Ann Thorac Surg 2003;75:1711-1714
© 2003 The Society of Thoracic Surgeons
Original article: general thoracic
Assessment of spontaneous pneumomediastinum: experience with 12 patients
Jacques B. Jougon, MD, FETCS,a*,
Michel Ballester, MD, PhDb,
Frédéric Delcambre, MDa,
Tarun Mac Bride, MDa,
Claire E. H. Dromer, MDa,
Jean-François Velly, MD, FETCSa
a Department of Thoracic Surgery, Haut-Lévêque Hospital, Bordeaux University Hospital, Pessac, France
b Department of Ear, Nose, Throat, and Cervicofacial Surgery, General Hospital, University Hospital, Dijon, France
Accepted for publication January 1, 2003.
* Address reprint requests to Dr Jougon, Service de Chirurgie Thoracique, CHU de Bordeaux, Hôpital du Haut-Lévêque, 33604 Pessac, France
e-mail: jacques.jougon{at}chu-bordeaux.fr
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Abstract
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BACKGROUND: The aim of this study is to report a series of spontaneous pneumomediastinum in a population of young, tall, and thin patients with a history of thoracic hyper pressure, and to analyze the assessment required in such patients.
METHODS: A retrospective study of an unicentric series and a review of the literature from 1980 to 2002 were performed.
RESULTS: Between December 1996 and January 2002, 12 patients (mean age, 25 years old; mean height, 172 cm; and mean weight, 63 kg) were admitted with spontaneous pneumomediastinum. In all patients, high intrathoracic pressure by cough or acute effort was the precipitating factor. Most frequent complaints were acute chest pain, asthenia, and subcutaneous emphysema. The following assessment was performed: chest roentgenogram in 12 of 12 patients (12/12); computer tomography (CT) scan in 8/12; bronchoscopy in 7/12; esophagoscopy in 6/12; esophagography in 2/12. Outcome was always uneventful without any recurrence. Hospital stay ranged from 0 to 6 days. The Medline research revealed that articles consist mainly of case reports. Two articles only report a multicentric series of 25 and 36 cases, respectively. No organ perforation was found either in our series or in our review of the literature.
CONCLUSIONS: Spontaneous pneumomediastinum follows alveolar rupture in the pulmonary interstitium. The dissection of gas towards the hilum and mediastinum is produced by an episode of acute high intrathoracic pressure. It affects mostly young people, and this is the case in our series. Endoscopic thoracic assessment may be risky and is not always necessary. Chest CT or esophageal contrast study should be performed in case of diagnostic doubt of esophageal perforation.
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Introduction
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Spontaneous pneumomediastinum (SPM) is an uncommon disorder arising most frequently in young adult men with an unknown precise incidence. The disease is little known by physicians, who often require endoscopic explorations to rule out perforation of a chest air-containing viscus. Endoscopic explorations, however, are not always necessary and the subject is still controversial [1, 2]. Previous series and case reports of SPM focused on precipitating factors, clinical presentation, and pathogenesis [3]. We report a unicentric series of 12 patients. The purpose of the study is to determine the minimal assessment required for spontaneous pneumomediastinum, to discuss the causes, and to review the literature.
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Patients and methods
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A retrospective study of a series of 12 patients admitted to our department for SPM was performed. Patients were first admitted to the emergency department of our university hospital or in a peripheral general hospital. They were secondarily referred to our department for suspicion of perforation of a chest air-containing viscus. In our department, bronchial and esophageal endoscopies are routinely performed. At the beginning of the study, no assessment was defined and each physician decided what the assessment for the patient suffering from pneumomediastinum would be. Data concerning patient history, presenting symptoms, endoscopic and radiologic findings, treatment, and outcome were carefully reviewed. Information concerning long-term recurrence or sequelae was obtained by phone calls to the patient or to his physician.
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Results
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Between December 1996 and January 2002, 12 patients were admitted for SPM to our department. During the same period 280 patients were admitted for spontaneous pneumothorax and 54 patients for esophageal perforation [4, 5]. There were 11 men and 1 woman ranging in ages from 16 to 46 years old (mean 25 years old). None of them had a medical history of pneumothorax or SPM. The mean height was 172 cm and the mean weight was 63 kg. Spontaneous pneumomediastinum always occurred after high intrathoracic pressure provoked by acute effort or a cough access. The most frequent complaints were acute chest pain, asthenia, noisy voice, and subcutaneous emphysema (Table 1).
Odynophagia was present in one patient. Laboratory indicators of infection were normal in all but one patient (patient 10) Chest roentgenogram was performed in all patients, thoracic computer tomography (CT) in 8 patients, bronchoscopy in 7 patients, esophagoscopy in 6 patients, and esophagography in 2 patients (Table 2).
Chest roentgenogram and CT revealed the pneumomediastinum in all patients (Figs 1 and 2).
Bronchoscopy was normal in all patients except in patient 10,
exhibiting a bronchial inflamed tree with clear but thick sputum. The patient was suffering from an acute bronchitis. Esophagoscopy and esophagography were normal in all patients. Treatment consisted of rest, analgesics for all patients, and nebulized therapy for patient 10. The outcome was always uneventful and discharge occurred from day 0 to 6 (mean hospital stay 4 days). None of the patients presented recurrence (follow-up: 98 days to 5 years, mean 19 months). The MEDLINE research revealed that publications consist mainly of case reports. Two articles only report a multicentric series of 25 patients [3] and 36 patients [6], respectively. No organ perforation was found in our review of the literature.
