Spontaneous Pneumothorax Caused by

Pulmonary Blebs and Bullae in 12 Dogs

Spontaneous pneumothorax caused by pulmonary blebs and bullae was diagnosed in 12 dogs
based on history, clinical examination, thoracic radiographs, surgical findings, and histopathologi-
cal examination of resected pulmonary lesions. Radiographic evidence of blebs or bullae was
seen in only one dog. None of the dogs responded to conservative treatment with thoracocente-
sis or thoracostomy tube drainage. A median sternotomy approach was used to explore the tho-
rax in all dogs. Pulmonary blebs and bullae were resected with partial or complete lung
lobectomy. Ten of the dogs had more than one lesion, and seven of the dogs had bilateral
lesions. The cranial lung lobes were most commonly affected. Histopathology results of the blebs
and bullae were consistent in all dogs and resembled lesions found in humans with primary spon-
taneous pneumothorax. None of the dogs developed recurrence of pneumothorax. Median fol-
low-up time was 19 months. The outcome following resection of the pulmonary blebs and bullae
was excellent. J Am Anim Hosp Assoc 2003;39:435–445.

Victoria J. Lipscomb, MA, VetMB, Introduction

MRCVS, CertSAS, Diplomate ECVS
Robert J. Hardie, DVM,
Diplomate ACVS, Diplomate ECVS
Richard R. Dubielzig, DVM,
Diplomate ACVP
RS
From the Department of Small Animal
Medicine and Surgery (Lipscomb),
Royal Veterinary College,
University of London,
Hawkshead Lane, North Mymms,
Hertfordshire, AL9 7TA England
and the Departments of Surgical
Sciences (Hardie)
and Pathobiological Sciences (Dubielzig),
School of Veterinary Medicine,
University of Wisconsin,
2015 Linden Drive,
Madison, Wisconsin 53706.
Address all correspondence to Dr. Hardie.
JOURNAL of the American Animal Hospital Association
Spontaneous pneumothorax occurs when air or gas enters the pleural
space in the absence of a traumatic or iatrogenic cause.1-4 The most com-
mon source of air is the lung parenchyma; however, other sources include
the trachea, bronchi, and esophagus or gas-forming organisms within the
pleural cavity.1 Spontaneous pneumothorax can be further classified as
either primary or secondary based on the history, clinical signs, and
whether an underlying cause can be determined from diagnostic tests,
such as thoracic radiographs, thoracic computed tomography (CT), or
thoracoscopy.4-7 Reported causes of spontaneous pneumothorax in dogs
include bacterial pneumonia, pulmonary abscesses, dirofilariasis, pul-
monary neoplasia, bullous emphysema, and pulmonary blebs and bullae.8
Based on previous reports, the most common cause of spontaneous pneu-
mothorax is pulmonary blebs or bullae.2,3,7,9
Pulmonary blebs are accumulations of air within the layers of the vis-
ceral pleura, most commonly located at the lung apices [Figure 1].6
They form when air escapes from within the lung parenchyma and trav-
els to the surface of the lung and becomes trapped between the layers of
the visceral pleura.6 Grossly, blebs appear as small “bubbles” or “blister-
like” lesions on the surface of the lung that range in size up to several
centimeters in diameter.
In contrast, pulmonary bullae are air-filled spaces within the lung
parenchyma that result from the destruction, dilatation, and confluence
of adjacent alveoli.6 Bullae can vary in size, with some being small
(involving only a few alveoli) and others being very large (involving a
majority of the lung).10 Bullae are confined by the connective tissue
septa within the lung and the internal layer of the visceral pleura. Bullae
have been classified into three types based on the size and connection
with surrounding lung tissue [Figure 1].6 Type 1 bullae are thin, with
empty interiors and a small, narrow connection to the pulmonary
parenchyma. They are usually found at the apices of the lung and
have outer walls that may or may not be lined by mesothelial cells on the
435
436 JOURNAL of the American Animal Hospital Association September/October 2003, Vol. 39

Figure 1—Line drawings illustrating the apex of the lung (shaded box in top drawing) and a pulmonary bleb (A), type 1
bulla (B), type 2 bulla (C), and type 3 bulla (D). Note the accumulation of air between the layers of the visceral pleura in
the pulmonary bleb and the different connections to the underlying pulmonary parenchyma in B, C, and D.

