What every physician needs to know:
Acute mediastinitis is an uncommon but potentially life-threatening infection that can affect any of the mediastinal compartments (anterior, middle, or posterior) from the thoracic inlet down to the diaphragm. 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, perforated viscus, or during procedures/surgery. Computed tomography (CT) of the neck, chest, and upper abdomen 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; mortality associated with this disease remains high.
Classification:
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 categorized 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, middle, and posterior). 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.
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Some anatomical classification systems also designate a superior compartment; acute mediastinitis in this compartment is usually associated with descending causes of infection from primary retropharyngeal infection or from trauma (including procedures or surgery) involving the head or neck. Procedures that can predicate superior compartment mediastinitis include dental procedures, intubation, upper endoscopy, and surgery of 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 appears toxic with clinical evidence of sepsis, including tachypnea, tachycardia, fever, chills/rigors, and hypotension/shock. Pneumothorax, subcutaneous emphysema, or pneumomediastinum can also be associated with the disease, especially if there is a disruption in the aerodigestive tract (pharynx, tracheobronchial tree, or esophagus).
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 dysphagia or dyspnea from deviation or compression of the trachea or esophagus, respectively, hoarseness from compression of the recurrent laryngeal nerve, Horner’s syndrome from stellate ganglion involvement, or tachycardia from vagus nerve involvement.
However, these signs and symptoms are non-specific; diagnosis is made by findings of acute inflammation, phlegmon, 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 non-specific and therefore ruling out other possible etiologies in the differential diagnosis is essential. A history of infections with potential for direct extension, recent oropharyngeal/neck or thoracic surgery, or recent procedures or trauma to the aerodigestive tract should prompt consideration for acute mediastinitis.
Other infections of the thorax (e.g., pneumonia, bronchitis) or even systemic infections/sepsis, that 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 from a retropharyngeal abscess.
Spontaneous mediastinitis
Primary mediastinitis is usually associated with anthrax, resulting 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 hide 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 wool sorter’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 hiatuses.
Postoperative
Post-surgical mediastinitis, now the most common source of acute mediastinitis, occurs in 1-4% of patients following cardiothoracic surgery. A wide variety of organisms are associated with post-surgical mediastinitis, including methicillin-sensitive Staphylococcus aureus (MSSA), methicillin-resistant Staphylococcus aureus (MRSA), gram negative bacilli, coagulase negative Staphylococcus, and Streptococcus. Recent reports suggest MRSA accounts for up to 65% of cases, resulting in an 11-fold increase in mortality relative to MSSA mediastinitis. In response, the Society of Thoracic Surgeons published a Class I recommendation for routine prophylaxis for cardiac surgery patients using intranasal mupirocin preoperatively, citing Level A evidence in its guidelines for antibiotic choice in 2007.
Disruption of mucosa
The other major etiology of acute mediastinitis is introduction of infection into the mediastinal space from perforated viscus. Procedural instrumentation accounts for 50-75 percent of esophageal perforations. Instrumentation includes unintentional esophageal intubation, transesophageal echocardiogram, and upper endoscopy with flexible or rigid esophagoscopy. Spontaneous perforations from Boerhaave’s syndrome or erosion from tumor or foreign bodies are the remaining most common causes of esophageal perforation.
Perforation of the tracheobronchial tree usually results from penetrating trauma or endotracheal intubation. Unlike rigid bronchoscopy, flexible bronchoscopy is much less likely to result in tracheobronchial injury unless therapeutic interventions are performed. Disruption of the tracheobronchial tree is less likely to lead to the development of acute mediastinitis compared to esophageal disruption.
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, Mycobacteria, 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 bilateral internal thoracic artery grafts (possible devascularization of the sternum) have also been shown to increase risk for mediastinitis.
What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?
Patients may have leukocytosis or metabolic acidosis 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 and the sensitivity may be limited, as antibiotics have usually already been administered.
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 for acute mediastinitis.
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. If esophageal perforation is suspected and esophagram does not show leakage of contrast, an upper endoscopy should be performed to rule out esophageal perforation or source. Surgical exploration, drainage, and debridement are the definitive treatment, but also offer the best means of confirming the diagnosis 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?
A patient with acute mediastinitis must be evaluated for drainage and debridement by a surgeon. If there are areas of undrained abscesses, these must be explored, via neck, chest or often both approaches, with side of surgery determined by the location of such collections. If there are no areas of undrained infection, occasionally non-operative management with antibiotics only is considered. Treatment with broad-spectrum antibiotics covering the most common pathogens including gram negatives, anaerobes and possible fungi for several weeks is recommended following drainage or in all patients treated medically. 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.
As stated above, surgical consultation is mandatory for suspected acute mediastinitis, as intervention with extensive surgical exploration and debridement is usually required. Surgical debridement is often achieved via a posterolateral thoracotomy; however, the approach must be tailored to the underlying pathology, which may require a cervical or subxiphoid approach, clamshell incision, or median sternotomy. Infrequently, percutaneous drainage with tube thoracostomy, pigtail catheter, or image-guided drain placement can be considered in cases of isolated mediastinal abscesses. Post-sternotomy mediastinitis requires early surgical debridement and possible partial or complete sternal excision. If feasible, primary sternal re-closure with a closed mediastinal suction/irrigation system is preferred. Temporary vacuum-assisted closure (V.A.C.®) therapy is another option as a bridge to sternal reconstruction with a vascularized tissue reconstruction, which may include pectoralis major, rectus abdominis, and/or omental flaps.
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 for osteomyelitis. CT scans are used to monitor the extent and progression of disease, with particular attention to areas of undrained collection if the patient does not demonstrate clinical improvement.
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 has significantly decreased the mortality associated with this uncommon but often fatal disease.
Early diagnosis and treatment, including antibiotics and early surgical debridement, is 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?
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Engelman, R, Shahian, D, Shemin, R, Guy, S, Bratzler, D, Edwards, F. “The Society of Thoracic Surgeons Practice Guideline Series: Antibiotic Prophylaxis in Cardiac Surgery, Part II: Antibiotic Choice”. Ann Thorac Surg. vol. 83. 2007. pp. 1569-76. (Society of Thoracic Surgeons workforce guidelines on antibiotic prophylaxis for cardiac surgery, including recommendations to prevent postoperative mediasitnitis.)
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 mediastinitis”. 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.)
Schimmer, C, Sommer, SP, Bensch, M, Elert, O, Leyh, R. “Management of Poststernotomy Mediastinitis: Experience and Results of Different Therapy Modalities”. Thorac Cardiov Surg. vol. 56. 2008. pp. 200-204. (Review post-sternotomy mediastinitis management.)
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.)
Tom, TS, Kruse, Michael, Reichman, RT. “Update: Methicillin-Resistant Staphylococcus aureus Screening and Decolonization in Cardiac Surgery”. Ann Thorac Surg. vol. 88. 2009. pp. 695-702. (Review of MRSA surveillance in cardiac surgery.)
Trouillet, JL, Vuagnat, A, Combes, A, Bors, V, Chastre, J. “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.)
**The original authors for this chapter were Drs. Ali Musani and David Hsia. The chapter was revised by Drs. Julian Horwitz and Andrea Wolf.
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