Tension Pneumothorax

Introduction
Pneumothorax, or air in the pleural space, is a common clinical problem. A

pneumothorax as a result of injury to the chest wall is termed traumatic. If
pneumothorax results from an invasive medical procedure (e.g., pacemaker or central
venous line insertion), it is referred to as iatrogenic. The term spontaneous
pneumothorax is reserved for cases arising without preceding trauma or injury. These are
typically further subdivided into primary spontaneous pneumothorax (PSP), developing in
patients with apparently “normal” lungs, and secondary spontaneous pneumothorax (SSP),
developing in patients with known lung disease. The British Thoracic Society (BTS)
guidelines suggest that pneumothorax in patients who are older than 50 years or with
significant smoking history should be labeled SSP, because there is a high likelihood of
pathologic lung changes, even in the presence of a normal chest radiograph (CXR). 1
Spontaneous Pneumothorax
Epidemiology
The best epidemiologic data for pneumothorax come from large national datasets, of
which there have been two recent publications. The largest, covering 50 years of hospital
admissions in England, included over 170,000 admissions. This study showed an
increase in the incidence of pneumothorax from 1968 to 2016, 2 although the reason for
this increase is unknown. In 2016, there were 14.1 pneumothorax admissions per
100,000 people aged 15 years or older. The rate was higher for men (20.8) than for
women (7.6 per 100,000), 2 and the study confirmed the classic bimodal age
distribution, with a first peak at age 15 to 34 years and an increasing incidence beyond
60 years in both men and women, which had been shown in smaller studies. 345 The
second large epidemiologic study from France showed similar incidence rates, but the
classic bimodal distribution was not seen. 6 The English study for the first time described
the admission rates by PSP and SSP on a large scale: 60.8% of patients in 2016 had
chronic lung disease and were classified as having SSP. 2
Etiology
Historically, patients with spontaneous pneumothorax are subcategorized into PSP and
SSP because the outcome and clinical course are very different; consequently,
management strategy differs significantly. The mortality and morbidity from patients
admitted with SSP is higher than PSP. 5 However, the traditional view that PSP presents
in the absence of lung disease is being challenged, and it is likely that these patients do
not have completely “normal” lungs. 7 , 8 This section focuses on the two spontaneous
entities, PSP and SSP. Other etiologies such as traumatic, iatrogenic, and catamenial are
covered separately.
Primary Spontaneous Pneumothorax

Ectomorphic Body Shape
The classic body shape for the patients with PSP is “tall and thin.” Indeed, PSP is more
common in taller patients with low body mass index and in smokers. 91011 A large-scale
study of 5604 cases of pneumothorax in Japan found a significantly lower weight/height
ratio in patients with pneumothorax compared to healthy individuals. 10 The risk of
recurrence (i.e., another episode of pneumothorax) in PSP patients was higher in taller
patients, but only in men. Interestingly, height (in women) and a lower body mass index
(in either sex) were not associated with increased risk of recurrence. 9
Abnormal Lung Parenchyma and Smoking

Although PSP may present in patients without overtly recognized lung pathology, there
is evidence that patients with PSP have macroscopic and microscopic structural
abnormalities characterized by microscopic evidence of distal airways inflammation,
“pleural porosity,” and emphysema-like changes. Such emphysema-like changes include
subpleural blebs and bullae, commonly seen in patients with PSP on surgical inspection
and on computed tomography (CT) scans, 12131415161718 but also in healthy volunteers
(both smokers and nonsmokers). 12 , 19 Therefore, one cannot assume that these
abnormalities are the sole cause of pneumothorax because they are not present in all
patients with PSP and may be present in healthy individuals without PSP.
Smoking is a well-known risk factor for pneumothorax. 20 , 49 Although the exact

mechanism is unclear, it has been postulated that small airways inflammation
associated with smoking results in weakening of the visceral pleura, or dilation of the
distal airways, resulting in increased airway pressure. However, it should be noted that
not all smokers get pneumothorax, and there is likely an underlying susceptibility to
cigarette smoke that results in the pneumothorax phenotype. Interestingly, risk of
recurrence is not consistently increased in smokers compared to
nonsmokers. 9 , 202122 It is not yet known whether pneumothorax and lung changes are
associated with the use of marijuana or e-cigarettes.
Blebs and Bullae

The anatomic lesion known as a bleb was first described in 1947 by Miller, as distinct
from a bulla (or bullous emphysema). 23 A bleb is defined as an outpouching (or vesicle)
of the visceral pleura caused by air in the interstitium, forming between the lamina
elastica interna and externa of the visceral pleura, typically less than 1 cm in diameter
( Figs. 110.1 and 110.2 ). In contrast, a bulla is an airspace measuring greater than 1 cm,
which is sharply demarcated by a thin wall (≤1 mm in thickness). In 1967, Reid further
subdivided bullae into three types: type I, a small amount of hyperinflated lung tissue
that is narrow (pedunculated) and contains no lung parenchyma; type II, a relatively
smaller amount of hyperinflated lung tissue that is broad (sessile); and type III, a large
amount of hyperinflated lung tissue extending to the pulmonary hilum, with ill-defined
margins and minimal parenchyma in each bulla. 24 These areas of disrupted mesothelial
cells at the visceral pleura, replaced by an inflammatory fibroelastic layer, along with
observed small pores, may contribute to a more general “pleural porosity.”
Open full size image