external surface. Type 2 bullae arise from the subpleural the outer walls are formed by intact pleura lined by
parenchyma and are connected to the rest of pulmonary mesothelial cells. Type 3 bullae can be very large and may
parenchyma by a neck of emphysematous lung. The interior contain emphysematous lung tissue that extends deep into
of the bullae is filled with emphysematous lung tissue, and the pulmonary parenchyma.
September/October 2003, Vol. 39
Several reports have described the clinical findings from
dogs with spontaneous pneumothorax due to pulmonary
blebs, bullae, or bullous emphysema; however, differences
in lesion terminology, lesion description, and histopatholog-
ical interpretation have resulted in conflicting information
about pulmonary bleb and bulla lesions.2,3,7,9 In particular,
the terms bleb, bulla, and bullous emphysema have been
used interchangeably in some reports, making it difficult to
determine the specific lesion being described. Also, the
location and extent of the pulmonary lesions were not
always reported, making it unclear as to whether lesions
were focal, multifocal, or diffuse. Finally, differing inter-
pretations of the histopathological findings has resulted in
uncertainty as to whether pulmonary blebs and bullae
should be considered primary lesions or lesions that
develop secondary to some other underlying cause.
The purpose of this study is to describe the clinical
signs, radiographic findings, surgical treatment, postopera-
tive complications, histopathological findings, and long-
term outcome of 12 dogs with spontaneous pneumothorax
caused by focal pulmonary blebs and bullae. In addition,
the findings of this study are compared to those described
for humans with primary spontaneous pneumothorax due to
pulmonary blebs and bullae.
Materials and Methods
Case Material
The records of dogs diagnosed with spontaneous pneu-
mothorax caused by pulmonary blebs and bullae at the
Royal Veterinary College, University of London, between
May 1991 and September 2000 were reviewed. The signal-
ment, history, prior treatment, physical examination find-
ings, complete blood count (CBC) and serum biochemical
profile findings, initial management, radiographic findings,
surgical technique, histopathological findings, postoperative
complications, and long-term outcome were recorded. Any
dog with a history of trauma or underlying pulmonary dis-
ease, such as neoplasia or pneumonia, was excluded from
the study.
Initial Management
Physical examination, CBC, and serum biochemical profile
were performed on all dogs. Pneumothorax was treated ini-
tially with intermittent thoracocentesis or placement of a
thoracostomy tube. Serial lateral and dorsoventral radio-
graphs of the thorax were made after thoracic drainage.
Spontaneous pneumothorax was diagnosed if evidence of
trauma was excluded based on history, clinical signs, and
thoracic radiographs. The duration and outcome of initial
treatment with thoracocentesis or thoracostomy tube
drainage were recorded.
Surgical Technique
A median sternotomy was performed on all dogs, and the
lungs were inspected for lesions. If the source of leakage was
not readily identified, the thorax was filled with warm, sterile
saline and leaks were located during ventilation. All visible
Pulmonary Blebs and Bullae 437
lesions were removed by partial or complete lung lobectomy.
Partial lung lobectomies were performed by stapling the lung
parenchyma using an automatic stapling devicea and resect-
ing the lesion distal to the staple line. Complete lung lobec-
tomies were performed by double ligating the pulmonary
vasculature, staplinga the bronchus, and resecting the lung
distal to the staples. Staple lines were checked for leakage by
filling the thorax with warm, sterile saline and inflating the
lungs. A thoracostomy tube was placed, and the thorax was
closed with stainless steel wire placed around the sternebrae
in a cruciate pattern. The description and location of the
resected lesions were recorded.
Postoperative Management
The dogs were monitored after surgery, and intramuscular
morphine,b intrapleural bupivacaine,c or both were given as
required for analgesia. The thoracostomy tubes were aspi-
rated as necessary, and the time of removal was recorded.
The sternotomy incisions were monitored, and complica-
tions were recorded.
Long-Term Follow-up
Follow-up information was obtained by clinical examina-
tion or by telephone conversation with the owner. Details of
exercise tolerance and respiratory effort were recorded. If
the dog was no longer alive, the cause of death and time
since the surgery were recorded.
Histopathological Examination
The resected lung tissue was preserved in 10% formalin,
embedded in paraffin, sectioned, and stained with hema-
toxylin and eosin. Histopathological examination was per-
formed by the same pathologist (Dubielzig).
Results
Signalment and History
Twelve dogs were identified with spontaneous pneumotho-
rax caused by pulmonary blebs or bullae [Table 1]. Eight
dogs were purebreds, and four were mixed-breed dogs. All
dogs were either large breed or had deep-chested conforma-
tion. The median age was 7.5 years (range, 3.5 to 12 years),
and the median weight was 25 kg (range, 9.9 to 42 kg).
There were seven males and five females. Eleven of 12
dogs had a history of intermittent or progressive dyspnea
that was acute in onset for some dogs. Other clinical signs
included lethargy, anorexia, depression, coughing, and exer-
cise intolerance. Eight dogs were treated with thoracocente-
sis, and one dog was treated with thoracostomy tube
drainage prior to referral.
Physical Examination, Radiography, and Initial
Management
Physical examination revealed varying degrees of tachycar-
dia, tachypnea, increased respiratory effort, and respiratory
distress. Auscultation of the thorax revealed decreased lung
sounds on one or both sides. Complete blood count and
serum biochemical profile results were within reference
 438

Table 1

Signalment, History, Initial Management, Radiographic Findings, Surgery, Complications, and Long-Term Outcome in 12 Dogs
With Spontaneous Pneumothorax

