applied
Respiratory Physiology. London: Butterworth & Co;
1989:23-45.
3. Noppen M, De Keukeleire T. Pneumothorax. Respi-
ration. 2008;76(2):121.
Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Acute Pneumothorax 187
usually occurs in the presence of anterior
or lateral fracture of 1 or more of first 3
ribs) and (2) pneumothorax with esophageal
rupture.
CONCLUDING REMARKS
Pneumothorax is a common clinical entity
that is encountered by critical care profes-
sionals frequently in everyday practice. An al-
gorithmic approach will help improve clinical
decisions and avoid unnecessary invasive pro-
cedures. Current advances in medical technol-
ogy and treatment have made early detection
and management of pneumothorax with
avoidance of complications. This has greatly
affected the overall morbidity and length of
hospital stay in patients with this condition.
Although spontaneous pneumothorax is
frequently noted on imaging studies with no
life-threatening complication, this is not so
true in the critical care settings. The high
prevalence of patient on mechanical ventila-
tion that requires a thoracic procedure makes
the incidence of tension pneumothorax very
significant. A very high clinical index of sus-
picion is required as the routine radiological
imaging is far from accurate in diagnosing this
medical emergency in a timely manner. Ultra-
sound machines that are now readily available
and more efficient than a radiograph in detec-
tion and initiating the appropriate treatment
step should be more widely incorporated in
the management algorithm of pneumotho-
races in all the intensive care units. Finally,
preventing recurrence of a pneumothorax is
equally important to decrease morbidity and
readmissions to the hospital.
4. Sahn SA, Heffner JE. Spontaneous pneumothorax.
N Engl J Med. 2000;342:868.
5. Daley BJ, Bascom R, Bhimji S, Alam S, Benninghoff
M, Mancini M. Pneumothorax. Medscape. 2015.
http://emedicine.medscape.com/article/424547-
overview. Published 2015. Accessed January 21,
2016.
188 CRITICAL CARE NURSING QUARTERLY/APRIL–JUNE 2016
6. Lesur O, Delorme N, Frogamet JM, et al. Com-
puted tomography in the aetiological assessment
of idiopathic spontaneous pneumothorax. Chest.
1990;98:341-347.
7. Bense L, Eklund G, Odont D, et al. Smoking and the
increased risk of contracting pneumothorax. Chest.
1987;92:1009-1012.
8. Graham RB, Nolasco M, Peterlin B, Garcia CK. Non-
sense mutations in folliculin presenting as isolated
familial spontaneous pneumothorax in adults. Am J
Respir Crit Care Med. 2005;172:39-44.
9. Gunji Y, Akiyoshi T, Sato T, Kurihara M, Tominaga S,
Takahashi K. Mutations of the Birt Hogg Dube gene
in patients with multiple lung cysts and recurrent
pneumothorax. J Med Genet. 2007;44(9):588-593.
10. Light RW, Hara O, Moritz VS, et al. Intrapleural tetra-
cycline for the prevention of recurrent spontaneous
pneumothorax: results of a department of VA coop-
eration study. JAMA. 1990;264:2224-2230.
11. Flume PA, Strange C, Ye X, et al. Pneumothorax in
cystic fibrosis. Chest. 2005;128:720-728.
12. Afessa B. Pleural effusion and pneumothorax in hos-
pitalized patients with HIV infection: the pulmonary
complications, ICU support and prognostic factors
of hospitalized patients with HIV (PIP) study. Chest.
2000;117:1031-1037.
13. Mendez JL, Nadrous HF, Vassallo R, et al. Pneumotho-
rax in pulmonary Langerhans cell histiocytosis. Chest.
2004;125:1028-1032.
14. de Lassence A, Timsit JF, Tafflet M, et al. Pneu-
mothorax in the intensive care unit: incidence, risk
factors, and outcome. Anesthesiology. 2006;104(1):
5-13.
15. Korom S, Canyurt H, Missbach A, et al. Catamenial
pneumothorax revisited: clinical approach and sys-
tematic review of the literature. J Thorac Cardiovasc
Surg. 2004;128(4):502-508.
16. Schramel FM, Golding RP, Haakman CD, et al. Expi-
ratory chest radiographs do not improve the visibility
of small apical pneumothorax by Enhanced Contrast.
Eur Respir J. 1996;9:406-409.
17. Beres RA, Goodman LR. Pneumothorax: detection
with upright versus decubitus radiography. Radiol-
ogy. 1993;186:19-22.
18. Kelly AM, Loy J, Tsang AYL, et al. Estimating the rate of
lung re-expansion of a spontaneous pneumothorax by
a formula derived from CT volumetry studies. Emerg
Med J. 2006;23:780-782.
19. Neff MA, Monk JS Jr, Peters K, et al. Detection of oc-
cult pneumothoraces on abdominal CT scan in trauma
patients. J Trauma. 2000;49:281-285.
20. Wilkerson RG, Stone MB. Sensitivity of bedside ultra-
sound and supine anteroposterior chest radiographs
for the identification of pneumothorax after blunt
trauma. Acad Emerg Med. 2010;17(1):11-17.