Figure 110.1
Blebs and bullae. The anatomy of emphysematous lung lesions is shown, representing a bleb and a
bulla.
From Lyra R de M. Etiology of primary spontaneous pneumothorax. J Bras Pneumol . 2016;42[3]:222-
226.
Figure 110.2
Thoracoscopic view of a bleb on the visceral pleural surface.
A bleb tends to be small (<1 cm in diameter) and forms within the visceral pleura.
Courtesy M. Noppen, Brussels University Hospital.
Microscopic Abnormalities
Microscopic abnormalities have been identified in the lungs of PSP patients. In an early
pathologic study of 20 young patients with PSP, resected lung parenchyma showed
features of chronic distal airway inflammation with lymphocyte and macrophage
infiltration alongside fibrotic changes. 25 In another study of 79 patients with
PSP, respiratory bronchiolitis (RB) was identified on surgical biopsy in
88.6%. 26 Unfortunately, all the patients in this study were smokers, a known cause of
RB. Thus, whether RB was a causal step in the development of pneumothorax or simply
a marker of smoking status remains unclear. A subsequent study of 126 surgical cases
found that RB was present in only 50% of patients. 27 In the same patients, light
microscopic assessment demonstrated thickening and fibroelastosis of the pleura. Reid
type I bullae were found to have microscopic changes in keeping with that originally
described by Miller with respect to blebs, with formation of small air-containing spaces
between lamina elastic interna and externa that contains no lung parenchyma (see Fig.
110.1 ). 24 , 27 Whether these microscopic changes lead to rupture of air into the pleural
space and PSP is speculative, the abnormalities found in this study support the
hypothesis that the underlying lung in PSP patients is not normal.
Historically, it has been postulated that rupture of blebs or bullae creates direct
communication between the alveolar air and the pleural space, thus creating a
pneumothorax. This view was contested by the observation that the presence of visible
air leaks at thoracoscopy or thoracotomy is highly variable, 28 with many blebs or bullae
remaining intact and, in some cases, with no macroscopic lesions at all. The concept of
pleural porosity as a possible driver of PSP, rather than bulla or bleb rupture, was
elegantly demonstrated in a study by Noppen et al. 19 (see Video 29.11 ). Twelve patients
with PSP were compared to 17 control subjects at thoracoscopy using fluorescein-
enhanced autofluorescence. Control subjects were undergoing sympathectomy (for
hyperhidrosis) and therefore did not have any lung disease or history of pneumothorax.
In both groups, there were areas of parenchymal abnormality, seen as areas of
subpleural fluorescence or visible fluorescence leak when inspected under ultraviolet
light, at regions of the lung that otherwise appeared normal with inspection under white
light. However, high-grade lesions were seen only in PSP patients. Two patients with
emphysema-like changes demonstrated air leak, but the leakage was not directly at the
site of the macroscopic blebs or bullae. 19 Thus, areas of porosity appeared to be more
closely associated with air leakage than did the blebs and bullae.
Abnormal Elastosis
Areas of porosity may be a consequence of airway inflammation. One theory is that
there is an imbalance in the protease-antiprotease systems. Matrix
metalloproteinases (MMPs) are a group of zinc- and calcium-dependent endopeptidases
that can damage basement membrane. 29 MMP-2 and MMP-9, two interstitial
collagenases, have been postulated to be pathogenic in other lung diseases, 30 including
asthma and COPD. 31 Two Taiwanese groups have examined surgical resection
specimens from patients undergoing surgery for PSP and demonstrated overexpression
of MMPs. 29 , 32 In the first study, immunohistochemistry showed overexpression of
MMP-2, MMP-7, and MMP-9 in the tissue of PSP patients compared to controls. 29 In
the second study, high MMP-2 and MMP-9 expression was found in patients
undergoing surgery for recurrence prevention, and higher levels were found in patients
presenting with a recurrent pneumothorax compared to those with a first
episode. 32 Although these studies present intriguing data on elevated MMP levels in
PSP, further prospective studies are required to confirm these findings and determine
their clinical applicability in terms of risk stratification of patients or potential treatment
options.
Familial Causes
Most episodes of PSP arise sporadically. However, an estimated 10% of patients have a
significant family history. 33 , 34 A number of important inherited conditions predispose to
pneumothorax, including Marfan syndrome, 35 Birt-Hogg-Dubé (BHD)
syndrome, 36 alpha 1 -antitrypsin deficiency, 37 and homocystinuria. 38 Marfan syndrome is
caused by mutations in the fibrillin 1 (FBN1) gene; the major manifestations include
increased height, disproportionately long limbs and digits, subluxation of the lens of the
eye, and dilation of the aortic root. 35 Apical blebs and spontaneous pneumothorax have
been described as minor diagnostic criteria for Marfan syndrome. 35 Whether mutations
in FBN1 predispose individuals to PSP in the absence of Marfan syndrome is not clear.
Mutations in FBN1 are not the cause of all autosomal dominant familial spontaneous
pneumothorax; an analysis of two pedigrees of patients with a strong family history of
spontaneous pneumothorax did not find associated mutations in FBN1 . 39 It is presumed
that the fibrillin mutation causes a weakness in the fibroelastic layer in the visceral
pleura, but this has not been proven. BHD syndrome is an autosomal dominant
inherited disease caused by mutations in the folliculin (FLCN) gene. BHD is
characterized by benign skin tumors, diverse types of renal cancer, pulmonary cysts, and
spontaneous pneumothorax. 36 , 40 It is likely that, as our understanding of pathogenesis
increases, more genes with a role in pneumothorax will be discovered.
Although familial patterns of inheritance of spontaneous pneumothorax, particularly

with autosomal dominance, are uncommon, a strong family history of pneumothorax
should prompt further investigation. In this situation, the pneumothorax event may be a
precursor to an unrecognized connective tissue disorder (Marfan or Ehlers-Danlos
syndrome), skin disease (BHD), or metabolic disorder (homocystinuria) with the need
for potential lifelong surveillance for other severe associations (e.g., renal cancer or
aortic rupture).
It seems likely that minor mutations in FBN1 or FLCN could predispose to the

development of PSP without causing the full clinical spectrum of Marfan or BHD
syndrome. This is an area that requires large-scale prospective studies with the
collection of genetic and clinical data. Such data, if successful in identifying causative
genetic mutation(s), could potentially determine an individual’s risk of
recurrence. 41 , 42 Clinicians should be vigilant for PSP being the first manifestation of a
systemic disease and should have a low threshold for referral for genetic
counseling. 41 , 42 At present, routine CT scan of the chest and pulmonary function testing
are not standard after uncomplicated treatment of a first episode of PSP. However, some
clinicians opt for a low-dose CT scan in female patients or males with a strong family
history to exclude important familial diagnoses (above) or underlying lung disease such
as lymphangioleiomyomatosis (LAM).
Secondary Spontaneous Pneumothorax

A host of airway and lung diseases can be complicated by SSP. In the United Kingdom,
the most common of these is COPD. 43 The most common cause worldwide remains
pulmonary tuberculosis. Other common causes include cystic fibrosis, lung cancer,
necrotizing pneumonias, and human immunodeficiency virus–related Pneumocystis
jirovecii lung infection. However, there are few large-scale epidemiologic studies
quantifying the risk of pneumothorax in these chronic diseases . Two rare infiltrative
lung diseases are commonly associated with SSP: pulmonary Langerhans cell
histiocytosis and LAM, with or without other features of tuberous sclerosis 44 ( eFig.
110.1 ). Indeed, spontaneous pneumothorax in younger women (30 to 40 years old) may
be the first manifestation of LAM. 44 Recurrent pneumothorax in women of childbearing
age should prompt consideration of catamenial pneumothorax due to thoracic
endometriosis. 45 , 46 The causes of SSP are summarized in Table 110.1 .
Table 110.1
Disorders Associated With Spontaneous Pneumothorax
Common COPD, pulmonary tuberculosis

Uncommon Cystic fibrosis, lung cancer, Pneumocystis jirovecii infection
Rare Interstitial lung diseases : idiopathic pulmonary fibrosis, sarcoidosis,
pulmonary Langerhans cell histiocytosis, lymphangioleiomyomatosis
Connective tissue diseases : rheumatoid arthritis, scleroderma, ankylosing
spondylitis, Marfan syndrome
Familial conditions: Birt-Hogg-Dubé syndrome, Ehlers-Danlos syndrome,
homocystinuria, catamenial pneumothorax
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Tension Pneumothorax
Tension pneumothorax is a medical emergency. Tension develops when the leak in the
visceral pleura functions as a one-way valve allowing air into the thorax but not allowing
escape, thus progressively increasing intrapleural pressure. The increased pressure
causes chest discomfort, reduces venous return, and eventually results in hypotension
and hemodynamic compromise due to compression of the right ventricle and
subsequent reduction in left ventricular end-diastolic filling pressure. These patients
require urgent decompression with a cannula placed anteriorly in the second intercostal
space in the midclavicular line. The unilaterality of the patient’s complaints and signs on
examination should be sufficient to identify the pneumothorax; in this setting,
treatment should not be delayed for radiologic confirmation. 1 Tension is relatively rare
in PSP and usually develops in the context of trauma or in ventilated patients in
intensive care units, 48 but it should be noted that the true incidence is unclear.
Diagnosis and Management

