Review Articles
Approach to Lung Biopsies
From Patients With Pneumothorax
Frank Schneider, MD; Rajmohan Murali, MD; Kristen L. Veraldi, MD, PhD; Henry D. Tazelaar, MD; Kevin O. Leslie, MD
Context.—Patients with pneumothorax occasionally
require limited lung resections to control persistent air
leaks. In some patients, especially smokers, histopathologic
findings suggest that a ruptured bulla or bleb caused the
pneumothorax. Other patients only exhibit histopathologic
changes related to the physical trauma of acute, and likely
occult recurrent, peripheral lung injury in the setting of
‘‘spontaneous,’’ or idiopathic, lung rupture. Sometimes,
pneumothorax occurs secondary to an underlying local-
ized or diffuse parenchymal lung disease. A comprehensive
description of the morphologic findings that may be seen in
these specimens will help the surgical pathologist distin-
guish patients with more common and indolent occur-
rences of pneumothorax from those requiring additional
workup or treatment.
Objective.—To develop a diagnostic approach for
surgical pathologists encountering lung specimens ob-
tained in the context of pneumothorax repair.
P neumothorax is defined as the presence of air in the
pleural cavity. Based on its underlying etiology,
pneumothorax may be divided into primary and secondary
types, the latter resulting from a variety of diseases (Table 1).
The pathogenesis, clinical features, and radiologic charac-
teristics of pneumothorax have been described extensively in
the literature, and interested readers are referred to the
sources cited in Table 1.
Pneumothorax is a condition of sudden onset that often
occurs in patients without a history of underlying lung
disease. Medical management of pneumothorax is the rule,
and surgical specimens are obtained infrequently. When
surgical biopsies are obtained, they may show blebs or
bullae, which are presumed to be antecedent lesions
Accepted for publication May 14, 2013.
From the Departments of Pathology (Dr Schneider) and Medicine
(Dr Veraldi), University of Pittsburgh Medical Center, Pittsburgh,
Pennsylvania; the Department of Pathology and the Human
Oncology and Pathogenesis Program Memorial Sloan-Kettering
Cancer Center, New York, New York (Dr Murali); and the
Department of Laboratory Medicine and Pathology, Mayo Clinic,
Scottsdale, Arizona (Drs Tazelaar and Leslie).
Drs Schneider and Murali contributed equally to this article.
The authors have no relevant financial interest in the products or
companies described in this article.
Reprints: Frank Schneider, MD, Department of Pathology, Univer-
sity of Pittsburgh Medical Center, 200 Lothrop St, Pittsburgh, PA
15213 (e-mail: schneiderf@upmc.edu).
Arch Pathol Lab Med—Vol 138, February 2014
Data Sources.—Literature review and consultation
experience of the authors.
Conclusions.—Two general categories of histopatholog-
ic changes can be identified: (1) nonspecific changes,
reflecting the lung’s acute and chronic response to
localized injury, and (2) changes suggesting an underlying
lung disease that may have played an etiologic role in the
development of pneumothorax. The latter changes are
important to recognize because they may require addi-
tional workup or treatment of clinically occult lung
disease. Difficulty arises when nonspecific histopathologic
changes overlap with those of an underlying lung disease.
Awareness of these diagnostic challenges and pitfalls,
together with clinicoradiographic correlation, is essential
in these situations and will help guide the surgical
pathologist toward an accurate diagnosis and the appro-
priate management of clinically occult disease.
(Arch Pathol Lab Med. 2014;138:257–265; doi: 10.5858/
arpa.2013-0091-RA)
resulting in the development of pneumothorax. A broad
spectrum of mainly nonspecific pathologic findings may also
be seen. On occasion, histopathologic changes will be
present that are more typical, and rarely pathognomonic, of
an underlying lung disease that is etiologically related to the
pneumothorax. Familiarity with the entire spectrum of
findings that may be seen in surgical biopsy specimens is
important to ensure accurate diagnosis, to avoid missing
histopathologic clues to the etiology of the pneumothorax,
and to distinguish pneumothorax-related changes from
other primary pathologies in the pleura and lung.