21. Alrajhi K, Woo M, Vaillancourt C. Test characteris-
tics of ultrasonography for the detection of pneu-
mothorax: a systemic review and meta-analysis. Chest.
2012;141:703-708.
Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
22. Lichtenstein D, Meziere G, Biderman P, Gepner A.
The comet-tail artifact: an ultrasound sign ruling out
pneumothorax. Intensive Care Med. 1999;25(4):383-
388.
23. O Rourke JP, Yee ES. Civilian spontaneous pneumoth-
orax: treatment options and long term results. Chest.
1989;96:1302-1306.
24. Kircher LTJ, Swartzel RL. Spontaneous pneumotho-
rax and its treatment. JAMA. 1954;155:24-29.
25. MacDuff A, Arnold A, Harvey J. Management of
spontaneous pneumothorax: British Thoracic Soci-
ety Pleural Disease Guideline 2010. Thorax. 2010;65
(suppl 2):ii18-31.
26. Baumann M, Strange C, Heffner J, et al. Manage-
ment of Spontaneous Pneumothorax: an American
College of Chest Physicians Delphi consensus state-
ment. Chest. 2001;119(2):590-602.
27. Northfield TC. Oxygen therapy for spontaneous
pneumothorax. Br Med J. 1971;4:86-88.
28. Chernick V, Avery ME. Spontaneous alveolar rupture
at birth. Pediatrics. 1963;32:816-824.
29. Zehtabchi S, Rios CL. Management of emergency de-
partment patients with primary spontaneous pneu-
mothorax : a needle aspiration or tube thoracostomy.
Ann Emerg Med. 2008;51:91-100.
30. Wakai A, O Sullivan RG, McCabe G. Simple aspira-
tion vs intercostal tube drainage for primary sponta-
neous pneumothorax in adults. Cochrane Database
Syst Rev. 2007;24(1):CD004479.
31. Conces DJ Jr, Traver RD, Gray WC, et al. Treatment
of pneumothoraces utilizing small caliber chest tubes.
Chest. 1988;94:55-57.
32. Mathur R, Cullen J, Kinnear WJM, et al. Time course
of resolution of persistent air leak in spontaneous
pneumothorax. Respir Med. 1995;89:129-132.
33. Mahfood S, Hix WR, Aaron BL, et al. Re-expansion
pulmonary edema. Ann Thorac Surg. 1988;45:340-
345.
34. Tsai WK, Chen W, Lee JC, et al. Pigtail catheters vs
large-bore chest tubes for the management of sec-
ondary spontaneous pneumothoraces in adults. Am J
Emerg Med. 2006;24:795-800.
35. Granke K, Fischer CR, Gago O, et al. The efficacy
and timing of operative intervention for spontaneous
pneumothorax. Ann Thorac Surg. 1986;42:540-542.
36. Chee CBE, Abisheganaden J, Yeo JKS, et al. Per-
sistent air-leak in spontaneous pneumothorax—
clinical course and outcome. Respir Med. 1998;92:
757-761.
37. Barker A, Maratos EC, Edmonds L, et al. Recurrence
rates of video-assisted thoracoscopic versus open
surgery in the prevention of recurrent pneumoth-
orax: a systematic review of randomised and non-
randomised trials. Lancet. 2007;370:329-335.
38. Sawada S, Watanabe Y, Moriyama S. Video-assisted
thoracoscopic surgery for primary spontaneous pneu-
mothorax: evaluation of indications and long-term
outcome compared with conservative treatment and
open thoracotomy. Chest. 2005;127:2226-2230.

39. Kennedy L, Sahn SA. Talc pleurodesis for the treat-
ment of pneumothorax and pleural effusion. Chest.
1994;106:1215-1222.
40. Alfegeme I, Moreno L, Heurtas C, et al. Spontaneous
pneumothorax: long term results with tetracycline
pleurodesis. Chest. 1994;106:347-350.
41. Dines DE, Clagett OT, Payne WS. Spontaneous
pneumothorax in emphysema. Mayo Clin Proc.
1970;45:481-487.
42. Boat TF, Di Sant’ Agnese PA, Warwick WJ, Handw-
erger SA. Pneumothorax in cystic fibrosis. JAMA.
1969;209:1498-1504.
43. Wait MA, Dal Nogare AR. Treatment of AIDS-related
spontaneous pneumothorax: a decade of experience.
Chest. 1994;106:693-696.
Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Acute Pneumothorax 189
44. Baumann MH, Sahn SA. Tension pneumothorax: di-
agnostic and therapeutic pitfalls. Crit Care Med.
1993;21:177-179.
45. Trupka A, Waydhas C, Hallfeldt KK, et al. Value of tho-
racic computed tomography in the first assessment of
severely injured patients with blunt chest trauma: re-
sults of a prospective study. J Trauma. 1997;43:405-
411.
46. Sassoon CSH, Light RW, O’Hara VS, et al. Iatrogenic
pneumothorax: etiology and morbidity. Respiration.
1992;59:215-220.
47. Kunisch-Hoppe M, Hoppe M, Rauber K, et al. Tra-
cheal rupture caused by blunt chest trauma: radi-
ological and clinical features. Eur Radiol. 2000;10:
480-483.