Symptoms
Patients usually present with chest pain and/or breathlessness. The cause of chest pain
is not clear but may be due to acute inflammation of the parietal pleura 47 or to tearing of
small adhesions as the visceral pleura moves away from the parietal surface. Tearing of
adhesions would be likely to cause some bleeding (hemopneumothorax), but significant
intrapleural bleeding is a rare complication of pneumothorax; on the other hand, the
CXR in many patients with pneumothorax demonstrates a basal air-fluid level if this is
carefully looked for, perhaps suggesting a small pleural bleed. The physiologic cause of
breathlessness is not clear—this may be due to expansion of the chest wall and
depression of the diaphragm or an alteration in respiratory mechanics and perception.
Such changes have been postulated to contribute to breathlessness in patients with
emphysema and in those with pleural effusion.
Clinical Examination
On examination, there is usually ipsilateral increased chest wall size, decreased chest
wall expansion with breathing, a hyperresonant percussion note (tympany), and
diminished breath sounds. However, signs can be subtle in patients with small
pneumothoraces or when the patient has underlying emphysema or cystic lung disease.
Deviation of the trachea to the contralateral side on examination, if present, with
hemodynamic compromise along with tympany and enlargement of the hemithorax on
the affected side would signify tension pneumothorax and the urgent need to intervene
(see later). Arterial blood gas measurements are not usually clinically indicated; in a
large and acute pneumothorax, these may demonstrate hypoxemia and an increase in
the alveolar-arterial oxygen tension difference. However, in most pneumothoraces
where the underlying lung is not diseased, very little disturbance to oxygen saturations
is seen, possibly because of matched perfusion-ventilation defects as a result of lung
collapse (see Chapter 44 ).
Imaging
In patients with suspected non–tension pneumothoraces, a CXR should be used to
confirm the diagnosis: the visceral pleura is clearly visible as a line with an absence of
lung markings distally ( Fig. 110.3 ). Often the distinction of the visceral pleural line and
other lines, such as skinfolds, can be challenging ( Fig. 110.4 ). A pleural line should have
air on both sides, have no lung markings distal to it, and be continuous along the length
of the pneumothorax.

Figure 110.3
Chest radiograph showing left-sided pneumothorax without mediastinal shift.
The visceral pleura is clearly visible ( arrows ) with an absence of lung markings distally.
Figure 110.4
Distinguishing a pneumothorax from a skinfold.
(A) Chest radiograph of a pneumothorax. The pleural line has lucency on either side, representing
air in the pleural space on one side of the line and air in the lung on the other. The line is sharply
demarcated and can be traced along its course ( lower arrow ) . No blood vessels can be seen
beyond the superior ( upper arrow ) and lateral ( middle arrow ) extent of the line. (B) Chest
radiograph of a skinfold ( arrows ) that could be mistaken for a pneumothorax. The border is more of
an edge, with lucency on only one side. The edge is poorly defined and cannot be followed
continuously ( lower arrow ) . Blood vessels can be traced beyond the border of the fold
( arrowhead ) .
In most cases, a standard erect frontal CXR is sufficient to confirm the diagnosis of
pneumothorax. Small pneumothoraces can be difficult to ascertain and may be missed
on a frontal CXR. In cases where there is a high clinical index of suspicion, lateral CXRs
are sometimes useful and can detect pneumothorax in up to an additional 14% of
cases. 49 In a supine patient, the intrapleural air of a pneumothorax will move and lie in
the anterior region of the pleural space, where it will have a different appearance on
CXR. As an example, in a supine patient, a pneumothorax can produce the deep sulcus
sign, in which the air collects between the diaphragm and chest wall ( Fig. 110.5 ).

Figure 110.5
Deep sulcus sign of pneumothorax in a supine patient.
Detailed views of the right costophrenic angle from successive supine chest radiographs taken
before (A) and after (B) the development of a pneumothorax. Both images show diffuse infiltration in
the right lower lung field. Note change in costophrenic angles ( arrows ) caused by air in the pleural
space between the diaphragm and chest wall: the deep sulcus sign. Air in the anterior pleural space
can also be recognized by an air-tissue interface ( arrowheads ) .
However, with ready access to CT scanning, many physicians opt for a chest CT to avoid
any doubt. This is particularly important in situations in which missing a small
pneumothorax may have detrimental consequences, such as in patients with extensive
lung disease or in those on positive-pressure ventilation. 50 Another indication for CT
scan is to differentiate pneumothorax from severe bullous lung disease because an
erroneous diagnosis and subsequent chest tube insertion could lead to puncture of the
lung, with risk of ongoing leak and bronchopleural fistula ( Fig. 110.6 ).

Figure 110.6
Bullae resembling pneumothorax.
(A) Frontal chest radiograph of a patient with cystic fibrosis and extensive bullous disease of the
right apex that was initially mistaken for a pneumothorax. Note lucent area ( arrows ) within the right
upper lung field. (B) Computed tomography scan confirms the presence of bullae ( asterisks ) and
excludes pneumothorax.
Midline Shift
Midline shift refers to deviation of the mediastinal structures away from the side of the
pneumothorax. Certainly, a tension pneumothorax will show a midline shift (unless the
mediastinum is fixed in place). However, midline shift can also be seen in patients
without hemodynamic compromise and thus does not equate to tension pneumothorax.
If the mediastinum is not fixed in place, the mediastinum can shift in response to a
difference in pressure between the two hemithoraces without one side having positive
intrapleural pressure indicative of tension physiology.
Use of Ultrasound in Pneumothorax

There is increasing interest in the use of thoracic ultrasound to diagnose pneumothorax
(see Chapter 23 ). The majority of the studies are prospective case series comparing
imaging modalities in diagnosing pneumothorax in the context of trauma, iatrogenic
(e.g., post–image-guided biopsy), or critical care. The absence of normal-appearing lung
on thoracic ultrasound (i.e., the absence of the normal findings of lung sliding and of B
lines) can be used to diagnose pneumothorax with very high sensitivity and specificity.
There are now randomized controlled trials (RCTs) assessing clinical impact or outcome
and four meta-analyses of these data comparing the accuracy of thoracic ultrasound for
pneumothorax compared to CXR. 51525354 Pooled sensitivity for ultrasound was 78–
90% with a specificity of greater than 98%. CXR performed more poorly with a pooled
sensitivity of 39–52% but a similar specificity. However, the vast majority of these
patients were trauma patients lying in a supine position in the emergency department,
which naturally reduces the sensitivity of CXR.
It is important to note that there are also false-positives for ultrasound in diagnosing
pneumothorax, particularly in patients with underlying lung diseases. This is
particularly evident in patients with COPD who may have bullae close to the pleural
surface, which can also show an absence of the lung sliding sign and thereby give an
appearance similar to pneumothorax. 55
Thoracic ultrasound can potentially be used to identify pneumothorax post–lung