CLINICAL MANAGEMENT OF PNEUMOTHORAX
The treatment of pneumothorax ranges from observation
to surgical intervention, depending upon patient character-
istics and the pathogenesis of the pneumothorax. Selection
of the appropriate management option requires an under-
standing of the natural history of pneumothorax, the risk of
recurrence, and the relative risks and benefits of the various
treatment options. For comprehensive discussions of the
epidemiology, pathophysiology, and initial evaluation and
management of pneumothorax, the reader is referred to
several outstanding clinical reviews and guidelines.1–6 When
a pneumothorax is refractory to chest tube drainage, closure
of the air leak may require surgical intervention and a
procedure to produce pleural symphysis. Indications for
surgical intervention include second ipsilateral or first
contralateral occurrence of pneumothorax, synchronous
Pathology of Pneumothorax—Schneider et al 257
 Table 1. Etiologic Classification of Pneumothorax
Primary (unknown etiology)
Secondary
Trauma
Traumatic41,42
Esophageal rupture43
Iatrogenic—lung biopsy, pleural biopsy, or fine-needle
biopsy; mechanical ventilation; thoracotomy; placement
of subclavian vein catheter, chemotherapy44–50
Primary lung diseases
Asthma51
Respiratory bronchiolitis21
Cystic fibrosis52,53
Usual interstitial pneumonia54
Pulmonary infarction55,56
Hypersensitivity pneumonitis34–36,57
Infections—necrotizing cavitary lesions (tuberculosis,
coccidioidomycosis), Pneumocystis jirovecii
pneumonia, human immunodeficiency virus
infection58–64
Emphysema
Distal acinar
Bullae (emphysematous cystic spaces larger than 1
cm)7
Secondary to other causes such as a1-antitrypsin
deficiency65–67
Pleuropulmonary blastoma68,69
Malignant (particularly necrotizing cavitary) tumors—
primary and metastatic70,71
Pleural conditions
Pleural blebs7
Malignant (particularly necrotizing cavitary) tumors—
mesothelioma and metastases70,71
Systemic conditions that involve lung and pleura
Endometriosis (catamenial pneumothorax)72–74
Lymphangioleiomyomatosis75–77
Langerhans cell histiocytosis78,79
Connective tissue diseases—Ehlers-Danlos
syndrome,80,81 Marfan syndrome82–84
Sarcoidosis85–87
Birt-Hogg-Dubé syndrome88,89
bilateral spontaneous pneumothoraces, or failure of pneu-
mothorax to resolve after more than 5 to 7 days of tube
drainage (defined as persistent air leak or incomplete re-
expansion of the lung).5 Although there are no firm
evidence-based guidelines for the timing of operative
intervention, a thoracic surgical opinion should be part of
the early management (2–5 days) of patients with difficult
pneumothoraces. Patients with pneumothorax secondary to
underlying lung disease may tolerate even a small pneu-
mothorax poorly and may therefore require earlier surgical
intervention. A clinical management approach to pneumo-
thorax is outlined in Figure 1.
PATHOLOGIC ABNORMALITIES IN SPECIMENS
FROM PATIENTS WITH PNEUMOTHORAX
Surgical intervention in the setting of pneumothorax
usually yields one or more wedge resections of peripheral
lung. Depending on the extent and nature of any underlying
lung disease, resections from any lobe may be obtained, but
for spontaneous pneumothorax, the upper lobes are the
dominant sites of occurrence and the location from which
most surgical specimens are taken. If associated pleural
disease or pleuropulmonary adhesions are present, pleural
decortication samples may be submitted (which usually
include some underlying lung tissue). Although some
authors suggest that ruptured preexisting bullae are the
causes of all spontaneous pneumothoraces, others consider
258 Arch Pathol Lab Med—Vol 138, February 2014
recurrences after bullectomy as evidence that ruptured
bullae are not always the site of an air leak.7
Morphologic findings in resection specimens for pneu-
mothorax fall into 2 broad categories: (1) nonspecific
changes that can confidently be classified as acute or
chronic response to localized injury (eg, eosinophilic
pleuritis), and (2) changes suggesting an underlying lung
disease. The latter category causes most diagnostic difficulty.
When features are pathognomonic for an underlying
disease, its diagnosis is straightforward (eg, Langerhans cell
histiocytosis or carcinoma in a bulla). When features merely
raise the possibility of an underlying lung disease (eg,
fibroblastic foci raising the possibility of a diffuse fibrosing
lung disease), clinical and radiographic correlation are
essential for interpretation. If clinical and radiologic findings
argue against an underlying lung disease, caution is
advisable.
