Adult Chest Surgery

Chapter 108. Pneumothorax and Pneumomediastinum 

Pneumo- is the Greek root for "air." This chapter concerns the presence of air in two separate anatomic compartments in the chest. Pneumothorax is defined as air in the pleural space and is extremely common.Pneumomediastinum is defined as air in the mediastinum and is quite rare. Despite their differences, the principles used to treat these two conditions are similar. Successful management requires a thorough understanding of the thoracic anatomy and pathophysiologic mechanisms that cause these conditions. Pneumothorax may signal a life-threatening condition, and pneumomediastinum may be a sign of an innocuous problem that requires no treatment. This chapter provides an overview of the incidence, causes, pathophysiology, symptoms, radiologic signs, diagnostic evaluation, and most important, techniques for treatment of both pneumothorax and pneumomediastinum.

PNEUMOTHORAX

Pneumothorax is a collection of air or gas in the pleural space. It is classified into three subtypes: spontaneous, traumatic, and iatrogenic pneumothorax (Table 108-1). A spontaneous pneumothorax is a collection of air or gas in the chest that causes the lung to collapse. It can be further classified as primary (i.e., collapse of lung for no apparent reason) or secondary (i.e., collapse of the lung secondary to underlying pulmonary pathology), as detailed in Table 108-2. The incidence of all types of pneumothoraces is greater in men than in women. For primary pneumothorax, the incidence is 7.4 per 100,000 population per year in men and 1.2 per 100,000 in women. Similarly, the incidence of secondary pneumothorax is 6.3 per 100,000 population per year in men and 2.0 per 100,000 in women. More specifically, the incidence is greatest in tall, thin young males younger than the age of 30 years.1

Table 108-1. Types of Pneumothoraces

Spontaneous pneumothorax

  Primary—no clinical lung disease

  Secondary—complication of lung disease

Traumatic pneumothorax

  Penetrating chest injury

  Blunt chest injury

Iatrogenic

  Transthoracic needle aspiration

  Subclavian vein catheter placement

  Thoracentesis

  Barotrauma

 

Used with permission from ref 30.

Table 108-2. Causes of Secondary Spontaneous Pneumothorax

Disease of airway

  Chronic obstructive pulmonary disease

  Cystic fibrosis

  Acute asthma

Parenchymal lung infection

  Pneumocystis carinii pneumonia

  Necrotizing infection

Malignancy

  Lung cancer

  Sarcoma

  Metastases

Interstitial lung diseases

  Sarcoid

  Connective tissue disease

  Tuberous sclerosis

  Idiopathic interstitial lung disease

Other

  Thoracic endometriosis

  Lymphangioleiomyomatosis

 

A tension pneumothorax occurs as a result of a pulmonary parenchymal or bronchial injury that acts as a one-way valve, permitting air to enter the pleural space but not escape. This causes a decrease in venous return and leads to hemodynamic compromise owing to low preload. Iatrogenic pneumothorax occurs as a consequence of inadvertent puncture of the lung during an invasive procedure.

Pathophysiology

The lung has an inherent tendency to collapse and the chest wall to expand. Hence the pressure in the pleural space is always negative in relation to atmospheric pressure. The alveolar pressure rises and falls on inspiration and expiration but is always greater than the intrapleural pressure (Fig. 108-1A ). Since air flows from an area of higher pressure to an area of lower pressure, when a fistula or air leak or other anomalous communication develops between an alveolus and the pleural space, the air flows down the pressure gradient until an equilibrium is reached or the communication is sealed (see Fig. 108-1B ). This condition is known as a pneumothorax.As the lung becomes smaller, the pneumothorax increases in size. The transpulmonary pressure, also known as elastic recoil of the lung, is the difference between alveolar pressure and pleural pressure (Palv –Ppl). When this value equals zero, the lung collapses. The primary physiologic consequence of this process is a decrease in the vital capacity of the lung, a decrease in the partial pressure of oxygen, and if the pressure becomes great enough, compression of the superior vena cava and tension pneumothorax. Young and healthy patients can tolerate these changes fairly well, with minimal changes in vital signs and symptoms, but individuals with underlying lung disease may develop respiratory or hemodynamic distress.