biopsy 565758 or to determine when pneumothoraces have resolved after chest tube
drainage. 59 However, further studies are required before this becomes standard practice.
We use thoracic ultrasound in the diagnosis of pneumothorax post–lung biopsy and
during pleural procedures but not as a primary diagnostic strategy in most cases, in
which a combination of CXR and CT is optimal.
Decisions on Intervention
The first treatment decision is whether intervention is required or not. Clinically stable
patients with a small PSP on CXR can be managed conservatively (i.e., observation
alone) with close CXR follow-up to ensure resolution. However, there is considerable
controversy about the optimal treatment of a minimally symptomatic PSP patient with a
large pneumothorax on CXR, and management therefore varies.
Size of Pneumothorax
The size of a pneumothorax is difficult to infer from the two-dimensional CXR image.
There are a number of methods of estimating pneumothorax size. One is the Light
index, calculated using the ratio of the cube of lung diameter to hemithorax
diameter. 37 Using this formula, a pneumothorax with a 2 cm depth at the level of the
hilum on CXR has an approximate volume of 50% of the hemithorax. Another method
suggested by Rhea et al. uses the average of the interpleural distances measured at the
apex, midpoint of the upper half of the lung, and midpoint of the lower half of the lung
on an erect CXR. 60 However, international guidelines do not agree on size measurement
criteria. 1 , 7 , 61 In clinical practice, the most commonly used methods are the two adopted
by the BTS and the American College of Chest Physicians, which rely on depth of
pneumothorax from the chest wall, possibly because these are relatively simple and
therefore applicable in clinical daily practice.
The BTS definition of a large pneumothorax is greater than 2 cm of air between the lung
margin and the chest wall measured at the level of the hilum on CXR. 1 The American
College of Chest Physicians consensus statement proposes that a large pneumothorax
has 3 cm or greater of air measured from the apex to the inner chest wall at the thoracic
cupola. 61 The Belgian Society of Pneumology proposed that a large pneumothorax has a
visible lung visceral pleural line along the whole length of the lateral chest wall 62 (also
referred to by some authors as complete dehiscence). However, it is clear that there is
little consensus and potentially limited use in size calculation. A study of 49 cases of
pneumothorax compared the classification of pneumothorax size across these three
guidelines and found agreement in only 47% 63 of cases. In addition, it is acknowledged
that size of the pneumothorax on CXR does not correlate to symptoms. The BTS
guidelines include the caveat that “in some patients with a large pneumothorax but
minimal symptoms, conservative management may be appropriate.” 1 Therefore, the
decision to treat or not is largely based upon clinical judgment rather than size; patients
with a small pneumothorax but severe symptoms may require intervention, whereas
stable patients with a pneumothorax classified as large may be initially managed
conservatively with observation only.
In a recently reported randomized trial in moderate to large PSP, conservative

management (i.e., no intervention) was compared to standard care (i.e., aspiration
and/or chest tube insertion). The conservative group did quite well, and the majority of
patients in both arms had resolution of their pneumothorax by 8 weeks. 64 These data
add evidence to the BTS guidance that patients with minimal symptoms can be safely
managed conservatively.
In contrast to PSP, in which observation or short-term treatment is encouraged as the

first treatment, current guidelines recommend that all patients with SSP should be
admitted to the hospital for at least 24 hours and receive supplemental oxygen. Most
SSP will require a chest tube. 1 This cautious approach is recommended in SSP because
the underlying lung disease is thought to increase the risk of complications (such as
respiratory failure) or prolonged ongoing air leak; indeed, there are data suggesting that
spontaneous resolution of pneumothorax is far less common in SSP versus PSP. 65 , 66
Initial Management Options

Once the decision is made to intervene, the next choice is whether to attempt needle
aspiration (NA) or to insert a small-bore chest tube. BTS guidelines recommend NA
(using a 16- to 18-gauge cannula) of up to 2.5 L of air as initial treatment. If NA is
unsuccessful in expanding the lung, chest tube insertion is required. 1 These
recommendations are based upon RCTs showing “equivalence” of NA and chest
drainage in terms of initial success rates, varying between 59% and
80%. 67686970 However, there were significant differences in the definition of “initial
success,” and trial design between the studies ( eTable 110.1 ), and none of the studies
was designed as a true noninferiority comparison.
eTable 110.1
Randomized Controlled Trials of Needle Aspiration vs. Chest Tube: Initial Success Rates
Study Year N Needle Aspiration Success Chest Tube Initial Success

Rate (%) Rate (%)
Harvey 67 1994 73 80 100
Andrivet 68 1995 61 67 93
Noppen 69 2002 60 59 64
Ayed 70 2006 137 62 68
Ho ∗ 136 2011 48 48 72 †
Parlak ‡ 73 2012 56 68 81
Thelle § 75 2017 77 74 38
Ramouz 74 2018 70 54 69
View full size
∗ Percentage discharged home after initial management.
† Chest tube with Heimlich valve.
‡ Includes traumatic (22/56).
§ Primary spontaneous pneumothorax data only.
In 2007, the first Cochrane review of this topic 71 included only one RCT. This study by
Noppen et al. included 60 patients with a first episode of PSP randomized to either NA
or chest tube. Initial success rates were not significantly different between the groups:
59.3% after NA and 63.6% after chest tube. 69
In 2017, Carson-Chahhoud et al. updated the Cochrane review, 72 this time with six
RCTs, 67686970 including Parlak, 73 who also recruited patients with traumatic (as well
as spontaneous) pneumothoraces. The Cochrane review concluded that immediate
success rates were higher in the chest tube group than the NA group. 72 However, there
was heterogeneity in the definitions of immediate success. Recurrence rates were no
different between the groups. Hospital stay was shorter in the NA group with fewer
complications compared to the chest tube group. 72
Since that review, two more RCTs have been published: Ramouz et al. enrolled patients
with PSP and again found similar immediate success rates with NA and chest tube and
shorter hospital stay in the NA group. 74 Thelle et al. recruited both PSP and SSP patients
and reported NA to be more effective than chest tube drainage for initial treatment
success (68.8% vs. 31.8%), although 37.5% of patients required a second
aspiration. 75 This was the first study to include significant numbers of patients with SSP
and to report the results separately; there was a higher success rate for NA in both PSP
and SSP patients. The authors suggest the guidelines should be changed to treat SSP in
the same way as PSP (i.e., with NA as initial treatment). 75 However, it should be noted
that the chest tube group had a lower success rate (31.8%) than in previous studies;
thus, first-line treatment of SSP with NA requires further validation before it can be
widely recommended.
Supplemental Oxygen
In patients who are not undergoing intervention to drain the pneumothorax,
supplemental oxygen can be prescribed. Evidence from a small study in 1971 suggests
that use of 100% oxygen in patients with spontaneous pneumothorax can increase the
rate of absorption fourfold compared to air (on the basis of mean reduction in
pneumothorax size of 4.8 and 18 cm 2 /day, respectively). 76 The rationale is that by
reducing the partial pressure of nitrogen in the inspired gas, and thus in pleural
capillaries, the rate of nitrogen absorption from the pneumothorax is increased, thereby
increasing the rate of resolution of the pneumothorax.
Reexpansion Pulmonary Edema