Case Initial Radiographic Long-Term

No. Signalment* History Management Findings Surgery Complications Outcome

1 7-yr, 15-kg, M Dyspnea for Thoracostomy Bilateral Bilateral lesions. None Lost to follow-up after 2-mos
mixed-breed 3 weeks, tube for 48 hrs pneumothorax Partial right middle reexamination. No
dog managed by and complete left recurrence of clinical signs at
thoracocentesis cranial lung that time
lobectomy

2 7.5-yr, 35.4-kg, Intermittent Thoracostomy Left pneumothorax Bilateral lesions. None Died of hepatic disease after
FS Old English dyspnea for 9 tube for 48 hrs Partial right cranial 36 mos; no recurrence of
sheepdog days, managed by and complete left clinical signs
thoracocentesis cranial lung
JOURNAL of the American Animal Hospital Association

lobectomy

3 7-yr, 42-kg, MN Acute-onset Thoracocentesis Bilateral Bilateral lesions. Recurrent Died acutely after 36 mos
mixed-breed dyspnea, managed for 24 hrs pneumothorax; Partial right cranial, pneumothorax after (cause of death unknown); no
wolfhound by daily bulla in left caudal partial left caudal, surgery due to recurrence of clinical signs
thoracocentesis for lung lobe and complete leakage from a staple
7 days accessory lung line; treated by
lobectomy restapling the lung

4 6-yr, 9.9-kg, F Dyspnea and Thoracostomy Left pneumothorax Unilateral lesions. None Lost to follow-up immediately
mixed-breed exercise intolerance tube for 6 days and Complete left after surgery
dog for 6 weeks, pneumomediastinum cranial lung
managed by lobectomy
thoracostomy tube
for 10 days

5 9.75-yr, 31.5-kg, Acute-onset Thoracostomy Bilateral Unilateral lesions. Edema around incision; Died of gastroenteritis after
M standard dyspnea and tube with pneumothorax Complete left suture removal delayed 24 mos; no recurrence of
poodle coughing, managed continuous cranial lung clinical signs
by thoracocentesis suction applied lobectomy
and emergency for several hours,
referral continued
leakage,
emergency
sternotomy
(continued on next page)
September/October 2003, Vol. 39
 Table 1 (cont’d)

Signalment, History, Initial Management, Radiographic Findings, Surgery, Complications, and Long-Term Outcome in 12 Dogs
With Spontaneous Pneumothorax

Case Initial Radiographic Long-term

No. Signalment* History Management Findings Surgery Complications Outcome
September/October 2003, Vol. 39

6 6.5-yr, 22.5-kg, Dyspnea and Thoracostomy Bilateral Bilateral lesions. None Died of splenic
FS German exercise tube for 24 hrs pneumothorax Complete right hemangiosarcoma after 6 mos;
shepherd dog intolerance for 18 cranial and partial no recurrence of clinical signs
days, managed by left cranial lung
thoracocentesis lobectomy
7 10-yr, 28.4-kg, Acute-onset Thoracostomy Bilateral Unilateral lesions. None Died of neoplasia on digit after 8
M Laborador dyspnea, managed tube for 24 hrs pneumothorax Partial right cranial mos; no recurrence of clinical
retriever by thoracocentesis lung lobectomy signs
for 5 days

8 8.6-yr, 37.6-kg, Dyspnea and Thoracostomy Bilateral Unilateral lesion. Seroma around incision, Alive at 40 mos; no
FS German anorexia for 5 days tube for 4 days pneumothorax Complete right resolved over 10 days recurrence of clinical signs
shepherd dog cranial lung
lobectomy

9 3.5-yr, 12-kg, M Dyspnea for 3 weeks, Thoracostomy Left pneumothorax, Bilateral lesions. Edema with Alive at 22 mos; no recurrence of
whippet managed by tube for 3 days pneumomediastinum, Partial left cranial, serosanguineous clinical signs
thoracocentesis cervical/thoracic partial right cranial, discharge from incision,
subcutaneous and partial right resolved with bandaging
emphysema middle lung and antibiotics
lobectomy

10 3.5-yr, 38-kg, F Dyspnea for 3 weeks, Thoracostomy Bilateral Unilateral lesion. Seroma around incision, Alive at 16 mos; no recurrence of
Old English managed by tube for 5 days pneumothorax Partial right cranial resolved over 2 weeks clinical signs
sheepdog thoracocentesis lung lobectomy

11 9.6-yr, 16.7-kg, Poor oxygen Thoracocentesis Right pneumothorax Bilateral lesions. None Alive at 10 mos; no recurrence of
MN rough-coated saturation during for 3 days Partial right and left clinical signs
collie routine anesthesia cranial lung lobectomy

12 12-yr, 14-kg, M Acute-onset dyspnea Thoracostomy Bilateral Bilateral lesions. None Alive at 6 mos; no recurrence of
mixed-breed dog over 1 day tube for 2 days pneumothorax Partial right and left signs
cranial lung
lobectomy
Pulmonary Blebs and Bullae