Figure 108-1.

 

A. Pressure in the intrapleural space is always negative (just below atmospheric pressure) and always lower than in the alveoli of the lung. B. Since air flows from regions of high to low pressure, when there is an anomalous communication between the alveolar tissues and the pleura, air flows down the pressure gradient and collects in the pleural space.

 

Tension pneumothorax has a far more dangerous outcome. As pressure within the intrapleural space increases, the mediastinum impinges on and compresses the heart and contralateral lung, thus decreasing the venous return (Fig. 108-2). Hypoxia results as the collapsed lung on the affected side and the compressed lung on the contralateral side compromise effective gas exchange. The hypoxia and decreased venous return caused by compression of the relatively thin walls of the superior vena cava and atria impair cardiac function. The decrease in cardiac output results in hypotension and may lead to hemodynamic collapse and death, if untreated.

Figure 108-2.

 

Chest x-ray of tension pneumothorax.

Causes

A spontaneous primary pneumothorax is commonly caused by rupture of subpleural apical emphysematous blebs, which are more prevalent in tall, thin males. Different mechanisms have been proposed; however, most concur that this process may occur because alveoli are subjected to a greater mean distending pressure over time, leading to subpleural bleb formation. Since pleural pressure is more negative at the apex of the lung than elsewhere, blebs located at the apex are more likely to rupture and cause pneumothorax.

Another risk factor for pneumothorax is smoking. Smoking increases the risk of spontaneous pneumothorax by 20-fold in men and by nearly 10-fold in women, as compared with similar risks in nonsmokers.2

Management

The goal of treatment of any pneumothorax is to remove air from the pleural space and prevent recurrence. Management depends on the symptoms and the radiologic size of the pneumothorax. Small, asymptomatic pneumothoraces may be followed with chest radiographs alone (Fig. 108-3). For larger pneumothoraces with more severe clinical symptoms and/or iatrogenic etiology, a chest tube should be inserted to protect the pleural space. If the cause is spontaneous, careful follow-up can be chosen.

Figure 108-3.

 

Chest x-ray of spontaneous pneumothorax.

Surgical Technique

We prefer surgical intervention when there is persistent air leak (>3 days), large air leak (>expiratory 4), failure of lung reexpansion, and in cases of recurrent spontaneous pneumothorax.Other indications for surgery include a space problem with air leak or occupations that predispose to pneumothorax, such as a pilot or scuba diver. Once the decision to proceed with surgery has been made, several different approaches can be taken, either by open or by video-assisted thoracoscopic surgery (VATS) technique. The latter is preferred by most surgeons because it affords the use of minimally invasive techniques, which can be particularly important when operating on patients with benign disease.However, newer techniques for thoracotomy have made this approach less painful with reduced morbidity. For example, open procedures can be performed using posterolateral muscle-sparing, rib-sparing, and nerve-sparing approaches.6,7 In addition, because this pathology requires access mainly to the upper hemithorax, axillary thoracotomy is also an option. Since VATS is by far the most common operation used for these patients, we will review the operative steps.

Video-Assisted Thoracoscopy

The goal of any operation in a patient with a recurrent pneumothorax is to prevent the patient from developing another symptomatic pneumothorax. Although one may not be able to prevent other parts of the lung from rupturing, the main goal is to prevent significant collapse and thus eliminate the risk of tension pneumothorax as well as shortness of breath. However, even when these goals are met, some patients still will have the sensation of an acute onset of chest pain postoperatively, and this probably signifies a small perforation in the lung. However, if the pleurodesis is successful, the lung will stay inflated, and the chest roentgenogram should be normal. To achieve these goals, some form of pleurodesis is needed. In this regard, we prefer to combine chemical with mechanical pleurodesis.