Unilateral pulmonary edema ( reexpansion pulmonary edema [RPE]) may develop in
certain patients whose lung has been rapidly reinflated after a period of collapse
secondary to a pneumothorax or a pleural effusion. This is likely due to mechanical
stress on the lung leading to increased permeability of the pulmonary vasculature
during rapid reexpansion. The incidence of RPE is likely to be low: retrospective series
suggest that the incidence may be as low as 0% 77 or 1% 78 in patients treated for
pneumothorax. More recent series report a high incidence of RPE (16%, 27/173), but
this was largely asymptomatic because only five patients (3%) required treatment. 79
Typically, patients with RPE will report cough or chest tightness. In extreme cases,
patients can be hypoxemic and hypotensive. Treatment is supportive with supplemental
oxygen and diuretics.
Ambulatory Care
With the increasing pressures on health care systems, ambulatory management has
been proposed for patients with a number of medical conditions. Given that patients
with PSP tend to have little comorbidity, this patient group might represent an ideal
cohort for outpatient management to reduce both inconvenience and risk for patients
and the economic costs of an inpatient hospital stay. This is not a new concept; a
number of studies have demonstrated the feasibility of outpatient management for PSP
using a chest tube attached to a one-way (also called a flutter or Heimlich) valve, but this
treatment has not been widely adopted. As far back as 1976, a case series of 226 patients
with PSP managed by observation or flutter valve concluded that outpatient
management was “safe, efficient, and economical.” 80 The first randomized trial of 30
PSP patients compared “thoracic vent” to standard chest tube. This study showed no
significant difference in complications or reexpansion rates, but 70% of the “vent”
patients were managed as outpatients and required fewer analgesics, with patients in
the control group (standard chest drain) hospitalized for a median of 8 days. 66 Since
then, a number of observational or retrospective studies also describe high rates of
success with outpatient management of PSP with one-way valves. 8182838485 These
data were summarized in a 2013 systematic review 86 in which an overall success rate
was reported as 85.8% and successful outpatient management reported in 77.9% with
“few complications.” However, the evidence was of poor quality with a high risk of
bias. 86 As a result, a large multicenter RCT was designed to answer the question of
efficacy and safety of ambulatory management. 87 In this trial, ambulatory management
(using an ambulatory device containing a one-way valve) was compared to standard care
(aspiration with or without chest tube, per BTS guidelines). Ambulatory management
significantly reduced hospital stay compared with standard care (median, 0 days
[interquartile range, 3 days] vs. 4 days [interquartile range, 8 days]; P < 0.0001).
Patients who underwent ambulatory treatment had fewer pleural procedures, but
serious adverse events were higher due to hospital readmission. 87
Suction
Suction refers to the application of negative pressure to the intrapleural space via the
chest tube. Use of suction is not recommended by the current guidelines. 1 There have
been two small RCTs, neither of which showed a significant difference in success rates
when comparing suction to standard underwater seal management. 88 , 89 However,
suction is advocated by some physicians in cases of nonresolution of pneumothorax
(particularly if the lung has not reinflated). Suction aims to remove air from the pleural
space at a rate faster than it can accumulate in the chest, hence, speeding resolution of
the pneumothorax; however, it should be noted that this does not treat the underlying
visceral pleural defect. However, some authorities state that full lung expansion allows
earlier healing of the pneumothorax due to apposition of the visceral and parietal
pleura. This hypothesis has not been proven, and recent data argue the opposite. 64 In a
recent RCT, those managed conservatively (e.g., without drainage of air) had a lower
recurrence of pneumothorax over the next year than those receiving standard
management (e.g., with aspiration and/or chest tube drainage), 64 suggesting that slow
reexpansion may improve healing.
Although the guidelines do not explicitly recommend suction, they state that a “high
volume” (up to 15–20 L/min) “low pressure” suction could be used. 1 The application of
suction is not without risk; rapid reinflation of the lung may precipitate RPE and,
perhaps more worryingly, the increased airflow through the visceral leak could increase
the size of the hole in the visceral pleura. Therefore, the use of suction needs to be
considered carefully.
Failure of Medical Management

In most patients with pneumothorax, the visceral pleural injury and therefore the air
leak will resolve spontaneously, with drainage intended to prevent symptoms and
complications such as tension. Failure of medical management for patients with
pneumothorax describes the clinical situation in which the lung has not reinflated with
chest drainage and/or there is a prolonged air leak.
A number of treatment options are possible in this situation. However, it is important to
understand the rationale behind each treatment before it is used in an unstructured
manner.
Prolonged Air Leak

Prolonged air leak (PAL) is typically defined as an ongoing leak despite 5 to 7 days of
chest tube drainage. There are data to suggest that most PSP patients with PAL will
eventually resolve given time. Chee et al. found that 100% of patients with PSP with PAL
for greater than 7 days had resolved by 14 days. 65 Therefore, any decision to define
failure must be considered as a balance between allowing time for the leak in the
visceral pleura to heal (with spontaneous cessation of PAL) and the inconvenience and
expense of having a chest tube in place while in the hospital for an extended period.
Current BTS guidelines suggest that drainage should be attempted for at least 3 days,
and a thoracic surgical opinion should be sought “early” at 3 to 5 days. 1 Presumably, this
recommendation was intended to allow the necessary arrangement for surgical
intervention as, in theory, PAL is not confirmed until at least day 5. 1 However, these
timings are somewhat arbitrary and not evidence based.
Chest Tube Size

In the presence of a large air leak, some physicians and surgeons may advocate
replacing a small-bore tube with a large-bore tube to allow a greater total flow rate of air
or using high-volume, low-pressure suction attached to the chest tube. The larger chest
tube allows a greater flow rate because turbulent flow is proportional to the fifth power
of the radius of the tube, as described by the Fanning equation: v = π 2 r 5 P/fl (where v is
flow, r is radius, P is pressure, l is length, and f is a friction factor). 89a The goal is to
remove air faster than air is entering, thereby reinflating the lung. This approach would
seem rational if there is clear evidence of insufficient drainage of air (e.g., subcutaneous
emphysema, increasing pneumothorax size, major bubbling through the water seal, or
worsening clinical condition). However, there is no good trial evidence to support the
use of larger drains or suction in stable patients with PAL.
Thoracic Surgery
Definitive treatment for failed medical treatment or recurrence prevention is thoracic
surgery. It is important to distinguish the two purposes of surgery in this situation. The
first is to repair the leaking lung, allowing full lung expansion and removal of the chest
drain, which is required only in cases of PAL. The second is recurrence prevention,
which is largely an elective operation; if air leak repair is to be performed at surgery, it
makes sense to conduct recurrence prevention surgery at the same time.
Surgery is performed by video-assisted thoracoscopic surgery (VATS), which has

superseded open thoracotomy in most countries as the approach of choice. During
surgery, the operator aims to identify and seal any areas of air leakage, resect any visible
blebs or bullae on the visceral pleura, and perform a pleurodesis procedure. Pleurodesis
is required alongside bleb/bullectomy to achieve lower recurrence
rates. 28 , 90 , 91 Pleurodesis can be achieved by pleural abrasion, pleurectomy, or chemical
pleurodesis (typically by insufflation of talc, called “poudrage”). A study of VATS for PSP
recurrence prevention (or for PAL) showed a lower rate of recurrence with talc poudrage
(1.8%) compared with subtotal pleurectomy (9.2%) regardless of whether ligation or
stapling of bullae was performed. 92 The low recurrence was confirmed in two large case
series of VATS with talc poudrage after bleb/bullectomy, which reported recurrence
rates of only 1.7% 93 and 1.9%. 94
Where the option exists, patients with PAL could undergo medical thoracoscopy
performed under conscious sedation (rather than under general anesthesia, as in VATS)
with talc poudrage. Although this is being performed in Europe, it is not current practice
in the United Kingdom or United States. An RCT comparing medical thoracoscopy with
talc poudrage to standard chest tube alone showed a reassuringly low recurrence rate of
5% compared to 34% for chest tube drainage. 95 It should be noted that deep conscious
sedation or general anesthesia is required to perform talc poudrage pleurodesis at
thoracoscopy in patients with pneumothorax because this procedure can be painful. 96
Recurrence Prevention After First Pneumothorax