It is critical for pathologists to be aware of both the
nonspecific and the specific pathologic findings seen in
pneumothorax specimens in order to identify conditions
requiring additional treatment or follow-up. A stepwise
approach to surgical pathology specimens from patients
with pneumothorax is proposed in Figure 2. The main
branch points, discussed in the following paragraphs,
require the pathologist to decide whether observed changes
are diagnostic for a certain lung disease, or whether the
features seen fall into the range of nonspecific findings
associated with pneumothorax.
Nonspecific Findings
Several nonspecific histopathologic findings may be seen
in lung and pleural tissue samples from patients with
pneumothorax (Table 2). Some of these changes are reactive
and reflect responses to the injury produced by the
pneumothorax. Others are associated with diseases that
predispose to pneumothorax but have no direct etiologic
involvement in its development. Common nonspecific
changes include eosinophilic pleuritis (Figure 3, A) with
varying degrees of pleural fibrosis (Figure 3, B) and of
underlying parenchyma (Figure 3, C).8–13 Tissue eosinophilia
can appear exuberant and involve the underlying lung
parenchyma with prominent infiltration of vessel walls.10
The presence of numerous eosinophils should also prompt
consideration of infectious/parapneumonic etiologies, as
well as systemic inflammatory diseases associated with
pleuritis (eg, rheumatoid arthritis, systemic lupus erythe-
matosus, ankylosing spondylitis) or peripheral blood eosin-
ophilia (such as hypereosinophilic syndromes). Fibrosis can
present as inactive, collagen-rich scars (Figure 3, D) as well
as immature fibrosis manifested by fibroblastic foci (Figure
4, A) or organizing intra-alveolar polyps. Scarring tends to
be more extensive in patients with a history of recurrent
pneumothoraces. Some of these reactive changes can also
be reflected in pleural fluid samples.14,15
Specific Findings
When pneumothorax occurs as a complication of an
underlying lung disease, histopathologic features of the
underlying disease are not always present in surgical
biopsies. A comprehensive description of these diseases is
beyond the scope of this manuscript; the reader is referred
to the references in Table 1 for lung diseases associated with
pneumothorax.
The histopathologic features corresponding to the most
common cause of pneumothorax are bullae and blebs.7
Pathology of Pneumothorax—Schneider et al
Figure 1. Diagnostic approach to patients with pneumothorax. The clinical diagnosis of pneumothorax involves assessment of the degree of
respiratory compromise and making decisions about the timing and extent of intervention. Abbreviation: VATS, video-assisted thoracoscopic surgery.
Spontaneous pneumothorax usually occurs in young, thin
men, particularly smokers, who have no obvious underlying
lung diseases. In these patients, pneumothorax is presumed
to result from rupture of bullae and blebs. The risk of
spontaneous pneumothorax is correlated with amount and
duration of tobacco smoke exposure.16 Pathologic changes
induced by cigarette smoke in small airways might also lead
to localized emphysema with subsequent development of
blebs or bullae.17–21 Bullae and blebs are each distinctive
lesions, found in different anatomic locations. A pleural bleb
is defined as airspace within the pleura and separated from
pleural space and alveoli by a thin pleural membrane (Figure
4, B). These thin membranes rupture and lead to pneumo-
thorax. Bullae are typically located subpleurally and, unlike
blebs, usually indicate destruction of lung tissue.22 In most
cases the diagnosis of one or the other is straightforward. In
occasional cases, the distinction may be impossible and a
descriptive diagnosis necessary, with both lesions cited as
possible underlying disease. Giant cells, similar in appear-
ance to those seen in pneumatosis intestinalis, are, in our
experience, more commonly associated with blebs and
persistent interstitial air (Figure 4, C).23 Such reaction can
extend along the interlobular septa into the lung parenchy-
ma and must be distinguished from true granulomatous
disease. Interestingly, the development of recurrent pneu-
mothorax was correlated with the severity of respiratory
bronchiolitis in one study.21 However, presence of respira-
tory bronchiolitis does not necessarily mean that the patient
has respiratory bronchiolitis–interstitial lung disease.
If clinicians or radiologists have concerns for a preexisting
lung disease (eg, lymphangioleiomyomatosis [LAM]), pa-
thologists can look for specific features and render a
diagnosis with reasonable certainty. In the absence of a
history of underlying lung disease, pathologists nevertheless
should always consider the possibility of an underlying lung
disease, and search for features associated with the entities
in Table 1 in a systematic fashion.
Diagnostic Challenges and Common Pitfalls
Diagnostic difficulty may arise when a biopsy shows
pneumothorax-related histopathologic features that in an
Arch Pathol Lab Med—Vol 138, February 2014
alternate clinicoradiologic setting would be highly sugges-
tive of a specific lung disease. Correlation with the clinical
and radiologic features is crucial to ensure accurate
diagnosis and detection of comorbid conditions.