PREOPERATIVE CARE

Patients should have a chest CT scan and pulmonary function testing performed before surgery. A CT scan is ordered to assess the number and severity of blebs, if any, and to ensure there are no indeterminate pulmonary nodules. In older patients with emphysema and hypercapnia, surgery would be ill-advised if numerous large blebs are found on CT scan. These patients should be managed with a chest tube and bedside sclerotherapy. This chapter, however, focuses on the more common phenomenon of a young patient with recurrent pneumothorax. We prefer to use an epidural, even when performing a VATS procedure because the need for pleurectomy as well as mechanical and chemical pleurodesis causes it to be more painful than a VATS wedge resection.

INTRAOPERATIVE CARE

After the induction of general anesthesia, bronchoscopy is performed. A double-lumen endotracheal tube is placed as well as appropriate lines. The patient is positioned with operative side up, and all indwelling chest tubes are removed. Three standard VATS incisions are made. These incisions should be placed in a triangle to permit complete inspection and access to all areas of the chest. The apical segment of the upper lobe and the superior segment of the lower lobe are examined carefully. Even if a bleb cannot be located, we prefer to excise a wedge of the upper lobe and a small part of the lower lobe by using an endoscopic stapler that is buttressed with pericardial strips (Bovine Pericardial Strips, Synovis Surgical Innovations, St. Paul, MN) (Fig. 108-4). The recurrence rate after VATS by means of endoscopic stapler is less than 5%.These strips help to create adhesions. A complete pleurectomy from the mammary artery to the vertebral bodies is performed. It extends from the top of the chest to the diaphragm. The pleura is scraped by attaching a Bovie scratch pad to the end of a long, curved VATS ringed forceps (Fig. 108-5). This technique creates a pleural edge that can be grasped. A blunt instrument, such as a Kittner dissector, a finger to start, and then a sucker (Ethicon Endo-Surgery, Cincinnati, OH) are used to slowly remove the entire pleura. If the pleura is grasped with a long, curved VATS ringed forceps, it can be twisted and rotated, and this helps the operator to perform a complete pleurectomy quickly, usually in 15–25 minutes (Fig. 108-6). After the pleurectomy is completed, we prefer to add a chemical pleurodesis as well. We do not use talc in these young patients because of some of its potential side effects. The intrapleural injection of talc has resulted in acute respiratory distress syndrome in some patients treated for malignant pleural effusion. In addition, extensive pleural thickening with calcifications can develop many years after intrapleural talc,causing restriction of pulmonary function. Instead we use 500 mg doxycycline in 250 mL normal saline. The intrapleural injection of a tetracycline derivative decreases the recurrence rate for pneumothorax. In a prospective, randomized study of 229 patients with spontaneous pneumothorax, for example, the recurrence rate was 25% in the group treated with intrapleural tetracycline compared with 41% in the control group.Thus we add this to our intraoperative technique. This fluid is instilled in the chest for 10 minutes and then evacuated. Two chest tubes are placed through the two more anterior incisions (the most inferior port used for the camera and the most anterior port). We prefer to place two soft 24F drains. One tube is placed anteroapically, and the other is placed posteroapically.

Figure 108-4.

 

A portion of the upper lobe is resected using an endoscopic stapler buttressed with pericardial strips, which help to create adhesions.

 

Figure 108-5.

 

A Bovie scratch pad is used to create a pleural edge.

 

Figure 108-6.

 

The pleural edge is grasped with a long, curved VATS ringed forceps, which is rotated and twisted as shown to facilitate the pleurectomy.

POSTOPERATIVE CARE

The chest tubes are placed on suction for a few days unless there is an air leak. Although we have written extensively about the benefits of the setting chest tubes to water seal, this applies to patients with an air leak. In these patients, often with large and expansive chests, the lungs have difficulty filling this space, and thus we prefer suction. The epidural is removed on postoperative day 2 (or 3), and the patient can be discharged home on day 3 or 4. We usually send the patient home for a week or two with the anterior apical tube in place on a Heimlich valve or, more recently, connected to an Atrium Express (Atrium Medical Corporation, Hudson, NH) device. The patient returns to the outpatient clinic 1-2 weeks later. If the device shows no air leak and the radiograph shows no or only a minor pneumothorax, the chest tube is removed. If there is a large pneumothorax that is new, we prefer suction for another few days to help promote visceral-pleural to parietal-pleural apposition. Even if an air leak is present, the tubes can be removed safely if there is no new pneumothorax or subcutaneous emphysema.10