In cases in which a recurrent pneumothorax is likely and would be accompanied by
serious clinical consequences, efforts to prevent recurrence are indicated. This can be
approached with a surgical, usually VATS, or medical thoracoscopy or with a medical,
usually talc, pleurodesis. Also, various additional procedures have been used to stop
ongoing air leaks to allow pleurodesis or discharge.
Surgical Pleurodesis
At present, recurrence prevention surgery after a first episode of spontaneous
pneumothorax is recommended only in certain circumstances and usually when the
patient’s occupation would increase risk in the event of a recurrence (e.g., airline pilot or
commercial diver). Otherwise, the indications for surgery are recurrence (either
ipsilateral or contralateral), synchronous bilateral pneumothorax, or PAL. 1 However,
there are advocates of surgical intervention after a first episode of PSP. There have now
been two RCTs comparing early VATS to conservative management after a first PSP.
The first study randomized 41 patients to either VATS within 24 hours of admission to
the hospital or to “conservative” treatment with chest tube drainage. 97 They found no
recurrence (0%) in the VATS group but 40.9% in the conservative group. It should be
noted that the recurrence rate in the conservative group is significantly higher than
expected from other studies in the literature, 2 , 6 and that this study was small and
therefore underpowered. A larger RCT by Olesen et al. 98 of 373 PSP patients showed a
significantly lower recurrence rate in those treated with VATS (13%) compared to
conservative treatment (34%). The 13% recurrence in the VATS group was unexpectedly
high but may be due to the use of abrasion rather than talc as the method of pleurodesis.
The main issue regarding recurrence prevention after the first event is determining
which patients would benefit. Around 28–30% of patients will have a recurrence after
simple chest tube drainage, 2 , 6 but 70% will not. It therefore follows that operating on all
patients results in approximately 70% having an unnecessary operation. Although VATS
or medical thoracoscopy is generally considered a safe procedure, there are still risks of
significant morbidity or mortality, especially persistent chest pain. 99 If patients at higher
risk could be identified, a more personalized approach could potentially shift the
balance of risks and benefits towards early surgery or thoracoscopy.
Risk stratification based on high-resolution CT scan findings was proposed by Ouanes-

Besbes et al. 100 Unfortunately, stratification by bullae size or “dystrophic score” has not
convincingly identified patients at higher risk of recurrence. As such, the case for early
surgery or thoracoscopy for PSP recurrence prevention has yet to be made. The
combination of clinical and radiographic findings may provide better information for
patients and clinicians on potential risks and benefits of early intervention, although
validated data are currently lacking.
Patients Unfit for Surgery

By definition, patients with SSP have demonstrable lung disease. Patients with long-
standing lung disease such as COPD and interstitial fibrosis are particularly susceptible
to PAL and recurrence. Unfortunately, the respiratory disease renders such patients
unfit for surgery due to the high risk of general anesthesia. These patients present a
significant management challenge for physicians and may have multiple episodes of
pneumothorax with prolonged hospital stays due to the presence of bronchopleural
fistulas. 101 Heimlich valves attached to chest tubes offer the option of discharge from the
hospital and outpatient follow-up, but this may only be feasible in the most stable
patients. Alternatively, a pleurodesis procedure could be performed via the chest tube,
via chemical pleurodesis or the instillation of autologous blood (blood patch
pleurodesis) in an attempt to reduce or stop the ongoing air leak.
Medical Pleurodesis
Pleurodesis is the application of chemical or mechanical injury to the pleura, inducing
inflammation and subsequent adhesion of the pleural layers, to prevent reaccumulation
of fluid or air. Medical pleurodesis is the instillation of a chemical irritant to the pleural
space. This is commonly performed to prevent the reaccumulation of pleural fluid
(usually in the context of malignancy) 102 (see Chapter 114 ). A number of pleurodesis
agents can be used for recurrence prevention in spontaneous pneumothorax, including
talc, tetracycline, minocycline, and autologous blood. 103 Graded talc (talc with the
smallest particles removed) is the most commonly used and successful agent for
pleurodesis. 1 , 7 , 8 In the treatment of malignant pleural effusion, the success rates of talc
for pleurodesis are high (around 70–80%). 102 , 104 It should be noted that for pleurodesis
of any form to work, there needs to be apposition of the visceral and parietal pleura;
therefore pleurodesis has no role in the presence of a pneumothorax with complete
separation of the visceral and parietal layers. The minimal amount of apposition
required to achieve success with pleurodesis is debated.
In an RCT by Chen et al, 105 pleurodesis was attempted for patients presenting with a first
episode of PSP. Minocycline was instilled via chest tube in the intervention arm,
compared with standard tube drainage only, and reduced the rate of recurrence at 1 year
to 29.2% compared to 49.1% in the control group. However, the recurrence rate in the
control arm was much higher than previously reported, 7 and this strategy results in
treating a significant number of patients who may never have a recurrence.
A systematic review has compared efficacy of chemical pleurodesis agents in

spontaneous pneumothorax via either medical or surgical approaches. 103 In the medical
approach (i.e., without surgery on the lung), talc poudrage during medical thoracoscopy
had the lowest recurrence rate at 2.5–10%. The recurrence rates following instillation
through the chest tube were 13–33% for tetracycline and 34% for talc (as a slurry). 95 On
this basis, medical pleurodesis is most commonly conducted using talc and, while
recurrence rates are lowest using VATS or medical thoracoscopy, slurry via chest tube
remains an option, especially for those not fit enough for surgery.
Blood Patch Pleurodesis

Blood patch pleurodesis involves the instillation of 1 to 2 mL/kg of autologous venous
blood into the pleural space via chest tube. Although this is technically not pleurodesis,
it can successfully resolve PAL in some cases. 106 It is presumed that the fibrin and
clotting factors within the blood aid the repair of the visceral leak and help resolve the
pneumothorax. Case series support the use of this technique using 2 to 4 mL/kg of
blood, but definitive data are lacking.
Endobronchial Valves
Another possible treatment option is the use of endobronchial valves, which are
increasingly used in COPD treatment to achieve lung volume reduction. These valves,
inserted at bronchoscopy, occlude the relevant lung segment corresponding to the site of
the air leak, thereby closing the bronchopleural fistula. 107 While there are case reports
and small case series suggesting successful treatment, high-quality evidence on their
efficacy is lacking, but they remain a useful option in difficult-to-treat patients. Once the
leak is controlled and the lung reinflates, a medical pleurodesis can be attempted to
reduce recurrence risk.
Total Pleural Covering

