Pulmonary Medicine

Non-Neoplastic Disorders of the Mediastinum: Acute Mediastinitis

What every physician needs to know:

Acute mediastinitis is an uncommon but potentially life-threatening infection that can affect any of the mediastinal compartments. Widespread use of broad-spectrum antibiotics makes this site of infection even less common, and spontaneous development of mediastinal infection is rare. The vast majority of cases result from introduction of microbes into the mediastinal space from trauma, from perforated viscus, or during surgery. Computed tomography (CT) of the chest is used to evaluate the extent of infection. These polymicrobial infections require early initiation of broad-spectrum antibiotics and surgical evaluation for drainage and debridement, and mortality associated with this disease remains high.


Acute mediastinitis is evaluated based on the origin of acute infection, with primary causes resulting from direct extension of infection or secondary causes following introduction of organisms from viscus perforation. Acute mediastinitis can also be considered based on the mediastinal compartment affected.

One of the most common clinically used designations of acute mediastinitis defines the disease based on the mediastinal compartment involved. Anterior compartment mediastinitis occurs in the region between the sternum and the anterior surface of the pericardium and great vessels. Middle compartment mediastinitis involves the region bordered by the anterior pericardium and posterior pericardium, and posterior compartment mediastinitis results from infection in the region that extends posteriorly from the posterior pericardium to the posterior vertebrae. Post-cardiac surgical complications usually affect the anterior compartment, esophageal perforations affect the middle compartment, and direct extension of infections from the spine or lung affect the posterior compartment.

Some anatomical classification systems also designate a superior compartment; acute mediastinitis in this compartment is usually associated with descending causes of infection from surgery or trauma involving the head or neck.

Are you sure your patient has acute mediastinitis? What should you expect to find?

Common symptoms associated with acute mediastinitis include rapid onset of dyspnea, and chest pain that worsens with deep inspiration. Patients usually display signs consistent with severe infection or sepsis, such as tachypnea, tachycardia, fever, chills/rigors, and hypotension/shock, and the patient often has a toxic appearance. Pneumothorax, subcutaneous emphysema, or pneumomediastinum can also be associated with the disease, especially if there is a disruption in the tracheobronchial tree or esophageal mucosa.

Pneumomediastinum, widened mediastinum, or mediastinal fluid can also be seen on chest radiography. Development of a localized mediastinal abscess can also result in findings related to mass effect, which can lead to dyspnea from deviation or compression of the trachea, hoarseness of voice from compression of a recurrent laryngeal nerve, Horner's syndrome from stellate ganglion involvement, or tachycardia from vagus nerve involvement.

However, these signs and symptoms are hardly specific; diagnosis is made by findings of acute inflammation, abscess formation, or other radiographic findings consistent with acute infection on radiographic imaging.

Beware: there are other diseases that can mimic acute mediastinitis:

Symptoms associated with acute mediastinitis are nonspecific. A history of infections with potential for direct extension, recent oropharyngeal/neck or thoracic surgery, or recent procedures or trauma to the gastrointestinal or tracheobronchial tree should prompt consideration for acute mediastinitis.

Other infections of the thorax (e.g., pneumonia, bronchitis) or even systemic infections/sepsis, which are much more prevalent, can mimic acute mediastinitis. Non-infectious etiologies, such as cardiac ischemia/arrhythmia or pneumothorax/pneumomediastinum can also present similarly. However, patients who present with pneumomediastinum warrant consideration for acute mediastinitis, as both etiologies have similar origins. Interruption of the esophageal or tracheal mucosa, such as from Boerhaave's syndrome or traumatic procedural instrumentation, can result in concurrent translocation of air and micro-organisms into the mediastinal space.

How and/or why did the patient develop acute mediastinitis?

Spontaneous development of mediastinal infection is rare. More commonly, microorganisms are introduced either by disruption of the skin or mucosa (trauma, surgery, or instrumentation/medical procedures) or by direct extension.