COMPLICATIONS

Chest tube insertion may result in empyema (1–3%), lung parenchyma perforation (0.2–0.6%), diaphragmatic perforation (0.4%), and subcutaneous placement (0.6%). In an analysis of 126 chest tube placements by pulmonologists at a teaching hospital, the complication rate was 11%; however, 10 of the 14 reported complications were related to clotting, kinking, or dislodgement of the chest tube.11

The most common short-term complication of VATS for a recurrent pneumothorax is an air leak. As described earlier, the initial treatment should be water seal, and if it persists, then outpatient management with an Atrium device is preferred. Persistent air leak commonly occurs in patients with secondary pneumothoraces. Pain is another common complaint after VATS, despite the fact that the ribs are not spread. The pain is usually secondary to impingement of the intercostal nerve. The best management is prevention. We do not use a trocar for the camera or for any of the ports. The trocar can be slipped over the camera once it is introduced into the chest. Pain can lead to inadequate ventilation of the lungs, thus promoting the incidence of atelectasis and pneumonia. Most patients have minimal postoperative discomfort; however, analgesics may be required to achieve adequate control of pain once the epidural is removed.

Recurrence of the pneumothorax is the most frequent and frustrating complication of primary spontaneous pneumothoraces; it occurs in up to 25–54% of untreated patients, and most recurrences occur within the first year of the first pneumothorax.12,13 After VATS, however, the incidence is much less. After a second pneumothorax, the risk of having a third increases by more than 50%.14 Hemorrhage related to VATS is uncommon. Arrhythmia, which is common after many thoracic procedures, should be managed as described in Chapter 8.

PNEUMOMEDIASTINUM

Pneumomediastinum (also known as mediastinal emphysema) is defined as air in the mediastinum. It occurs in approximately 1 per 10,000 hospital admissions per year in adults and in 2.5 per 1000 live births per year.15 It is generally a benign, self-limited condition. Very few, if any, reports of fatal outcomes in patients with spontaneous pneumomediastinum in the absence of underlying disease exist in the recent literature. These data are in sharp contrast to tension pneumomediastinum, which often results in fatality unless there is immediate surgical intervention.

PATHOPHYSIOLOGY

Pneumomediastinum can be caused by air that originates in the pharynx, the tracheobronchial tree, or the esophagus. Excessive intraalveolar pressure, for example, can lead to rupture of perivascular alveoli (Fig. 108-7). Air escapes into the perivascular connective tissue and subsequently dissects into the mediastinum. From there, the air may dissect superiorly into the visceral, retropharyngeal, and subcutaneous spaces of the neck. From the neck, the subcutaneous compartment is continuous throughout the body; thus air can diffuse widely. Mediastinal air also can pass inferiorly into the retroperitoneum and other extraperitoneal compartments. It even can enter the pericardium and cause pneumopericardium. A study by Clements and colleagues showed that 85% of patients developed pneumomediastinum after esophageal procedures.16 When it dissects throughout the body, it usually stops at the level of the inguinal ligament. If the mediastinal pressure rises abruptly, or if decompression in not sufficient, the mediastinal parietal pleura also may rupture, causing pneumothorax (in 10–18% of patients). Table 108-3 lists the common causes of pneumomediastinum. Mihos and colleagues have described sports that commonly lead to pneumomediastinum, including SCUBA diving, basketball, and soccer.17

Figure 108-7.

 

In pneumomediastinum, excessive intraalveolar pressure can lead to rupture and escape of air into perivascular connective tissues and eventually mediastinum.