Fibroblastic Foci.—Fibroblastic foci can be found in a
subset of pneumothorax specimens and should not be
interpreted as being diagnostic of an idiopathic interstitial
pneumonia.24 It has been suggested that the presence of
fibroblastic foci defines a subset of pneumothoraces, mostly
affecting young, male smokers.25 Because fibroblastic foci
are common in smokers and other lung injuries, the authors
prefer to consider their presence a nonspecific finding
indicative of repair rather than a diagnostic feature of a
specific entity.26 Although pneumothorax specimens can be
severely scarred (and may even resemble end-stage lung
disease), a diagnosis of diffuse interstitial pneumonia should
not be rendered in this context if chest imaging does support
this hypothesis.
Thick Vessels.—Thickening of pulmonary vessels is a
common occurrence in areas of lung fibrosis. Alone, such
changes do not imply hemodynamic compromise, especially
if only veins are affected.27 Hemosiderin deposition and
increased capillary density in areas not involved by fibrosis
have been shown to predict pulmonary hypertension in
patients with idiopathic pulmonary fibrosis, but there are no
data to support a similar conclusion in other lung diseases or
in pneumothorax specimens.28
Inflammatory Cells in Vessel Walls.—Infiltration of
vessel walls by inflammatory cells, including eosinophils, is
a feature not only of primary systemic small vessel vasculitis
such as anti-neutrophil cytoplasmic antibody–associated
vasculitis or Goodpasture syndrome, but also of pneumo-
thorax and should not be overinterpreted.10 The presence of
alveolar hemorrhage with hemosiderosis, coexisting capil-
laritis, and a history of extrathoracic disease should prompt
the pathologist to suggest further serologic testing.
Smooth Muscle Nodules.—Small, often stellate, sub-
pleural smooth muscle nodules may be seen in pneumo-
thorax resections obtained from smokers.29 They must be
distinguished from the abnormal smooth muscle that occurs
in the walls of LAM cysts. Chest computed tomography is
Pathology of Pneumothorax—Schneider et al 259
Figure 2. Pathologists interpreting pneumothorax specimens should identify the (nonspecific) features expected in such samples, followed by a
search (both in the submitted tissue and by correlation with clinical and radiologic findings) for underlying lung disease or evidence of other potential
etiologies of the pneumothorax. Sampling error needs to be considered if clinical or radiographic features do not support the histopathologic changes
seen. Abbreviation: Ptx, pneumothorax.

helpful in this differential, as it will reveal diffuse cystic lung

Table 2. Nonspecific Histopathologic Features disease if the patient has LAM. When considering cyst-poor
Seen in Surgical Specimens From Patients LAM, patient sex may resolve the issue, as LAM is
With Pneumothoraxa extraordinarily rare in males.30 An appropriate immunohis-
Changes in pleura tochemical workup may be necessary to exclude LAM if
Eosinophilic pleuritis9,11 there is a strong clinical suspicion.31
Fibrinous exudate (can be therapy related90) Round Atelectasis.—Specimens showing atelectatic lung
Columnar, squamous, or mucous cell metaplasia of with apparent fibrosis and overlying pleural fibrosis,
pleura91–93
Mesothelial hyperplasia13 especially in patients with a history of pleural effusions,
Changes in lung should prompt consideration of round atelectasis.32 Al-
Subpleural fibrosis though round atelectasis carries no dire implications for the
Vasculopathy8 patient, its presence can explain a radiologically identified
Eosinophilic infiltration of vessels10 peripheral mass lesion. Sections typically show fibrotic
Arteriovenous malformation–like vascular lesion94
Fibroblastic foci25
pleura with deep invaginations of pleura into the pulmonary
Atelectasis parenchyma.