Spontaneous mediastinitis

Primary mediastinitis is usually associated with anthrax, which results from infection by Bacillus anthracis. This organism is most prevalent in the Middle East, and the primary reservoir is farm animals, such as cattle, sheep, and goats. Human infection typically afflicts individuals who handle the skin or hides of infected animals.

More than 90 percent of cases are limited to the cutaneous form of the disease, which is transmitted by direct inoculation. The inhalational form, or woolsorter's disease, results from inhalation of B. anthracis spores. The development of spores in the distal airways and subsequent transfer to mediastinal lymph nodes by alveolar macrophages results in fever and rapid progression to hemorrhagic mediastinitis, bacteremia, sepsis, and likely death. Fortunately, anthrax mediastinitis is rare, although concern regarding inhalational anthrax has risen, given its potential use as a biological weapon.

Direct extension

Mediastinitis can result from direct extension of infection along tissue planes that originate from other regions of the body. The most common sites of origin are the head and neck, which can result in a necrotizing mediastinitis.

Descending necrotizing mediastinitis originates from other infectious sites, such as retropharyngeal abscess, epiglottitis, pharyngitis, deep cervical infections, or complications of head/neck/dental surgery with polymicrobial gram negative and/or anaerobic oropharyngeal organisms. The infection can then spread to the mediastinum through the pretracheal space (posterior to the strap muscles and pretracheal fascia and anterior to the trachea), through the perivascular space along the carotid sheath and the associated neurologic and vascular structures, or (most frequently) through the retrovisceral space extending from the base of the skull to the posterior mediastinal compartment. Spread of infection from the head and neck to the mediastinum may be influenced by gravity and negative intrathoracic pressure.

Other sources of direct extension are relatively uncommon, although extension from the lungs can occur with invasive tumors and from the chest wall in injection drug users. Pancreatitis has also been described as a source of mediastinitis with presumed infection spread via the aortic and esophageal hiatus.


Post-cardiac surgery infections, now the most common source of acute mediastinitis, feature a wide variety of associated organisms, but a single organism is identified in more than 80 percent of post-cardiac cases of mediastinitis. The most commonly identified organisms, listed in order of prevalence, are methicillin-susceptible S. aureus, methicillin-resistant S. aureus, gram negative bacilli, coagulase-negative Staphylococcus, and Streptococcus.

While the overall incidence is relatively low, with most reports ranging from 0.5-2.0 percent, the high volume of cardiac surgeries results in a significant number of post-surgical complications of acute mediastinitis.

Disruption of mucosa

The other major etiology of acute mediastinitis is introduction of infection into the mediastinal space from perforation of a viscus. Procedural instrumentation accounts for 50-75 percent of esophageal perforations. Spontaneous perforations from Boerhaave's syndrome or erosion from tumor or foreign bodies are other possible causes of esophageal perforation.

Perforation of the tracheobronchial tree usually results from penetrating trauma or endotracheal intubation. Flexible bronchoscopy is a significantly less likely cause unless therapeutic interventions are performed. Disruption of the tracheobronchial tree is less likely to lead to the development of acute mediastinitis than are perforations of the esophageal mucosa.

Which individuals are at greatest risk of developing acute mediastinitis?

Immunocompromised states can predispose patients to infections from the aforementioned sources, especially via direct extension and with less common organisms, such as Aspergillus, Mycobacterium, and Nocardia.Increased risk of post-sternotomy mediastinitis has also been associated with tobacco use, peripheral artery disease, prolonged preoperative hospitalization, blood transfusions, and repeat operations, such as exploration for bleeding. Diabetes mellitus and the use of internal thoracic artery grafts (possible devascularization of the sternum) have also been shown to be significant risk factors.

What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?

Patients may have leukocytosis or acid-based disturbances consistent with acute infection. Blood cultures are often helpful, but they are not always sensitive to the organism that is causing mediastinitis. Wound cultures should be performed for postoperative patients in whom acute mediastinitis is suspected. A culture of infected mediastinal tissue is helpful, but it is usually performed at the time of surgical debridement.

What imaging studies will be helpful in making or excluding the diagnosis of acute mediastinitis?