The visceral pleura can be covered with an absorbable cellulose mesh via VATS in an
attempt to reinforce the visceral pleura and reduce recurrence without creating a
pleurodesis. This novel approach has been attempted in selected patients with a high
risk of recurrence (e.g., innumerable cysts that preclude resection) and reasons to avoid
pleurodesis. Pleurodesis in patients with LAM increases bleeding complications at the
time of future lung transplantation and, although pleurodesis is not a contraindication
for lung transplantation, alternatives to pleurodesis are desirable. Total pleural covering
has been used in both BHD 108 and LAM, 109 where it appears to be a promising approach
to reduce recurrence. An ATS treatment guideline advocates further study of this
option. 110
Follow-up
Patients should be counseled about risk of recurrence and recommendations regarding
air travel and scuba diving. Patients should be advised to return to the emergency
department if they experience similar chest pain or breathlessness. 1 During follow-up,
the possibility of underlying lung disease should be considered and investigated.
Lifestyle advice on smoking cessation should be reinforced because continued smoking

increases the risk of recurrence. 4 , 94 Advice on air travel is mandatory (see Chapter 106 ).
An undrained pneumothorax will increase in size as a result of the decreased ambient
pressure in the aircraft cabin and potentially cause respiratory compromise; thus, an
untreated pneumothorax is an absolute contraindication to air travel. Current guidance
recommends waiting for 7 days after full resolution of pneumothorax on CXR before it is
considered safe to fly. 111 Patients who have had definitive surgical management with
pleurodesis for pneumothorax can fly once they have fully recovered from surgery, but
they should be aware that their recurrence risk is still around 1–2%. In patients with
SSP who are not fit for surgery, patients should seek safer modes of transportation (road
or rail) instead of flying. 111
Scuba diving (using compressed gas) should be avoided lifelong after pneumothorax
unless recurrence prevention surgery with pleurodesis has been
conducted 112 (see Chapter 107 ). There is no evidence to link recurrence with physical
exertion, but general advice is that patients can return to work and normal physical
activities once symptoms have resolved. Pragmatically, patients should refrain from
high-impact physical sports in the short term.
Traumatic Pneumothorax
The incidence of pneumothorax after blunt trauma depends on the severity of trauma.
Data on incidence of pneumothorax are limited but, in some series, the incidence
exceeds 35%. 113
A traumatic pneumothorax can result from either penetrating or nonpenetrating chest

trauma (see Figure 104.4, Figure 104.7, Figure 104.8 eFigs. 104.10 and 116.5 ). In penetrating
chest trauma, air can enter the pleural space from the outside via a wound in the chest
wall, or from the lung via a break in the visceral pleura. With nonpenetrating trauma, a
pneumothorax may develop if the visceral pleura is lacerated secondary to a rib fracture
or dislocation. However, in the majority of patients with pneumothorax secondary to
nonpenetrating trauma, there are no associated rib fractures. In this circumstance,
pneumothorax may result from the sudden chest compression abruptly increasing the
alveolar pressure, thereby causing alveolar rupture. Air then enters the interstitial space
and dissects toward either the visceral pleura or the mediastinum. A pneumothorax
develops when either the visceral or the mediastinal pleura ruptures.
Diagnosis
The diagnosis of pneumothorax is commonly made by CXR or CT. However, patients
with significant trauma will commonly be lying in a supine position and may be
immobilized. As mentioned earlier, pneumothorax on CXR in the supine position can be
easily missed. CT scans, increasingly used in major trauma, will identify many more
pneumothoraces, even small ones. A pneumothorax detectable on CT, but not on CXR,
is called an occult pneumothorax and accounts for about 40% of traumatic
pneumothoraces 114 (see Fig. 104.7 ). FLOAT NOT FOUND
Treatment
There is some controversy about whether treatment is required for traumatic
pneumothorax. Most clinicians initiate treatment with chest tube for a large
pneumothorax. However, whether to intervene in patients with occult or small
pneumothoraces is not clear. In one series of 803 patients, 300 with pneumothoraces
less than 1.5 cm were initially managed without chest tubes, and only 33 (10%)
subsequently required chest tube insertion. 115 The remaining 504 patients were treated
with chest tubes, but 66% had the chest tube removed within 24 hours because the lung
reexpanded and air leak ceased. 115 As discussed earlier in regard to PSP and SSP, if the
leak persists for more than a few days, consideration should be given to performing
thoracoscopic surgery to identify and repair the site of the air leak. 116
Iatrogenic Pneumothorax
On the basis of two large series, iatrogenic pneumothoraces are probably more common
than PSPs and SSPs combined. 117 , 118 A leading cause of iatrogenic pneumothorax is
transthoracic needle aspiration. Historically, the incidence of iatrogenic pneumothorax
postaspiration was as high as 25%, although this has reduced since the introduction of
ultrasound for all pleural procedures. 119 Another leading cause of iatrogenic
pneumothorax is CT-guided transthoracic lung biopsy. This procedure is more likely to
result in a pneumothorax if the patient has COPD, if the lesion is deep within the lung,
or if larger needles are used. In a meta-analysis, the pneumothorax rate was 25.3% for
core lung biopsy and 18.8% for fine-needle aspiration. 120
Other common causes of iatrogenic pneumothorax (with approximate incidences) are

subclavian vessel puncture (e.g., during cardiac pacemaker insertion; 22%), pleural
biopsy (8%), mechanical ventilation (7%), and transbronchial lung biopsy
(6%). 1 Iatrogenic pneumothorax also frequently complicates cardiopulmonary
resuscitation. Radiofrequency ablation is increasingly used to treat lung tumors but
carries a high incidence of pneumothorax (≈30%). 121 , 122 A series of 137 radiofrequency
ablation procedures found 27 symptomatic pneumothoraces requiring chest tube
drainage. 123 In another series, the risk for pneumothorax was associated with the
number of tumors ablated, electrode positions, and the electrode trajectory through
aerated lung. 122
Diagnosis
The diagnosis should be suspected in any patient who becomes more dyspneic or whose
condition deteriorates after an intervention procedure. Importantly, the pneumothorax
can present late and therefore may not be evident for 24 hours or longer after the
procedure. 124 The diagnosis needs confirmation by ultrasound or radiographic imaging.
In patients with extensive pulmonary opacities, there may be little evidence of lung
collapse; the air in the pleural space may instead be indicated by the deep sulcus sign
( Figs. 110.5 and 104.8 ).
Iatrogenic pneumothorax should be suspected in any patient treated by mechanical
ventilation whose clinical condition suddenly deteriorates. A sensitive indicator of the
development of a pneumothorax in such patients is increased peak and plateau
pressures if the patient is on a volume-cycled ventilator or a decreased tidal volume if
the patient is on a pressure-cycled ventilator.
Treatment
The treatment of iatrogenic pneumothorax differs from that of spontaneous
pneumothorax in that preventing recurrence is not an issue. If the patient has minimal
or no symptoms and the pneumothorax is small, the patient can be observed. However,
in cases of symptomatic patients or larger pneumothoraces, practice varies
significantly. 125 Simple needle aspiration can be attempted, but many patients require
chest tube insertion. More recently, two studies have postulated an “early discharge
strategy” in which patients with significant pneumothoraces are managed as outpatients
with small-bore chest tubes attached to Heimlich valves. 126 , 127
The management of patients with an iatrogenic pneumothorax secondary to positive-