Table 108-3. Causes of Spontaneous Pneumomediastinum

Increased intrathoracic pressure31,32

  Excessive or forceful coughing

  Sneezing

  Vomiting

  Valsalva maneuvers (childbirth, defecation)

Neonate

  Gas trapping associated with neonatal respiratory distress syndrome

  Use of mechanical ventilation

  Aspiration of meconium or blood

  Birth-related trauma

Sports or occupational hazard

  Rapid altitude changes (scuba diving, skydiving, pilot)

  Basketball

  Soccer

Iatrogenic

  Laparoscopic surgery (usually esophageal)

 

A more serious variant of pneumomediastinum, termed tension pneumomediastinum (or malignant by some), often mimics cardiac tamponade and should be treated immediately with cervical mediastinoscopy.18 It arises from interference of air in the lung and mediastinum, causing compression of pulmonary and mediastinal vessels and interference with respiration by the splinting action of air in the interstitial tissue of the lung. If unrelieved, it may progress to pulmonary edema and circulatory failure.

Signs, Symptoms, and Diagnosis

The signs and symptoms of pneumomediastinum vary from asymptomatic to severe chest pain below the sternum that may radiate to the neck and arms. The pain may be exacerbated by breathing or swallowing. On examination, subcutaneous air is present in approximately 50% of cases. Hammam's sign (i.e., precordial crunching noise synchronous with heartbeat and often accentuated during expiration)19 is also commonly present. Tension pneumomediastinum is characterized by dyspnea, cyanosis, engorged neck veins, and hypotension.

The diagnosis of pneumomediastinum can be confirmed with a chest x-ray that reveals streaky gas densities along the fascial planes of the mediastinum (Fig. 108-8). This is most clearly demonstrated on the lateral view. Once diagnosed, a thorough workup is needed to ensure that no life-threatening causes have been missed. An upper gastrointestinal swallow and a contrast chest CT scan, bronchoscopy, and esophagoscopy can be performed depending on the index of suspicion. These are all usually normal. VATS also has been recommended but, in our opinion, is rarely necessary.20

Figure 108-8.

 

X-ray of patient with pneumomediastinum showing air around the right and left pulmonary arteries.

Management and Surgical Techniques and Approaches for Pneumomediastinum

The treatment of tension pneumomediastinum, most commonly seen in neonates on ventilators,21 often requires urgent evacuation of air from the mediastinum.20 This can be achieved by incisions into the subcutaneous tissues or, less commonly, by a cervical mediastinoscopy.18 Moore and colleagues used a tube to drain subcutaneous air through a subxiphoid incision in neonates. The dissection is carried out bluntly along the entire length of the sternum, exposing the anterior mediastinum and the pericardium.20 Other incisions also have been used for this purpose, such as the transverse suprasternal with or without full sternotomy, infraclavicular,22 and tracheostomy.23

The aim of management of pneumomediastinum is to ensure that a serious underlying cause is not missed. Most patients with a pneumomediastinum do not require surgical intervention, and in most cases, the condition resolves without intervention.24,25 A study by Mihos and colleagues evaluated the treatment course of 25 cases of pneumomediastinum resulting from sports accidents. All patients were treated by observation alone. Complete resorption of the pneumomediastinum occurred in 3–8 days in all patients, and hospital stay ranged from 2 to 6 days (mean 3.8 days).17 This experience has led some to avoid the expensive battery of usually normal diagnostic tests. Perhaps in the hemodynamically stable patient observation alone is safe as well as cost-effective.

However, once the need for surgery has been decided, the underlying cause of the pneumomediastinum dictates the surgical approach. If the cause is a ruptured bleb, the previously described approach for pneumothorax should be followed as indicated. If the cause is a perforated esophagus, the location of the tear can be revealed on upper gastrointestinal barium swallow. A posterolateral thoracotomy is performed ipsilateral to the infected effusion. Thus the empyema can be treated and the esophagus repaired. If the tear is limited to the mediastinum and does not drain into a pleural space, surgical intervention may not be needed because the tear is contained. However, if surgery is chosen, the side opposite the aortic arch (usually the right) offers better exposure and greater access to the entire length of the intrathoracic esophagus.