The initial study performed is typically chest radiography, which may show a widened mediastinum or pneumomediastinum. Since air in the mediastinum can be a normal post-surgical finding, computed tomography (CT) is more helpful in differentiating between mediastinitis and post-surgical changes, wound dehiscence, sites of trauma, hemorrhage, edema, and inflammation. Contrast with CT, which is also helpful in visualizing the mediastinal soft tissue, should be added unless contraindicated.

For patients in whom esophageal perforation is suspected, CT or esophogram with water-soluble contrast is usually diagnostic, although false-negative tests can occur in up to 10 percent of cases with esophogram. Other modalities, such as MRI and ultrasound, have been used, but CT remains the study of choice because of considerations related to cost, availability, and image quality.

What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of acute mediastinitis?

Non-invasive pulmonary diagnostic studies are not a primary method of disease diagnosis.

What diagnostic procedures will be helpful in making or excluding the diagnosis of acute mediastinitis?

Radiography is the primary means of evaluating for acute mediastinitis in patients with the appropriate history and presentation. Surgical exploration, drainage, and debridement are commonly required for diagnostic evaluation of and therapeutic intervention in suspected cases of mediastinitis.

What pathology/cytology/genetic studies will be helpful in making or excluding the diagnosis of acute mediastinitis?

Culture results from surgical debridement may be helpful in identifying microbial pathogens and antibiotic management. Pathology results of debridement are consistent with acute inflammation from infection.

If you decide the patient has acute mediastinitis, how should the patient be managed?

Acute mediastinitis is routinely treated with several weeks of broad-spectrum antibiotics, including coverage for gram negative and anaerobic organisms. Typical coverage includes a third-generation cephalosporin and metronidazole or an extended-spectrum beta-lactam, such as piperacillin-tazobactam. If skin flora are possible pathogens, such as in postoperative mediastinitis, initial empiric use of vancomycin should be considered to cover resistant strains of S. aureus.Antibiotic regimens can be tailored once culture results are available.

However, surgical evaluation should also be made, as intervention with extensive surgical exploration and debridement is usually required. In rare circumstances, percutaneous drainage can be used. Studies in mediastinitis from visceral perforation suggest that aggressive, early surgical debridement may be associated with decreased mortality. For postoperative patients, early surgical intervention is recommended with either immediate closure or open-wound management followed by delayed primary or subsequent flap closure.

Patients are treated with antibiotics for two to three weeks after surgical debridement, although the antibiotic duration can be extended if the infection is slow to resolve or if there is a concern about bone involvement/osteomyelitis. CT scans are used to monitor the extent and progression of disease.

What is the prognosis for patients managed in the recommended ways?

Unfortunately, mortality is high in acute mediastinitis. with rates of 10-40% reported. Acute mediastinitis secondary to esophageal rupture or post-surgical causes is associated with higher rates of mortality (up to 50%). Early management with broad-spectrum antibiotics is thought to have significantly decreased the mortality associated with this uncommon but often fatal disease.

Early diagnosis and treatment, including antibiotics and early surgical debridement, are associated with a significant decrease in mortality in postoperative and visceral perforation cases, resulting in survival rates up to 80% and 90%, respectively. The impact is significantly less in mediastinitis secondary to direct extension, which has mortality rates of 23-42%, despite aggressive therapy and intervention.

What other considerations exist for patients with acute mediastinitis?

Primary considerations for the diagnosis and treatment of the disease have been outlined above.

What’s the evidence?

Akman, C, Kantarci, F, Cetinkaya, S. "Imaging in mediastinitis: a systematic review based on aetiology". Clin Radiol. vol. 59. 2004. pp. 573-585.

(Review of radiographic findings associated with acute mediastinitis.)

Berry, B, Ochsner, J. "Perforation of the esophagus: a 30-year review". J Thorac Cardiovsc Surg. vol. 65. 1973. pp. 1-7.

(Retrospective review of complications associated with esophogeal perforation.)

Braxton, J, Marrin, C, McGrath, P, Ross, CS, Morton, JR, Norotsky, M. "Mediastinitis and long-term survival after coronary artery bypass graft surgery". Ann Thorac Surg. vol. 70. 2000. pp. 2004-2007.