* M=male; FS=female spayed; MN=male neutered; F=female

439
440 JOURNAL of the American Animal Hospital Association September/October 2003, Vol. 39

ranges. Radiographs of the thorax revealed bilateral pneu-

mothorax in eight dogs and unilateral pneumothorax in four
dogs [Table 1]. Two dogs had pneumomediastinum, and one
dog had subcutaneous emphysema over the cervical and tho-
racic areas. A 2-cm bulla was identified in the left caudal lung
lobe on dorsoventral radiographs in case no. 3. None of the
other dogs had pulmonary lesions identified on radiographs.
Initial treatment consisted of thoracostomy tube drainage
for 10 of the dogs and thoracocentesis for two dogs. For
case no. 3, thoracocentesis was performed as necessary, and
surgery was performed the following day. For case no. 5,
placement of a thoracostomy tube and the use of continuous
suction could not control the pneumothorax, and an emer-
gency median sternotomy was performed the day of admis-
sion. For the other 10 dogs, thoracostomy tubes were in
A
place for 1 to 5 days prior to surgery. Pneumothorax per-
sisted in all of the dogs despite conservative treatment with
either thoracocentesis or thoracostomy tube drainage.

Surgical Findings
Bleb and bulla lesions appeared as thin, focal, translucent,
“bubble-like” lesions on the apical margins of the affected
lung lobes in all dogs, varying in size up to several centime-
ters in diameter [Figure 2]. In some dogs, the bleb and bulla
lesions had a similar appearance, and it was not possible to
distinguish the differences between the lesions on gross
inspection. Ten of the 12 dogs had more than one lesion,
and seven of 12 had bilateral lesions [Table 1]. In all of the
dogs, one or both cranial lung lobes had lesions. The acces-
sory lung lobe and left caudal lung lobe (bulla identified on
radiographs) were also affected in case no. 3, and the right
middle lung lobe was also affected in case nos. 1 and 9. In
dogs with multiple lesions, not all were leaking at the time
of surgery. The rest of the lungs appeared grossly normal.
B
Postoperative Management and Complications Figures 2A, 2B—Intraoperative photographs of pulmonary
bullae on the apical margin of the right and left cranial lung
Pneumothorax occurred in the immediate postoperative lobes from case no. 12.
period in case no. 3 due to leakage from the staple line of a
partial lung lobectomy. A second surgery was performed to
restaple the lung, and the pneumothorax resolved. Thora- disruption of the superficial portion of the lesion during
costomy tubes were removed between 1 and 6 days after preservation made it difficult to accurately determine
surgery. A seroma developed at the sternotomy incision in whether the lesion was a bleb or bulla, although the sur-
four dogs. In three of the dogs, the seroma resolved without rounding changes were similar to those found in the other
any treatment. In the fourth dog (case no. 9), the incision bleb and bulla lesions. Five dogs (case nos. 1, 2, 6, 11, 12)
was bandaged and antibiotic therapy was continued for 2 had bullae that most closely resembled the type 1 classifica-
weeks before resolution. There were no recurrences of tion, and two dogs (case nos. 5, 10) had bullae that resem-
pneumothorax due to pulmonary blebs or bullae in the bled the type 2 classification. The focal changes
immediate postoperative period. surrounding the bleb and bulla lesions included dilated
alveoli and peripheral emphysema, smooth-muscle hyper-
Histopathological Findings trophy surrounding the respiratory ducts, mild to moderate
Histopathological examination was performed on represen- perivascular lymphoplasmacytic inflammation, chronic col-
tative samples of resected lung tissue from all dogs except lapse of adjacent parenchyma, and black foreign particulate
case nos. 3 and 7 [Table 2]. Histopathological findings of matter. No underlying cause for the lesions was identified
the pulmonary lesions were similar in all dogs. Focal bleb in any dog, although smooth-muscle hypertrophy was sug-
lesions were identified in two dogs (case nos. 8, 10) [Figure gestive of a chronic change. The foreign particulate mate-
3], focal bulla lesions were identified in six dogs (case nos. rial present in the lungs was most likely carbon from
1, 5, 6, 10-12) [Figure 4], and multiple bullae were identi- inhaled smoke or other pollutants in the environment,
fied in one dog (case no. 2). In two dogs (case nos. 4, 9), which is often seen in the lungs of normal dogs.
September/October 2003, Vol. 39
Figure 3—Photomicrograph of a pulmonary bleb from case
no. 8. Air has accumulated between the layers of the vis-
ceral pleura. There is marked pleural thickening but note the
lack of an epithelial lining, and there is no indication of a
connection between the air-filled space and the pulmonary
parenchyma. There is peripheral emphysematous change
and muscular hypertrophy around the respiratory ducts
(Hematoxylin and eosin stain, 200×).
Long-term Outcome
Long-term information was available from 10 of the dogs
[Table 1]. Five dogs were still alive at the time of writing,
