Keywords
Asthma - pneumomediastinum - spontaneous pneumothorax - subcutaneous emphysema
Introduction
Subcutaneous emphysema, pneumothorax, and pneumomediastinum are usually a consequence
of thoracic and cervical blunt trauma, esophageal perforation (Boerhaave syndrome),
or are iatrogenic in nature. Causes include assisted positive pressure ventilation,
interstitial lung disease, and perforation of a hollow abdominal viscus with subsequent
dissection of air into the mediastinum using the diaphragmatic hiatus and dental procedures
as well as several diseases. It can also spontaneously occur because of cocaine inhalation,
vomiting and forceful straining, such as in childbirth or strenuous exercise.[[1]],[[2]],[[3]] However, simultaneous subcutaneous emphysema, pneumothorax, and pneumomediastinum
are complications rarely observed synchronously during an acute asthma attack. This
case illustrates an unusual sudden complication of an asthmatic attack.
Case Study
A 67-year-old woman, with a past medical history of bronchial asthma, was admitted
to our emergency department with pleuritic chest pain, dysphagia, and odynophagia,
followed by progressive swelling of her upper chest, neck, and face, which began 2
h prior to admission. She previously had consulted her general physician with a history
of malaise, violent dry cough, and wheezing for 3 days, for which she had received
treatment with inhaled albuterol and oral prednisone. She had no current history of
trauma or foreign body aspiration. She denied any lip or tongue swelling, difficulties
swallowing saliva, or retching, prior to presentation. She did not smoke, and her
family history was not remarkable.
On physical examination, she was not in acute distress. Vital signs revealed a temperature
of 99.3°F (37.4°C), blood pressure of 115/67 mmHg, the pulse was 92 beats per minute,
regular, respirations were 21 breaths per minute, and her arterial blood oxygen saturation
was 91% on room air. Examination of the neck and chest revealed symmetrical swelling
with crepitations on palpation consistent with subcutaneous emphysema. In the auscultation
of the lungs, reduced respiratory sounds were observed in both hemithoraces with expiratory
and inspiratory wheeze. The remainder of the physical examination was unremarkable.
The patient’s history and physical findings were consistent with subcutaneous emphysema.
Treatment with oxygen therapy was started.
Laboratory tests revealed 18800/mm3 leukocytes, a hematocrit of 39%, and a platelet count of 207000/mm 3. C-reactive
protein was 3 mg/l. Liver and kidney function tests, and serum electrolytes were all
within normal limits. The arterial blood gas analysis (breathing room air) showed
pH 7.49, hypoxemia (PaO2 58 mmHg), hypocapnia (PaCO2 31 mmHg), and HCO3 28 mmol/l.
A 12-lead electrocardiogram showed a sinus rhythm with 95 beats per minute. On chest
and neck radiograph, we observed a subcutaneous emphysema [[Figure 1]]. She was subsequently put on antibiotics, analgesia, and low molecular weight heparin
for prevention of venous thromboembolism. The patient was admitted to our thoracic
surgery department. The diagnosis of pneumothorax and pneumomediastinum were established
according to the chest computed tomography scan findings. Computerized tomography
scan of the neck and chest revealed moderate sized pneumothorax on the left side,
extensive pneumomediastinum, and soft tissue emphysema in the neck and chest [[Figure 2]].
Figure 1: Chest X-ray on the day of admission showing vast subcutaneous emphysema. Pneumothorax
and pneumomediastinum are obscured by the extensive subcutaneous air.
Figure 2: Chest computed tomography scans showing subcutaneous emphysema, pneumomediastinum
(yellow arrows), and pneumothorax on the left side (red arrow)
The patient evolved favorably after oxygen therapy, antibiotic prophylaxis, and conventional
medical treatment. Seven days later, subcutaneous emphysema had almost resolved spontaneously
on the follow-up chest X-ray [[Figure 3]].
Figure 3: Chest X-ray showing significant resolution of subcutaneous emphysema after 7 days
Discussion
This case illustrates an unusual sudden complication of an asthmatic attack. In our
patient, subcutaneous emphysema, pneumothorax, and pneumomediastinum were likely caused
by what we believed to be a complication after a coughing attack. Simultaneous subcutaneous
emphysema, pneumothorax, and pneumomediastinum are complications rarely observed synchronously
during an acute asthma attack. Although spontaneous pneumothorax has already been
reported in asthma patients in the literature, its concurrence with subcutaneous emphysema
and pneumomediastinum is extremely rare except for iatrogenic conditions, with only
one case reported.[[4]]
The relationship between asthma and pneumothorax is not widely known. Making a differential
diagnosis between pneumothorax and asthma is usually hard. Both asthma and tension
pneumothorax are manifested by tachycardia, tachypnea, respiratory distress, desaturation
and decreased air entry, causing difficulty to perform a differential diagnosis. Therefore,
the diagnosis of pneumothorax in asthmatic patients may often be delayed or missed.