The goal of the operation is to drain the empyema, decorticate the lung to control the pleural space, and if possible, identify and repair the esophageal tear. Importantly, the latter is the least important goal because if there is no distal obstruction, no cancer, and no foreign body, the tear will heal on its own if there is adequate drainage of the infected surrounding space. Patients who have esophageal perforation due to instrumentation or a penetrating injury have a better prognosis than those with spontaneous perforation largely because of earlier diagnosis in the former group.26 We prefer to identify the tear and close it primarily if the chest is entered within 48–72 hours of the injury, depending on the quality of the tissue. Primary repair alone is never enough. The suture line must be reinforced to reduce the risk of esophageal leaks, mediastinitis, and sepsis by buttressing with a pedicled flap.27 We prefer an intercostal flap that should be harvested before chest retraction.Other options include a diaphragmatic patch, although this has the potential to introduce infection in the subphrenic space. A pericardial fat pad is another option, but its blood supply is not reliable. A pleural flap also can be used, but it is often too thin. The postoperative care depends on the underlying cause and the treatment strategy chosen.

Recurrence of spontaneous untreated pneumomediastinum is rare, although it has been reported in a few smaller series. Abolnik reported a recurrence incidence of 2 in 25 patients over a 2-year period.28 While the physiologic mechanism of recurrence has not yet been elucidated, some attribute recurrence from a pulmonary cause to a congenital weakness of the alveolar wall.29

EDITOR'S COMMENT

The basic objective of surgery to prevent recurrent pneumothorax is to remove the source of the leak: typically a few blebs at the apex of the lung or a rare secondary site (e.g., apical portion of the superior segment). If the site of the pneumothorax is identified and removed, mechanical or chemical pleurodesis is unnecessary. Alternatively, if pleurodesis is performed without removing the source of the pneumothorax, subsequent pneumothoraces may present as basilar air collections (because effective basilar pleurodesis is unlikely with a functioning diaphragm), and these can be difficult to manage with tube thoracostomy or thoracoscopy.

–SJM

REFERENCES

1. Primrose W: Spontaenous pneumothorax: A retrospective review of aetiology, pathogenesis and management. Scott Med J 29:15–20, 1984. [PubMed: 6531673]

2. Bense L, Eklund G, Wiman LG: Smoking and the increased risk of contracting spontaneous pneumothorax. Chest 92:1009–12, 1987. [PubMed: 3677805]

3. Cerfolio RJ, Bass C, Katholi CR: Prospective, randomized trial compares suction versus water seal for air leaks. Ann Thorac Surg 71:1613–7, 2001. [PubMed: 11383809]

4. Baumann MH, Strange C: Treatment of spontaneous pneumothorax: A more aggressive approach? Chest 112:789–804, 1997. [PubMed: 9315817]

5. Ayed AK, Al-Din HJ: The results of thoracoscopic surgery for primary spontaneous pneumothorax. Chest 118:235–8, 2000. [PubMed: 10893385]

6. Cerfolio RJ, Price TN, Bryant AS, et al: Intracostal sutures decrease the pain of thoracotomy. Ann Thorac Surg 76:407–11; discussion 11–2, 2003. 

7. Cerfolio RJ, Bryant AS, Patel B, Bartolucci AA: Intercostal muscle flap reduces the pain of thoracotomy: A prospective, randomized trial. J Thorac Cardiovasc Surg 130:987–93, 2005. [PubMed: 16214509]

8. Lange P, Mortensen J, Groth S: Lung function 22–35 years after treatment of idiopathic spontaneous pneumothorax with talc poudrage or simple drainage. Thorax 43:559–61, 1988. [PubMed: 3212753]

9. Light RW, O'Hara VS, Moritz TE, et al: Intrapleural tetracycline for the prevention of recurrent spontaneous pneumothorax: Results of a Department of Veterans Affairs cooperative study. JAMA 264:2224–30, 1990. [PubMed: 2214100]

10. Cerfolio RJ, Bass CS, Pask AH, Katholi CR: Predictors and treatment of persistent air leaks. Ann Thorac Surg 73:1727–30; discussion 30–1, 2002. 