with no recurrence of pneumothorax 6, 10, 16, 22, and 40
months after surgery. Four dogs died from unrelated prob-
lems, with no recurrence of pneumothorax 6, 8, 24, and 36
months after surgery. One dog (case no. 3) collapsed and
died suddenly 36 months after surgery. The cause of death
was unknown; however, signs of pneumothorax had not
been reported previously. Information was not available for
two dogs 1 week and 2 months after surgery. The median
follow-up time for the 10 dogs with long-term information
was 19 months (range, 6 to 40 months).
Figure 4—Photomicrograph of a pulmonary bulla from case
no. 1. Note the connection between the bulla and the under-
lying lung parenchyma and the presence of an epithelial lin-
ing. There is marked peripheral emphysematous change
and focal atelectasis. There is muscular hypertrophy around
respiratory ducts and a moderate amount of particulate for-
eign material around the bronchioles (Hematoxylin and
eosin stain, 20×).
Pulmonary Blebs and Bullae 441
Discussion
Diagnosis and treatment of spontaneous pneumothorax
caused by pulmonary blebs and bullae in dogs can be par-
ticularly challenging since the source of air leakage is not
usually evident from the history, clinical examination, or
thoracic radiographs.2,3,7,9 Understanding the typical clini-
cal signs, radiographic findings or lack thereof, response to
conservative and surgical treatment, and gross and
histopathological characteristics is essential for making the
diagnosis and providing appropriate treatment. In addition,
understanding how bleb and bulla lesions in dogs compare
to those found in humans is necessary so that diagnostic
and treatment strategies developed for humans can be
applied appropriately to dogs.
Based on the results of this study, pulmonary blebs or
bullae are found most often in healthy, middle-aged, large-
breed or deep-chested dogs that have no previous history of
respiratory problems or lung disease. The most common
clinical signs include lethargy, anorexia, depression, cough-
ing, tachypnea, exercise intolerance, increased respiratory
effort, and various degrees of respiratory distress. For some
dogs, respiratory signs may develop rapidly and be very
obvious, whereas for other dogs, initial clinical signs may
be very nonspecific and respiratory signs may not develop
until the pneumothorax progresses over days.
Initial treatment should focus on stabilizing the dog with
strict rest, oxygen supplementation, and thoracic drainage.
Thoracocentesis should be performed as often as necessary
to maintain adequate respiration. For dogs with more rapid
accumulation of air, a thoracostomy tube should be placed
to allow more frequent drainage of the thorax or the use of
continuous suction.
Definitive diagnosis of pulmonary blebs and bullae can
be difficult since the lesions are not usually apparent on
thoracic radiographs.2,7 Due to their relatively small size
and location on the margins of the lungs, most blebs and
bullae are not usually seen unless they become very large or
develop thickened walls. Nevertheless, serial thoracic radio-
graphs should be taken to identify other potential causes of
pneumothorax such as pulmonary neoplasia, abscesses, or
dirofilariasis.2,7,8 In this study, all of the dogs had various
degrees of unilateral or bilateral pneumothorax, and in only
one dog (case no. 3) was a bulla identified on radiographs.
The bulla was located in the left caudal lung lobe; however,
at surgery, additional bullae were discovered on other lung
lobes. The use of thoracic computed tomography (CT) or
thoracoscopy for the diagnosis of pulmonary blebs and bul-
lae has not been reported in a series of dogs; however, their
use warrants investigation and may prove more accurate
than radiographs for identifying small pulmonary lesions.
Other diagnostic tests, such as a CBC and serum biochemi-
cal profile, are not usually helpful for determining the cause
of pneumothorax, although they may identify other concur-
rent problems.3,9
Conservative treatment with thoracocentesis or thoracos-
tomy tube drainage was not effective in resolving the pneu-
mothorax in any of the dogs in this study. Pneumothorax
 442

Table 2

Histopathological Findings in 12 Dogs With Pulmonary Blebs or Bullae

Case No. Histopathological Findings From Various Representative Lesions Submitted for Examination

1 Bulla (type 1). Peripheral emphysematous change. Extensive atelectasis and moderate muscular hypertrophy around airways. Moderate
particulate foreign material surrounding bronchioles. Dilated, blood-filled vascular anomaly of unknown significance.

2 Bullae (type 1). Extensive peripheral emphysematous change. Minimal perivascular lymphocytic inflammation. Marked central atelectasis and
prominent muscular hypertrophy around airways. Moderate particulate foreign material surrounding bronchioles.

3 No histopathology obtained.

4 Mild peripheral emphysematous change. Extensive atelectasis and mild muscular hypertrophy around airways. Abundant particulate foreign material.
Superficial portion of bulla or bleb not included in section.

