Mediastinitis

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40 Mediastinitis


Ravi Karra and Keith S. Kaye


The mediastinum is the space in the thorax between the lungs; it houses the heart, great vessels, esophagus, trachea, thymus, and lymph nodes. The connective tissues of the mediastinum are continuous with the long fascial planes of the head and neck, one reason why mediastinitis was primarily a complication of pharyngeal infections until the advent of thoracic surgery. By virtue of its deep position within the thorax, the mediastinum is a relatively protected organ space. There are four major portals of entry into the mediastinum: (1) direct inoculation of the mediastinum following sternotomy (i.e., postoperative mediastinitis [POM]); (2) spread along the long fascial planes of the neck (i.e., descending mediastinitis); (3) rupture of mediastinal structures, such as the esophagus; and (4) contiguous spread of infection from adjacent thoracic structures.


Postoperative mediastinitis


Postoperative mediastinitis (POM) is classified as an organ/space infection by Centers for Disease Control and Prevention (CDC) criteria and is a dreaded complication of median sternotomy. POM classically presents as a febrile illness with sternal wound dehiscence and purulent drainage, usually 2 to 4 weeks after sternotomy. Occasionally POM presents as a more chronic, indolent infection months to years after sternotomy. Sometimes, only superficial signs of infection are present, making POM difficult to diagnose. Frequently, a high index of clinical suspicion is required to differentiate POM from a more superficial sternal wound infection.


Pathogenesis

Infection most often occurs as the result of direct inoculation of host bacteria into the mediastinum during surgery. Bacteria that colonize the skin and oral mucosa, such as coagulase-negative Staphylococcus (CoNS) and Staphylococcus aureus are the most common causes of POM. Gram-negative bacilli, a less common cause of POM, are believed to spread to the mediastinum from the abdomen. Infrequently, pathogens such as S. aureus might be introduced into the mediastinum by a member of the surgical team or by contaminated operative instruments. Whether bacterial contamination develops into full-blown infection is a combination of three major factors: (1) inoculum of bacterial contamination, (2) the degree of local tissue and vascular damage, and (3) host immunity. Larger inoculum and greater perioperative tissue damage both increase the risk for infection. Decreased host immunity increases susceptibility to the development of POM, contributing to an elevated risk for mediastinitis after cardiac transplantation.


Epidemiology and outcomes

Despite advances in surgical techniques and the use of preoperative prophylactic antibiotics, rates of POM in the modern era remain around 1.0%. The high number of median sternotomies performed annually makes POM a frequently encountered problem.


Risk factors for the development of POM comprise three categories: (1) host-related factors, (2) hospital-related factors, and (3) technical or operative factors. Host-related factors include diabetes, obesity, advanced age, prior sternotomy, chronic obstructive pulmonary disease, and New York Heart Association (NYHA) class III or IV heart failure. Hospital factors include prolonged postoperative mechanical ventilation and prolonged postoperative stay in an intensive care unit. Operative factors include mobilization of an internal mammary artery, increased duration of surgery, and surgical complexity. Complex surgeries are simultaneous coronary artery bypass grafting and valve repair, “repeat” or “redo” median sternotomy, and surgical re-exploration following initial sternotomy.


POM is associated with significant attributable morbidity and mortality. Estimates of postoperative mortality range from 11.8% to 14% in patients with POM compared to 2.7% to 5.5% in uninfected operative controls. Some series report mortality rates as high as 40%. Risk factors for mortality in the immediate postoperative period are related to the patient (advanced age and postoperative bacteremia), the hospitalization (e.g., mechanical circulatory support and prolonged postoperative mechanical ventilation), technical factors (prolonged operative duration, surgical re-exploration, blood transfusion), and the specific pathogen. POM due to methicillin-resistant S. aureus (MRSA) is associated with particularly adverse clinical outcomes. Patients with POM are not only at increased risk for mortality during the immediate postoperative period but also carry a two- to four-fold increased risk for death for up to 10 years following cardiothoracic surgery. Risk factors for long-term mortality in patients with POM include age >65 years, serum creatinine >2.0 mg/dL prior to surgery, infection with MRSA, delay of sternal closure more than 3 days following therapeutic debridement for POM, and failure to treat POM with effective antimicrobial agents within 7 days of therapeutic sternal debridement.


Descending necrotizing mediastinitis


Mediastinitis arising from the migration of pathogens from head or neck infection, as opposed to direct inoculation of the mediastinum, is classified as descending necrotizing mediastinitis. Pharyngeal infections cause nearly 50% of all descending necrotizing mediastinitis. However, virtually any infection of the head and neck can spread into the mediastinum. If infections of the head and neck are treated with appropriate antimicrobial agents, descending necrotizing mediastinitis can be prevented. In the modern age of antibiotics, descending mediastinitis is becoming increasingly rare.


Pathogenesis

Spread to the mediastinum can occur via each of the three spaces of the head and neck: the pretracheal space (suppurative thyroid and tracheal infections), the perivascular space (oropharyngeal infections), and the retrovisceral space (oropharyngeal infections). Negative intrathoracic pressure during inspiration acts to draw infection into the mediastinum from these spaces. The retropharyngeal space houses the “danger” space, so named because it extends from the base of the skull all the way to the diaphragm. Spread within the retropharyngeal space is involved in the pathogenesis of approximately 70% of cases of descending mediastinitis. Infections of the perivascular space can also be complicated by thrombophlebitis of the jugular vein (Lemierre’s disease) and direct extension of infection into the carotid artery. (See Chapter 10, Deep neck infections.)


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Jun 18, 2016 | Posted by in INFECTIOUS DISEASE | Comments Off on Mediastinitis

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