pressure mechanical ventilation should include urgent tube thoracostomy to reduce the
risk of tension pneumothorax. If the patient continues to receive mechanical ventilation,
the chest tube should be left in place for at least 48 hours after the air leak stops. Two
studies have demonstrated that high-frequency ventilation does not consistently
improve gas exchange or decrease air leak through the fistula. 128 , 129
Catamenial Pneumothorax
A catamenial pneumothorax is a pneumothorax that develops in conjunction with
menstruation. It is probably underdiagnosed and underreported. 130 With catamenial
pneumothorax, respiratory symptoms usually develop within 24 to 48 hours of the onset
of menstruation. 131 Most pneumothoraces are right-sided, but left-sided and bilateral
pneumothoraces have been reported. Catamenial pneumothoraces tend to be recurrent;
patients typically have five pneumothoraces before the diagnosis is recognized. 131
Case series report an incidence of catamenial pneumothorax in 3–6% 45 of

pneumothoraces in young women, but the rate may be as high as 30–40% 46 in patients
requiring surgery for recurrence or ongoing air leak.
Pathogenesis
The pathogenesis of catamenial pneumothorax is unclear. When the syndrome was
initially described, 132 it was hypothesized that air gained access to the peritoneal cavity
during menstruation and then entered the pleural cavity through a diaphragmatic
defect. In a subsequent review of 28 patients who had undergone thoracoscopy,
endometriosis (primarily diaphragmatic) was present in 18 and diaphragmatic
perforations or nodules were present in 21. 133 It has been suggested that diaphragmatic
endometriosis tissue undergoes cyclical necrosis, leading to a diaphragmatic
defect. 134 These authors concluded that diaphragmatic abnormalities play a fundamental
role in the pathogenesis of catamenial pneumothorax. 133 , 134 Alternatively, endometriosis
of the visceral pleura could lead to alveolar pleural air leaks during menstruation.
Treatment
Any woman who has a spontaneous pneumothorax within the first 48 hours of her
menstrual period should be suspected of having a catamenial pneumothorax. The
treatment of catamenial pneumothorax is aimed at treating endometriosis, known or
suspected, by suppressing the ectopic endometrium. This can be attempted by
suppression of ovulation with oral contraceptives or by suppression of gonadotropins
with danazol or gonadotropin-releasing hormone to produce a medical oophorectomy.
Alternative treatments include thoracoscopy with stapling of blebs, closure of
diaphragmatic defects, and parietal abrasion or pleurectomy, or pleurodesis. 130 One
study reported significantly reduced recurrence by combining surgical treatment with
hormonal therapy over a 4-year follow-up period. 135
Key Points
 ▪
Patients with pneumothorax present with chest pain, perhaps due to inflammation of
the pleura or pleural tethering, and dyspnea, potentially caused by expansion of the
chest wall.
 ▪
Mediastinal shift on imaging indicates a difference in pleural pressures on the right and
left sides without necessarily indicating tension. Tension pneumothorax signifies
positive intrapleural pressure that completely collapses the lung, reduces venous return
causing hemodynamic compromise, and requires emergency decompression.
 ▪
Pneumothorax in a young woman should raise the possibility of catamenial

pneumothorax or lymphangioleiomyomatosis.
 ▪
In primary spontaneous pneumothorax (PSP) a conservative approach with no drainage

may also be an option for patients with mild or moderate symptoms who can be
followed as outpatients. Those with severe symptoms should be managed initially by
needle aspiration followed by chest tube insertion in those who do not respond to
treatment.
 ▪
Secondary spontaneous pneumothorax should be treated initially with chest tube

drainage; consideration should then be directed to prevent recurrence, usually with talc
pleurodesis.
 ▪
Patients with PSP are now recognized to have abnormal underlying lung, with
inflammation and emphysema-like changes (blebs, bullae, and pleural porosity) that
represent areas of abnormal tissue beneath the visceral pleura.
 ▪
PSP may be the first manifestation of a systemic disease (e.g., Birt-Hogg-Dubé

syndrome or Marfan syndrome) that may require further investigation for associated
abnormalities.
 ▪
All patients require advice on flying, scuba diving, and smoking cessation.
eFigure Image Gallery

eFigure 110.1
Chest computed tomography scan of a patient with lymphangioleiomyomatosis.
Note the numerous thin-walled cysts, rounded and relatively uniform in shape, and a pneumothorax
on the left.
Courtesy Dr. Lisete Teixeira, University of Sao Paulo, Brazil.
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Tension Pneumothorax

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Tension Pneumothorax

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Introduction

Pneumothorax, or air in the pleural space, is a common clinical problem. A

Primary Spontaneous Pneumothorax

Abnormal Lung Parenchyma and Smoking

Smoking is a well-known risk factor for pneumothorax. 20 , 49 Although the exact

Blebs and Bullae

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Although familial patterns of inheritance of spontaneous pneumothorax, particularly

It seems likely that minor mutations in FBN1 or FLCN could predispose to the

Secondary Spontaneous Pneumothorax

Common COPD, pulmonary tuberculosis

Diagnosis and Management

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Use of Ultrasound in Pneumothorax

Thoracic ultrasound can potentially be used to identify pneumothorax post–lung

In a recently reported randomized trial in moderate to large PSP, conservative

In contrast to PSP, in which observation or short-term treatment is encouraged as the

Initial Management Options

Study Year N Needle Aspiration Success Chest Tube Initial Success

† Chest tube with Heimlich valve.

‡ Includes traumatic (22/56).

§ Primary spontaneous pneumothorax data only.

Reexpansion Pulmonary Edema

Failure of Medical Management

Prolonged Air Leak

Chest Tube Size

Surgery is performed by video-assisted thoracoscopic surgery (VATS), which has

Recurrence Prevention After First Pneumothorax

Risk stratification based on high-resolution CT scan findings was proposed by Ouanes-

Patients Unfit for Surgery

A systematic review has compared efficacy of chemical pleurodesis agents in

Blood Patch Pleurodesis

Total Pleural Covering

Lifestyle advice on smoking cessation should be reinforced because continued smoking

A traumatic pneumothorax can result from either penetrating or nonpenetrating chest

Other common causes of iatrogenic pneumothorax (with approximate incidences) are

The management of patients with an iatrogenic pneumothorax secondary to positive-

Case series report an incidence of catamenial pneumothorax in 3–6% 45 of

Pneumothorax in a young woman should raise the possibility of catamenial

In primary spontaneous pneumothorax (PSP) a conservative approach with no drainage

Secondary spontaneous pneumothorax should be treated initially with chest tube

PSP may be the first manifestation of a systemic disease (e.g., Birt-Hogg-Dubé

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 Macduff A., Arnold A., Harvey J.: Management of spontaneous pneumothorax:

 Noppen M., Dekeukeleire T., Hanon S., et. al.: Fluorescein-enhanced

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 3. Melton L.J., Hepper N.G.G., Offord K.P.: Incidence of spontaneous

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 8. BintcliffeOJ , Hallifax R.J., Edey A., et. al.: Spontaneous pneumothorax:

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