Fluid accumulation Infection.—Inflammation in pneumothorax specimens
Bronchiolar, alveolar, and mesothelial cell proliferation13 may be acute or chronic. Infection should be considered in
Exuberant type II pneumocyte hyperplasia95 specimens showing necrosis and neutrophilic microabscess-
Changes in pleura and lung
Eosinophilic pneumonia–like changes with eosinophilic
es. Histochemical stains may be helpful adjuncts to
pleuritis microbiology cultures in this setting.33 Chronic inflamma-
Chronic inflammation13 tion associated with pneumothorax can be rich in eosino-
Hemosiderin deposition phils, lymphocytes, or plasma cells. The composition of the
a
Specific histopathologic features often associated with disease inflammatory infiltrate is not specific for a certain disease. If
etiology are described in Table 1. a lymphoid inflammatory infiltrate is exuberant, care should
260 Arch Pathol Lab Med—Vol 138, February 2014 Pathology of Pneumothorax—Schneider et al
Figure 3. Histopathologic findings in patients with pneumothorax. The features illustrated here are nonspecific because the patients from whom
they were obtained had no underlying lung disease. A, Eosinophilic pleuritis, a common response to the pleura’s exposure to air. B, Pleural fibrosis, a
result of recurrent or long-standing injury, is a nonspecific finding that can also be seen in connective tissue diseases such as rheumatoid arthritis or
systemic lupus erythematosus. C, Fibrosis in a patient with a clinical history of pneumothorax. If histopathologic features overlap with those of
interstitial lung diseases, radiologic correlation is necessary to confirm their presence or absence. D, Fibrosis in the setting of pneumothorax can range
from absent or subtle (in recent or primary pneumothoraces) to extensive, mimicking a chronic fibrosing interstitial pneumonia (hematoxylin-eosin,
original magnifications 3200 [A], 320 [B and D], and 340 [C]).

be taken to exclude lymphoma. A preponderance of B
lymphocytes (outside of germinal centers) combined with
similar features in the underlying lung such as expansion of
the interstitium and ‘‘tracking’’ along lymphatic routes in
the interlobular septa are helpful clues to the diagnosis of
lymphoma. Additional workup of such specimens is
warranted.
Hypersensitivity Pneumonitis.—Hypersensitivity
pneumonitis has been associated with pneumothorax
primarily in the Japanese literature.34–36 A centrilobular
distribution of the interstitial inflammatory infiltrate, even in
the absence of nonnecrotizing granulomas, may enable the
pathologist to include hypersensitivity pneumonitis in the
differential diagnosis and prompt additional investigation.
Because radiologic features are often characteristic in the
setting of subacute hypersensitivity pneumonitis, clinico-
radiologic correlation is most helpful in resolving this
differential diagnosis.
Small Airway Fibrosis.—Constrictive (obliterative)
bronchiolitis has been associated with pneumothorax
Arch Pathol Lab Med—Vol 138, February 2014
following allogeneic bone marrow transplant.37,38 Although
data on patients without such transplants are limited, the
authors routinely look for bronchiolar findings that might
suggest this possibility.39 Due to the patchy nature of
constrictive bronchiolitis, a concomitant finding of air
trapping on chest computed tomograms, usually manifest-
ing as mosaic pattern of decreased attenuation, may help to
confirm the diagnosis.40
Pneumocyte Hyperplasia.—Exuberant pneumocyte hy-
perplasia is frequently related to localized atelectasis or
acute lung injury. In the setting of pneumothorax, atypical
pneumocyte hyperplasia may be so severe as to suggest
adenocarcinoma (Figure 4, D). The history of pneumotho-
rax, along with clinical and radiologic correlation, is
important in making the correct diagnosis.
DIAGNOSTIC TERMINOLOGY
When direct communication with clinicians and radiolo-
gists is not possible, the pathologist often has to extract
relevant information from clinical notes and radiology
Pathology of Pneumothorax—Schneider et al 261
Figure 4. Histopathologic findings in patients with pneumothorax. A, Fibroblast foci (arrows) are thought to be a reparative phenomenon in the
setting of pneumothorax and should not be reflexively interpreted as being diagnostic of usual interstitial pneumonia. B, Pleural bleb, defined as
airspace within the pleura, should be distinguished from subpleural bullae, which indicate destruction of lung tissue. C, Giant cells at the air-tissue
interface in a patient with intrapleural air. If such reaction extends into the lung parenchyma it must be distinguished from a granulomatous interstitial
pneumonia. D, Exuberant pneumocyte hyperplasia is uncommon but may raise suspicion for neoplastic disease. Absence of cytologic atypia is
helpful in recognizing the process as reactive (hematoxylin-eosin, original magnifications 3100 [A], 340 [B], and 3200 [C and D]).

reports. Table 3 lists a collection of terms frequently seen in
the context of the entities listed in Table 1. Such supporting
information may help the pathologist to render a more
specific diagnosis.