5 Bulla (type 2) with low cuboidal epithelial lining and multifocal smooth muscle indicating continuity with respiratory ducts. Moderate peripheral
emphysematous change. Marked atelectasis. Moderate particulate foreign material surrounding bronchioles. Moderate peribronchiolar
JOURNAL of the American Animal Hospital Association

lymphoplasmacytic inflammatory infiltrate and inspissated mucinous secretion seen in some airways.

6 Bulla (type 1) with low cuboidal epithelial lining and multifocal smooth muscle indicating continuity with respiratory ducts. Marked peripheral
emphysematous change. Pleural thickening. Prominent atelectasis and muscular hypertrophy around airways. Moderate particulate foreign material
surrounding bronchioles.

7 No histopathology obtained.

8 Bleb dissecting within the pleural capsule. Extensive peripheral emphysematous change. Extensive central atelectasis and prominent smooth
muscle hypertrophy around airways. Moderate particulate foreign material surrounding bronchioles.

9 Extensive peripheral emphysematous change. Minimal perivascular lymphocytic inflammation. Small number of peripheral lung foci with lymphocytic
infiltrate and interstitial fibrosis. Marked central atelectasis and minimal muscular hypertrophy around airways. Small amount of particulate foreign
material surrounding bronchioles. Superficial portion of bulla or bleb not included in section.

10 Bulla (type 2) and bleb. Marked peripheral emphysematous change. Marked pleural capsule fibrosis and intermittent interstitial fibrosis.
Multifocal areas of extensive atelectasis. Slight amount of particulate foreign material surrounding bronchioles.

11 Bulla (type 1) with low cuboidal epithelial lining and multifocal smooth muscle indicating continuity with respiratory ducts. Extensive peripheral
emphysematous change. Increased perivascular lymphoplasmacytic inflammation with inspissated mucous secretions in some bronchi. Prominent
muscular hypertrophy around airways and central atelectasis. Increased particulate foreign material surrounding bronchioles.