11. Collop NA, Kim S, Sahn SA: Analysis of tube thoracostomy performed by pulmonologists at a teaching hospital. Chest 112:709–13, 1997. [PubMed: 9315804]

12. Light R: Pleural Diseases. Philadelphia, Williams & Wilkins, 2001:284–319.

13. Sadikot RT, Greene T, Meadows K, Arnold AG: Recurrence of primary spontaneous pneumothorax. Thorax 52:805–9, 1997. [PubMed: 9371212]

14. Cran I, Rumball C: Survey of spontaneous pneumothoraces in the Royal Air Force. Thorax 22:1967. 

15. Hacking D, Stewart M: Images in clinical medicine: Neonatal pneumomediastinum. N Engl J Med 344:1839, 2001. [PubMed: 11407345]

16. Clements RH, Reddy S, Holzman MD, et al: Incidence and significance of pneumomediastinum after laparoscopic esophageal surgery. Surg Endosc 14:553–5, 2000. [PubMed: 10890964]

17. Mihos P, Potaris K, Gakidis I, et al: Sports-related spontaneous pneumomediastinum. Ann Thorac Surg 78:983–6, 2004. [PubMed: 15337032]

18. Beg MH, Reyazuddin A, Ansari MM: Traumatic tension pneumomediastinum mimicking cardiac tamponade. Thorax 43:576–7, 1988. [PubMed: 3212757]

19. Hammam L: Spontaneous mediastinal emphysema. Bull Johns Hopkins Hosp 64:1–21, 1939. 

20. Moore JT, Wayne ER, Hanson J: Malignant pneumomediastinum: Successful tube mediastinostomy in the neonate. Am J Surg 154:688–91, 1987. [PubMed: 3425819]

21. Rosenfeld DL, Cordell CE, Jadeja N: Retrocardiac pneumomediastinum: Radiographic finding and clinical implications. Pediatrics 85:92–7, 1990. [PubMed: 2296498]

22. Shennib HF, Barkun AN, Matouk E, Blundell PE: Surgical decompression of a tension pneumomediastinum: A ventilatory complication of status asthmaticus. Chest 93:1301–2, 1988. [PubMed: 3286149]

23. Kirchner J: Cervical mediastinal emphysema. Arch Otolaryngol 9:368–75, 1980. 

24. Miura H, Taira O, Hiraguri S, et al: Clinical features of medical pneumomediastinum. Ann Thorac Cardiovasc Surg 9:188–91, 2003. [PubMed: 12875642]

25. Jougon JB, Ballester M, Delcambre F, et al: Assessment of spontaneous pneumomediastinum: Experience with 12 patients. Ann Thorac Surg 75:1711–4, 2003. [PubMed: 12822604]

26. Bladergroen MR, Lowe JE, Postlethwait RW: Diagnosis and recommended management of esophageal perforation and rupture. Ann Thorac Surg 42:235–9, 1986. [PubMed: 3753071]

27. Wright CD, Mathisen DJ, Wain JC, et al: Reinforced primary repair of thoracic esophageal perforation. Ann Thorac Surg 60:245–8; discussion 248–9, 1995. 

28. Abolnik I, Lossos S, Breuer R. Spontaneous pneumomediastinum. A report of 25 cases. Chest 100:93–95, 1991. [PubMed: 1824034]

29. Hammam L: Mediastinal emphysema. JAMA 128:1–6, 1945. 

30. Sahn SA, Heffner JE: Spontaneous pneumothorax. N Engl J Med. 342:868–74, 2000. [PubMed: 10727592]

31. Ba Salamah A, Schima W, Umek W: Spontaneous pneumomediastinum. Eur Radiol 9:724–7, 1999. 

32. Miguil M, Chekairi A: Pneumomediastinum and pneumothorax associated with labour. Int J Obstet Anesth 13:117–9, 2004. [PubMed: 15321418]



If you find an error or have any questions, please email us at admin@doctorlib.info. Thank you!