Surgical pathology reports in the setting of pneumothorax
are often descriptive. There is no single correct or superior
style. Below, we present a few examples of how these cases
are handled by the authors.
If all of the histopathologic findings fall into the
nonspecific category (see Table 2), and the clinical and
radiographic features are not suggestive of an underlying
lung disease, our diagnosis generally reads, ‘‘Features
consistent with pneumothorax.’’
If the histopathologic features are not specific but the
clinician suspects an underlying lung disease, we pay careful
attention to features associated with conditions listed in
Table 1. If these features are absent, we keep in mind that
the pneumothorax may have no etiologic association with
the underlying disease, and also consider sampling issues
(for example, diagnostic features of a lower lobe–predom-
262 Arch Pathol Lab Med—Vol 138, February 2014
inant usual interstitial pneumonia may not be present in the
resection of an upper lobe pleural bleb). If the radiology
report confirms the presence of a diffuse lung disease, we
tend to report the case descriptively with a diagnostic
comment outlining the limitations of the specimen.
If the histopathologic features suggest an underlying lung
disease, but clinical and/or radiologic correlation are
unavailable, we use generic terminology, for example,
‘‘Acute pleuroparenchymal changes consistent with history
of pneumothorax, superimposed on a chronic fibrosing
interstitial pneumonia. Please correlate with the clinical and
radiologic findings.’’ Such reports typically also include a
comment indicating what type of interstitial pneumonia is
most likely.
If diagnostic features of a specific entity are present and
supported by clinical and radiographic findings, the
pathologist should feel comfortable placing the disease into
a defined diagnostic category. Such a report, for example,
may read, ‘‘Usual interstitial pneumonia with superimposed
features of pneumothorax.’’
Pathology of Pneumothorax—Schneider et al
 Table 3. Commonly Encountered Terminology in Patients With Diffuse Lung Diseasea
96,97
Clinical symptom/sign or test
Antibodies (RF, ANA, SS-A, SS-B, anti-topoisomerase (Scl-70),
anti-centromere, Jo-1, PL-7, PL-12, EJ, OJ, Mi-2, Ku, SRP,
Smith, RNP, ANCA, anti-phospholipid)
Elevated angiotensin-converting enzyme level
’’Velcro’’-type crackles
Clubbing
Restrictive pattern pulmonary function tests (reduced VC,
increased FEV1/FVC ratio)
Obstructive pattern pulmonary function tests (decreased FEV1
and FEV1/FVC ratio)
Reduced diffusing capacity or increased PAO2 PaO2
Radiologic feature98
Reticular pattern
Traction bronchiectasis
Honeycomb change
Innumerable small nodules
Centrilobular nodules
Tree-in-bud pattern
Lymphangitic distribution
Basilar/lower zone distribution of disease
Peripheral/subpleural distribution of disease
Apical/upper zone distribution of disease
Cysts
Nodules/masses/consolidation
Wedge-shaped opacity
Abbreviations: ANA, anti-nuclear antibody; ANCA, anti-neutrophil cytoplasmic antibody; CF, cystic fibrosis; COPD, chronic obstructive pulmonary
disease; DAD, diffuse alveolar damage; DLCO, diffusing capacity for carbon monoxide; FEV1, forced expiratory volume in 1 second; FVC, forced vital
capacity; HP, hypersensitivity pneumonitis; NSIP, nonspecific interstitial pneumonia; PAO2
pulmonary Langerhans cell histiocytosis; RF, rheumatoid factor; RNP, ribonucleoprotein; SRP, signal recognition particle; UIP, usual interstitial
pneumonia; VC, vital capacity.
a
Pathologists often have limited access to clinical and radiographic information. In cases in which no specific question is posed, these findings may
indicate the presence of an underlying lung disease.
CONCLUSIONS
When evaluating pathologic specimens from patients with
pneumothorax, a multidisciplinary approach involving
discussions among pathologists, pulmonologists, and radi-
ologists and correlation of the pathologic findings with the
clinical and radiologic features is often extremely helpful in
arriving at the correct diagnosis. From the pathologist’s
perspective, it is important to confirm the pathologic
changes associated with the presence of pneumothorax
(Table 2), as well as to examine carefully the submitted
tissue for potential disease entities that might be associated
with the etiopathogenesis of the pneumothorax (Table 1).
Identification of the latter (which might be mild, patchy and/
or overshadowed by florid reactive nonspecific changes)
might prove to be critical in patient management, particu-
larly in cases in which the pneumothorax is the first
manifestation of the underlying disease process.
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