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Table 1. Patient Demography, Causing Factors, Symptoms, and Follow-Up: Young, Tall, and Thin Patients Mainly Present With Spontaneous Pneumomediastinum
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Fig 2. Computer tomographic scan illustrating air infiltrating the mediastinum (arrows) without pneumothorax.
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Comment
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The first description of pneumomediastinum is attributed to Laennec [7] in a context of chest trauma. Hamman [8] was the first who described the disease of spontaneous pneumomediastinum so SPM is also called Hammans syndrome. He described a typical sign, which consists of crackles, bubbles, or churning sounds heard with each contraction of the heart [8]. The clinical diagnosis is based on the symptom triad of chest pain, dyspnea, and subcutaneous emphysema. Subcutaneous emphysema may be either discreet or evident inducing crepitus and facial swelling. The chest pain may be posterior or retrosternal with radiation to the jaw creating odynophagia. Many other signs and symptoms can be associated including rhinolalia [9], sore throat, cough, tachycardia, dysphagia, and anxiety. All those signs are secondary to tissue dissection by air or compression. When clinical signs are evident, the diagnosis is confirmed by a chest roentgenogram illustrating multiple thin, lucent streaks outlining mediastinal structures, elevating the mediastinal pleura, and often extending into the neck or chest wall [10] (Fig 1). However, it may be missed by a standard chest roentgenogram when it is of small volume. The lateral view is more sensitive in making the diagnosis. Computer tomography scan is the critical test for diagnosis (Fig 2). By reviewing chest roentgenogram and CT scans of 33 patients, Kaneki and colleagues [6] concluded that it seemed likely that 30% or more in clinical practice underdiagnosed SPM. Indeed, SPM must be looked for in cases of unclear chest pain especially in young men, and must not be misdiagnosed for chest pain of anxiety origin.
Demography of our series is similar to others [3, 9]: young, tall, and thin men are mainly concerned. It seems likely that they present predisposing anatomic factors, such as elastic tissues fragilities.
The pathophysiology was initially described by Macklin and Macklin in 1944 [11] on the basis of laboratory animal experiments, and more recently in a case report by Kaneki and coworkers [12]. SPM would result from the rupture of distal pulmonary alveoli, allowing bubbles to dissect along the vascular sheaths and connective tissue planes to the mediastinum. In the case report by Kaneki and coworkers [12], the CT scan revealed the presence of air in a tubular shape along the pulmonary artery in one segment of the left lung. This can be caused by sustained Valsalva maneuvers such as coughing, vomiting, forceful defecation, strenuous effort, labor [13, 14], asthma attack [15], sneezing [2], or inhalational drug use [16].
Potential serious complications, such as tension pneumomediastinum leading to cardiac compression, are possible. They were induced in laboratory experiments by Macklin and Macklin [11], but were never reported in humans. Cessation of high pressure in the alveoli stops the passage of air.
The main differential diagnosis is spontaneous esophageal perforation (Boerhaaves syndrome) and worrisome symptoms, signs and abnormal results from simple investigations requires prompt surgery [1]. They include fever, hypotension, odynophagia, pronounced dysphagia, leukocytosis, and pleural effusion. Vomiting is often found as a preceding symptom [17]. The initial investigation should include a CT scan or a water-soluble contrast esophagogram. To us, the esophagoscopy may be a dangerous procedure in such patients when it is not performed by trained surgeons accustumed with the pathology, which may turn a contained into a noncontained perforation. Inducing cough may even, like bronchoscopy, facilitate the passage of air from the ruptured alveoli to the mediastinum along the bronchovascular tissue sheath, thus enhancing pneumomediastinum. For these reasons, some reports argue it is contraindicated. We routinely perform rigid esophagoscopy in the management of esophageal perforation and have noticed no incident [5], preferring it to flexible esophagoscopy, which can also be dangerous by inducing air insufflations into the mediastinum. In our series, 6 patients underwent a rigid esophagoscopy performed immediately after the bronchoscopy: no increasing swelling was noticed. Only one patient (patient 10) had worrisome signs, dysphagia and fever, which justified endoscopic explorations. At the end of our study, which is more than 4 years after its beginning, we drastically reduced the assessment in patients presenting SPM. Only a chest roentgenogram was performed in patients 11 and 12.
Treatment of SPM should consist of reassuring the patient, rest, and analgesia when needed. Symptoms usually resolve quickly and the patient can be discharged a few days later. In our series the hospital stay was gradually reduced along the study from 6 days to few hours, although 48-hour medical supervision seems necessary when a CT scan or a contrast esophageal study is not performed.
Recurrence is rare but has been reported in 2 patients [3, 18], with no predicting factor identified. In case of SPM occurring in children, pulmonary function tests are necessary after the acute episode to rule out asthma [15].
Spontaneous pneumomediastinum is probably a more frequent disorder than usually reported because it is underdiagnosed or misdiagnosed. It is usually limited and resolves spontaneously with rest. Assessment should be tailored to each patients history and clinical status. Endoscopies should not be recommended routinely. Young, tall, and thin men, who have a history containing any mechanism responsible for the creation of a high intrathoracic pressure and present with neither fever nor pleural effusion, can only be kept under close supervision a minimum of 2 days. Computer tomography scan and esophageal contrast roentgenogram study are needed in case of worrisome associated symptoms, signs, and abnormal results from simple investigations to rule out an esophageal perforation.
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Acknowledgments
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We thank Dr Steven Plume for language editing this manuscript.
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References
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