(Retrospective review of more than 15,000 post-surgical cases of acute mediastinitis.)

El Oakley, R, Wright, J. "Postoperative mediastinitis: classification and management". Ann Thorac Surg. vol. 61. 1996. pp. 1030-1036.

(Review of management of post-surgical acute mediastinitis.)

Estera, A, Landay, M, Grisham, J. "Descending necrotizing mediastinitis". Surg Gynecol Obstet. vol. 157. 1983. pp. 545-552.

(Retrospective review of necrotizing mediastinitis from oropharyngeal causes.)

Farinas, M, Gald Peralta, F, Bernal, J, Rabasa, JM, Revuelta, JM, Gonzalez-Macias, J. "Suppurative mediastinitis after open-heart surgery: a case-control study covering a seven-year period in Santander, Spain". Clin Infect Dis. vol. 20. 1995. pp. 272-279.

(Retrospective case-control evaluation factors associated with post-surgical acute mediastinitis.)

Kiernan, P, Hernandez, A, Byrne, WD, Bloom, R, Dicicco, B, Hetrick, V. "Descending cervical mediastinitis". Ann Thorac Surg. vol. 65. 1998. pp. 1483-1488.

(Retrospective case presentation and literature review of causes and outcomes from descending acute mediastinitis.)

Loop, FD, Lytle, BW, Cosgrove, DM, Mahfood, S, McHenry, MC, Goormastic, M. "J Maxwell Chamberlain memorial paper. Sternal wound complications after isolated coronary artery bypass grafting: early and late mortality, morbidity, and cost of care". Ann Thorac Surg. vol. 49. 1990. pp. 179-186.

(Retrospective review of sternal wound complications associated with coronary artery bypass graft surgery.)

Milano, CA, Kesler, K, Archibald, N, Sexton, DJ, Jones, RH. "Mediastinitis after coronary artery bypass graft surgery: risk factors and long-term survival". Circulation. vol. 92. 1995. pp. 2245-2251.

(Discussion of risk factors for mediastinitis following coronary artery bypass graft surgery.)

Ohri, SK, Liakakos, TA, Pathi, V, Townsend, ER, Fountain, SW. "Primary repair of iatrogenic thoracic esophageal perforation and Boeerhaave's syndrome". Ann Thorac Surg. vol. 55. 1993. pp. 603-606.

(Discussion of surgical intervention for esophageal perforation.)

Pierce, TB, Razzuk, MA, Razzuk, LM, Luterman, DL, Sutker, WL. "Acute mediastiniti". Proc (Bayl Univ Med Cent). vol. 13. 2000. pp. 31-33.

(Case presentation and review of acute mediastinitis.)

Risnes, I, Abdelnoor, M, Almadahl, S, Svennevig, JL. "Mediastinitis after coronary bypass grafting risk factors and long-term survival". Ann Thorac Surg. vol. 89. 2010. pp. 1502-1509.

(Retrospective, case-control study of 107 patients with post-surgical acute mediastintis.)

Sakamoto, Y, Tanaka, N, Furuya, T, Ueno, T, Okamoto, H, Nagai, M. "Surgical management of late esophageal perforation". Thorac Cardiovasc Surg. vol. 45. 1997. pp. 269-272.

(Retrospective review and discussion of surgical management for esophageal perforation.)

Singhal, P, Kejriwal, N, Lin, Z, Tsutsui, R, Ullal, R. "Optimal surgical management of descending necrotising mediastinitis: our experience and review of literature". Heart, Lung and Circ. vol. 17. 2008. pp. 124-128.

(Review of surgical management for descending etiologies of acute mediastinitis.)

Trouillet, JL, Vuagnat, A, Combes, A, Bors, V, Chastre, J, Gandj. "Acute poststernotomy mediastinitis managed with debridement and closed-drainage aspiration: factors associated with death in the intensive care unit". J Thorac Cardiovasc Surg. vol. 129. 2005. pp. 518-524.

(Retrospective review of surgical intervention for post-surgical acute mediastinitis.)
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