Consequently, it is important to carefully monitor these patients. There is a 1.2%
probability of pneumothorax in an asthma exacerbation.[[5]] Although pneumomediastinum prognosis is usually excellent with conservative treatment,
its concurrence with complications such as pneumothorax may prove fatal during a severe
asthma attack. In asthma exacerbations, pneumothorax and pneumomediastinum develop
because the obstruction in the minor airways leads to air-trapping and barotrauma
of distal airways, and the subsequent alveolar rupture. The abrupt increase in intra-alveolar
pressure is a phenomenon known as the Macklin effect.[[6]] Negative pressure generated between the pulmonary interstitium and the mediastinum
explains the occurrence of pneumomediastinum.[[2]] Subcutaneous emphysema is caused by increased intra-alveolar pressure with an extrapleural
outflow of air.[[2]] The escape of air out of the alveolar spaces into the interstitial tissues around
the pulmonary vasculature travels back toward the hilum, leading to pneumomediastinum,
and this eventually tracts into the soft tissue of the neck, face, and chest wall.
The clinical symptoms of pneumothorax and/or subcutaneous emphysema critically depend
on the amount of extravasated gas and the extension of the affected areas. Most frequently,
they include chest pain, dyspnea, dysphonia, and dysphagia.[[2]],[[3]] Massive accumulation of air in the subcutaneous tissue, when associated to tension
pneumothorax, may also compromise the life of the patient, causing acute respiratory
distress syndrome.[[7]] Whereas subcutaneous emphysema causes swelling and crepitus over the involved anatomical
site, pneumomediastinum characteristically gives a positive Hamman’s sign (crunching
or clicking noise heard synchronously with the heartbeat on auscultation, in left
lateral decubitus position) when it is clinically significant.[[8]] It is not only found in Hamman’s syndrome and spontaneous pneumomediastinum but
also in patients with pneumothorax.
Conventional chest X-ray is the first investigation performed to assess pneumothorax
because it is simple, rapid, and noninvasive; however, non-contrast computed tomography
of the chest is more sensitive in detecting small amounts of gas.[[9]]
Subcutaneous emphysema, pneumothorax, and pneumomediastinum secondary to cough or
Valsalva maneuver are considered benign conditions and amenable to conservative management.[[10]] Subcutaneous emphysema is usually a benign, self-limiting condition only requiring
conservative management. Indications of observation as an initial management for pneumothorax
remain controversial. Management depends on the clinical setting, etiology, and size
of the pneumothorax, and whether it is open or closed, and simple or tension pneumothorax.[[11]] There are two main tasks in the treatment of pneumothorax: re-expansion of the
lung and prevention of recurrence. Although it is difficult to obtain high quality
consensus evidence because of differences in classification systems and management
guidelines, conservative treatment with observation and supplemental oxygen has been
considered as a more viable option for the treatment of pneumothorax in a healthy
patient, with a success rate of 79%.[[12]] Observation alone as the primary therapeutic option should be determined by the
size of pneumothorax, the presence of significant breathlessness, pre-existing lung
disease, the presence of a persistent air leak, and whether the pneumothorax is primary
or secondary 13. British Thoracic Society guidelines 2010 for the management of spontaneous pneumothorax recommend observational
one as the first-line treatment for patients without pre-existing lung disease, with
small closed pneumothorax (<15–20%) with minimal symptoms and asymptomatic patients
with large-size pneumothorax (>20%)11. Patients with small closed pneumothorax and
who are not breathless can be managed with outpatient follow-up with appropriate analgesia
and early review to ensure satisfactory resolution. If the patient is admitted for
observation, supplemental high flow oxygen should be given. The rate of re-expansion
of primary spontaneous pneumothorax is 2.2% of the volume of hemithorax per day, and
complete re-expansion usually occurs in 7 weeks.[[13]] Most studies reveal low recurrence rates after conservative treatment.[[14]] However, observation is inappropriate in pneumothorax patients suffering an underlying
lung disease with decreased pulmonary reserve. Secondary pneumothorax usually occurs
in patients with overt underlying lung disease, most commonly chronic obstructive
pulmonary disease. In these cases, the clinical symptoms associated are more severe
in general than those associated with primary pneumothoraces and require more aggressive
treatment. However, there is a significant rate of recurrence of secondary pneumothoraces,
eventually with serious consequences. Therefore, observation is not the preferable
option for secondary pneumothorax.[[10]] In conclusion, the clinical status is determined by the size of pneumothorax and
cardiopulmonary reserve. Thoracic catheter drainage is recommended for a first large
(rim of air in the thorax >2 cm according to the British Thoracic Society 2010 criteria)
or symptomatic episode of primary spontaneous pneumothorax.
Conclusions
This report presents a patient with simultaneous subcutaneous emphysema, pneumothorax,
and pneumomediastinum as an unusual complication of an asthma attack. Extra-pulmonary
extravasations of air manifested as subcutaneous emphysema, pneumothorax, and pneumomediastinum
can be a rare but very important complication of acute exacerbation of bronchial asthma.
When there is no serious cause for subcutaneous emphysema, it usually resolves promptly.
We suggest that occult pneumothoraces should be considered in the differential diagnosis
of patients presenting with an acute asthma attack failing to respond to conventional
medical therapy.
Declaration of patient consent
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understand that their names and initials will not be published and due efforts will
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