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Mediastinitis is a life-threatening condition that carries an extremely high mortality if recognized late or treated improperly. [1, 2, 3, 4] Although long recognized as a complication of certain infectious diseases, most cases of mediastinitis are associated with cardiac surgery (>300,000 cases per year in the United States). [4, 5] This complication affects approximately 1-2% of these patients. Although small in proportional terms, the actual number of patients affected by mediastinitis is substantial. This significantly increases mortality and cost.

After years of evolution, optimal therapy for mediastinitis is more clearly understood. Future directions for research should focus on prevention, including timely antibiotic administration, sterile technique, prophylactic measures such as topical bacitracin, and meticulous hemostasis. The focus should also include more accurate methods of diagnosis during the first 14 days after surgery, when computed tomography (CT) findings are not reliable.

However, the keys to successful management remain early recognition and aggressive treatment, including sternal reopening and debridement. Further research should also focus on the optimal timing and method of wound closure and the duration of antibiotic therapy required for optimal treatment.

The portion of the thorax defined as the mediastinum extends from the posterior aspect of the sternum to the anterior surface of the vertebral bodies and includes the paravertebral sulci when the locations of specific mediastinal masses are defined. It is limited bilaterally by the mediastinal parietal pleura and extends from the diaphragm inferiorly to the level of the thoracic inlet superiorly.

Traditionally, the mediastinum is artificially subdivided into three compartments (anterior, middle, and posterior) for better descriptive localization of specific lesions. When the location or origin of specific masses or neoplasms is discussed, the compartments or spaces are most commonly defined as follows:

Infection from either bacterial pathogens or more atypical organisms can inflame any of the mediastinal structures, causing physiologic compromise by compression, bleeding, systemic sepsis, or a combination of these.

The origin of infection following open heart operations is not known in most patients. Some believe that the process begins as an isolated area of sternal osteomyelitis that eventually leads to sternal separation. Others hold that sternal instability is the inciting event, and bacteria then migrate into deeper tissues. Inadequate mediastinal drainage in the operating room may also contribute to the development of a deeper chest infection.

The patient’s own skin flora and the bacteria in the local surgical environment are possible sources of infection as well. Because some bacterial contamination of surgical wounds is inevitable, host risk factors are likely critical in promoting an active infection.

Most cases of mediastinitis in the United States occur following cardiovascular surgery. Risk factors for the development of mediastinitis in this setting include the following:

A study by Perrault et al found that higher body mass index, higher creatinine level, the presence of peripheral vascular disease, preoperative corticosteroid use, and ventricular assist device or transplant surgery were all associated with an increased risk of mediastinal infection; in nondiabetic patients, postoperative hyperglycemia was associated with an increased infection risk. [13]

Additional causes include the following:

Most mediastinitis cases involve gram-positive cocci, [9] with Staphylococcus aureus [19] and Staphylococcus epidermidis accounting for 70-80% of cases (see the image below). [12] Mixed gram-positive and gram-negative infections account for approximately 40% of cases. Isolated gram-negative infections are rare causes.

Fibrosing mediastinitis is most commonly associated with Histoplasma capsulatum and Mycobacterium tuberculosis, though mediastinitis is an extremely rare complication of these infections. [16]

Acute mediastinitis has also been reported as a complication of Epstein-Barr virus infection. [20]

In the United States, mediastinitis most commonly occurs in the postoperative setting following CABG. [4]  The reported incidence of mediastinitis after cardiac surgery has ranged from 0.3% to 3.4%. [5]  At most large surgical centers, the incidence is in the range of 1-2%; however, certain subsets of patients, such as patients who have undergone a heart transplant, are at much higher risk.

The development of mediastinitis dramatically increases mortality. One study showed that postoperatively, a patient’s chance of dying was twice as high when mediastinitis developed as it was when mediastinitis was absent (12% vs 6%). In a review by Goh, in-hospital mortality for poststernotomy mediastinitis ranged from 1.1% to 19%. [5]  Some studies have reported death rates as high as 47%. Mediastinitis also raises the 2-year mortality from 2% to 8% following CABG.

Mediastinitis substantially lengthens the hospital stay as well. Patients with postoperative mediastinitis stay in the hospital six to seven times longer than those without the condition, and total costs may triple. [21]

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Dale K Mueller, MD Co-Medical Director of Thoracic Center of Excellence, Chairman, Department of Cardiovascular Medicine and Surgery, OSF Saint Francis Medical Center; Cardiovascular and Thoracic Surgeon, HeartCare Midwest, Ltd, A Subsidiary of OSF Saint Francis Medical Center; Section Chief, Department of Surgery, University of Illinois at Peoria College of Medicine

Dale K Mueller, MD is a member of the following medical societies: American College of Chest Physicians, American College of Surgeons, American Medical Association, Chicago Medical Society, Illinois State Medical Society, International Society for Heart and Lung Transplantation, Society of Thoracic Surgeons, Rush Surgical Society

Disclosure: Received consulting fee from Provation Medical for writing.

Michael J Dacey, MD Consulting Staff, Department of Internal Medicine, Division of Critical Care, Kent County Hospital

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Shreekanth V Karwande, MBBS Chair, Professor, Department of Surgery, Division of Cardiothoracic Surgery, University of Utah School of Medicine and Medical Center

Shreekanth V Karwande, MBBS is a member of the following medical societies: American Association for Thoracic Surgery, American College of Chest Physicians, American College of Surgeons, American Heart Association, Society of Critical Care Medicine, Society of Thoracic Surgeons, Western Thoracic Surgical Association

Disclosure: Nothing to disclose.

Mary C Mancini, MD, PhD, MMM Surgeon-in-Chief and Director of Cardiothoracic Surgery, Christus Highland

Mary C Mancini, MD, PhD, MMM is a member of the following medical societies: American Association for Thoracic Surgery, American College of Surgeons, American Surgical Association, Phi Beta Kappa, Society of Thoracic Surgeons

Disclosure: Nothing to disclose.

Benson B Roe, MD 

Benson B Roe, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Thoracic Surgery, American College of Cardiology, American College of Surgeons, American Heart Association, American Medical Association, American Society for Artificial Internal Organs, American Surgical Association, California Medical Association, Society for Vascular Surgery, Society of Thoracic Surgeons, Society of University Surgeons

Disclosure: Nothing to disclose.


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