12 Bulla (type 1) with low cuboidal epithelial lining and multifocal smooth muscle indicating continuity with respiratory ducts. Extensive peripheral
emphysematous change. Moderate muscular hypertrophy around airways and extensive central atelectasis. Moderate particulate foreign material
surrounding bronchioles.
September/October 2003, Vol. 39
September/October 2003, Vol. 39
persisted in all of the dogs, despite 1 to 5 days of conserva-
tive treatment. Similar results were also found in two previ-
ous studies where pneumothorax persisted or recurred in
eight of 11 (73%) and seven of eight (88%) dogs with con-
firmed or presumed blebs and bullae after treatment with
thoracocentesis or thoracostomy tube drainage.2,7 Based on
these results, conservative treatment should not be consid-
ered a reliable means of treating pneumothorax caused by
pulmonary blebs and bullae in dogs, and surgical treatment
should be pursued once other obvious causes of pneumo-
thorax have been ruled out. For dogs in which surgical
treatment is not an option, prolonged conservative treatment
may eventually resolve the pneumothorax; however, this
possibility must be balanced against the extended hospital-
ization time and potential complications associated with
repeated thoracocentesis or thoracostomy tube drainage.
Ultimately, the decision regarding how long to pursue con-
servative treatment should be based on the severity of clini-
cal signs, the rate of air accumulation, the ability to rule out
underlying lung disease, and the availability of appropriate
surgical expertise and postoperative care.
Definitive treatment for dogs involves resecting the pul-
monary blebs and bullae with a partial or complete lung
lobectomy. A median sternotomy approach is recommended
so that the entire thorax can be explored. Lesions may be
present on multiple lung lobes, so each lobe should be thor-
oughly examined. Bleb and bulla lesions typically appear as
focal, translucent, “bubble-like” lesions on the apices of the
lungs, although they may be located anywhere within the
lung. Blebs and type 1 and 2 bullae may look very similar
depending upon their size and location, and in most cases it
is not possible to distinguish the difference between the
lesions on gross inspection.6 The size, number, and location
of the lesions on each lobe will determine the amount of
lung tissue that needs to be removed. For dogs with lesions
involving multiple lobes, it may not be possible to com-
pletely resect all of the lesions without significantly reduc-
ing lung capacity. For these dogs, other treatments that
preserve lung capacity such as mechanical or chemical pleu-
rodesis may be of benefit; however, these treatments have
had limited success in creating pleural adhesions in experi-
mental studies, and their use for the treatment of pneumo-
thorax due to blebs and bullae has not been reported.
The use of an automatic stapling device is recommended
for partial lung lobectomy, because it is faster and results in
fewer complications compared to conventional suturing
techniques.11 In this study, one dog (case no. 3) experi-
enced leakage of air from a staple line after partial lobec-
tomy. The precise reason for the leakage was not
determined, although it was most likely due to staples fail-
ing to engage tissue properly.11 Other treatments such as
mechanical and chemical pleurodesis have been described
in dogs in both experimental studies and in a small number
of clinical cases. However, these treatments have had lim-
ited success in creating pleural adhesions, and their use for
the specific treatment of pneumothorax due to blebs and
bullae requires further investigation.12,13
Pulmonary Blebs and Bullae 443
Results of surgical treatment were considered excellent
for the dogs in this study. None of the dogs developed
signs of recurrent pneumothorax due to blebs or bullae in
the follow-up period. For the one dog (case no. 3) that col-
lapsed and died suddenly 36 months after surgery, the
cause of death was not determined; however, sudden death
without prior respiratory signs would not be typical for
recurrent pneumothorax due to pulmonary blebs or bullae.
Unfortunately, necropsies were not performed on any of
the dogs, so the condition of the lungs at the time of death
was not known.
In humans, spontaneous pneumothorax due to pul-
monary blebs and bullae is typically classified as primary
spontaneous pneumothorax.4,14,15 It occurs most com-
monly in young men, between 20 and 40 years of age, who
have no previous history of lung disease.6,14,16 In contrast
to dogs, the pneumothorax in humans is typically unilateral
and does not usually progress or result in immediate respi-
ratory compromise.4,16 Clinical signs include chest pain,
tachypnea, and dyspnea, although some patients may be
asymptomatic or only mildly affected.4,14 As is often the
case with dogs, thoracic radiographs in humans usually do
not reveal any underlying pulmonary disease as a cause of
the pneumothorax, although rarely bulla lesions may be
detected.14,15 In cases where thoracic CT has been per-
formed, blebs or bullae have been identified on the margins
of the lungs and have been described as emphysema-like
changes.15,17
Treatment for humans with primary spontaneous pneu-
mothorax caused by blebs or bullae is typically conserva-
tive, involving strict rest and, if necessary, thoracic drainage
with thoracocentesis or, less commonly, a thoracostomy
tube.14,15,18 In contrast to dogs, conservative treatment in
humans is generally successful, with minimal morbidity
and recurrence rates ranging between 16% and
52%.14,15,18,19 The reason for the improved results with
conservative treatment in humans compared to dogs is not
known; however, it may be related to differences in the
thrombolytic and fibrinolytic systems that ultimately lead to
adhesion formation and the sealing of bleb or bulla
lesions.12
For humans that do not respond to conservative treat-
ment, conventional surgical treatment is performed by
resecting pulmonary blebs and bullae through a thoracot-
omy incision.15,18 In humans, the average recurrence rate
for pneumothorax after conventional surgical treatment is
1.5%.14,15 More recently, the use of minimally invasive,
video-assisted thoracoscopic techniques has been described
for resection of pulmonary lesions.14,15,20 The average
recurrence rate for video-assisted thoracoscopy techniques
is slightly higher (4%), but complication rates and surgical
times are reduced.15 Other forms of treatment that have
been described for bleb and bulla lesions include chemical
pleurodesis, mechanical pleurodesis, and partial pleurec-
tomy, with recurrence rates ranging from 8% to 25%.15,18
The bulla lesions from the dogs in this study most closely
resembled the type 1 and type 2 bullae described in Figure
444 JOURNAL of the American Animal Hospital Association
1.6 Histopathological examination revealed a consistent pat-
tern of focal abnormalities, including subpleural emphysema,
atelectasis, muscular hypertrophy of the respiratory ducts,
increased foreign particulate matter, and varying degrees of
inflammation. Similarly, bleb and bulla lesions from humans
with primary spontaneous pneumothorax exhibit consistent
focal changes, including emphysema, atelectasis, chronic
inflammation, fibrosis, increased particulate foreign material,
bronchial lesions, and vascular changes, with the remainder
of the lungs appearing macroscopically normal.21-23 It is not
clear whether the muscular hypertrophy found surrounding
the respiratory ducts in the dogs was the cause or result of
bleb and bullae formation; however, it does suggest a chronic
change and indicates that the lesions may exist for some time
before clinical signs develop. In addition, the fact that no
obvious cause for the lesions was identified in these sections
supports the idea that focal blebs and bullae represent a dis-
tinct or “primary” disease in dogs and that they are not the
result of some other disease process.
Previous veterinary reports have suggested that there are
marked differences between the histopathological findings
from bleb and bulla lesions in dogs compared to those
found in humans with primary spontaneous pneumotho-
rax.2,7,9 These comments were based on the idea that bleb
and bulla lesions in humans had no associated pathological
changes and that the pathological changes associated with
the bleb and bulla lesions in dogs represented significant
underlying disease such as diffuse emphysema.2,7,9 These
findings were not substantiated in the authors’ study, and
the histopathological findings from these dogs clearly illus-
trate the similarities with bleb and bulla lesions observed in
humans with primary spontaneous pneumothorax.21-23
The pathogenesis of pulmonary bleb and bulla lesions in
both dogs and humans is not completely understood; how-
ever, the histopathological similarities between species may
suggest a similar pathogenesis. In humans, one theory sug-
gests that increased distensile forces generated at the apices
of the lungs in tall individuals are responsible for bleb and
bulla formation.24 Increases in transpulmonary pressure
resulting from changes in atmospheric pressure have also
been implicated as a potential cause for formation and rup-
ture of pulmonary bleb and bulla lesions.25 Cigarette smok-
ing has been determined to be a significant risk factor for
developing pulmonary bleb and bulla lesions in humans, due
to its effect on degradative enzymes in the alveoli and
increased inflammation in the lower airways.16 One study
revealed a 22-fold increase in relative risk for developing
pneumothorax in male smokers and a nine-fold increase in
relative risk in female smokers.16 Alpha-1 antitrypsin may
be inactivated by smoking, creating a focal imbalance
between elastase and alpha-1 antitrypsin. This results in
increased elastase-induced degradation of elastic fibers and
progressive destruction of pulmonary parenchyma.26 Smok-
ing also increases the number of macrophages and neu-
trophils in the distal airways. This influx of inflammatory
cells may create a partial obstruction that acts as a “check-
valve” leading to increased pressures in the distal air spaces,
September/October 2003, Vol. 39
hyperinflation of alveoli, and eventual bulla formation.4
Influx of inflammatory cells has also been associated with
bronchiolitis, bronchiolar wall fibrosis, and destruction of
pulmonary parenchyma leading to the formation of emphy-
sematous-like changes.27 Bronchoalveolar lavage in humans
with primary spontaneous pneumothorax has shown a close
relationship between the total cell count, especially
macrophages, and the extent of emphysematous-like
changes seen on CT.28 Another theory suggests that there
may be anatomical differences in the lower airways that pre-
dispose humans who have never smoked to spontaneous
pneumothorax. A significant number of bilateral airway
anomalies, including abnormal airway branching, smaller
diameter airways, and accessory airways, have been identi-
fied with bronchoscopy in humans having spontaneous
pneumothorax.29
In addition to the many theories regarding the formation
of bleb and bulla lesions, the actual source of pneumotho-
rax and the mechanism of leakage from the bleb and bulla
lesions are also debatable.22 It is generally accepted that
rupture of a bleb or bulla lesion is the cause of pneumotho-
rax.4,18 However, the potential for leakage of air through
the wall of a bulla, without actual rupture, has been sug-
gested by a study that examined the interior and exterior
surfaces of type 1 to 3 bullae using scanning electron
microscopy.22 A marked absence of mesothelial cells on the
external surface of type 1 bullae was found, supporting the
theory that air may diffuse between mesothelial cells and
that integrity of the mesothelial cell layer may play an
important role in the pathogenesis of spontaneous pneu-
mothorax.22
Further investigation into the anatomical, biochemical,
inflammatory, and epidemiological aspects of spontaneous
pneumothorax in dogs is needed. Prospective examination
of the histopathology of multiple areas of grossly normal
and abnormal lung is necessary to further define the origin
and distribution of the lesions. Analysis of degradative
enzymes present in the lung parenchyma may help deter-
mine if an imbalance exists that may be responsible for pro-
gressive weakening of the alveolar wall and bulla
formation, as has been suggested in humans. Analysis of
bronchoalveolar lavage samples from affected and unaf-
fected lobes may help determine if inflammation of the dis-
tal airways is present that may potentially contribute to a
partial obstruction and the “check-valve” effect. Also, epi-
demiological evaluation of potential risk factors such as
“second-hand” smoke in the environment or chest height-
to-width ratios may help identify dogs at risk for develop-
ing spontaneous pneumothorax.
Conclusion
Pulmonary blebs and bullae are the most common cause of
spontaneous pneumothorax in dogs. The lesions should be
suspected in any dog with spontaneous pneumothorax when
no other obvious source of air leakage can be identified
from the history, clinical examination, or thoracic radio-
graphs. Affected dogs are typically healthy, middle-aged,
September/October 2003, Vol. 39
large breeds or have deep-chested conformation, with no
previous history of lung disease. Clinical signs include vari-
ous degrees of respiratory distress that may progress over
several hours to days. Bleb and bulla lesions are not usually
evident on thoracic radiographs; however, the use of CT or
possibly diagnostic thoracoscopy may be more helpful for
detecting small pulmonary lesions. Persistence of pneu-
mothorax is common after treatment with thoracocentesis
or thoracostomy drainage. Surgical treatment involves par-
tial or complete lung lobectomy. A median sternotomy
approach is recommended to allow thorough examination
of all the lungs. Multiple lesions are common and are usu-
ally located on the apices of the cranial lung lobes.
Histopathological findings are similar to those found in
humans with primary spontaneous pneumothorax. Although
the pathogenesis of bleb and bulla lesions is still not com-
pletely understood, the long-term outcome appears to be
excellent after surgical resection of pulmonary lesions.
a Proximate Linear Cutter, 30-mm stapler; Ethicon Endosurgery, Inc.,
Edinburgh, Scotland
b Numorph; Evans Medical Ltd, Slough, Berkshire, England
c Marcaine; Astra Pharmaceuticals Ltd, Kings Langley, England
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