Acute mediastinitis is a life-threatening disorder that causes severe morbidity in the afflicted patient. All three mediastinal compartments can be affected; the anterior compartment most commonly after sternotomy for cardiac surgery, the middle compartment usually from esophageal perforation, and the posterior compartment from direct extension from the neck, lung, or spine. Instrumental perforation of the esophagus is the most common cause of acute mediastinitis in the United States.
Mediastinitis from Esophageal Perforation
Instrumental perforation of the esophagus now accounts for almost one-half of all esophageal perforations.9 Perforation is more common after rigid esophagoscopy, dilation of a stricture, and pneumatic dilation for achalasia, but it also occurs after variceal sclerosis, esophageal tube placement (nasogastric, Sengstaken–Blakemore, and salivary bypass tubes), and simple flexible esophagoscopy. Boerhaave syndrome (postemetic rupture) was described in 1724 but still represents a diagnostic challenge and remains a major consideration in patients with otherwise unexplained mediastinitis (Fig. 80-8). Patients usually present with the abrupt onset of severe substernal chest pain, which is pleuritic after forceful vomiting or retching. Dyspnea is common even in the absence of pneumothorax. Shock develops quickly and the patient usually appears gravely ill. Examination reveals tachypnea, tachycardia, fever, hypotension, splinting of the chest and abdomen, and cervical emphysema. Radiographic findings include cervical or mediastinal emphysema, pneumothorax, and pleural effusion. A contrast esophagogram (usually with water-soluble contrast) should be performed immediately when the diagnosis is suspected, but one should be aware that this study has a false-negative rate of 10%. A chest CT scan is the next best study in a patient in whom esophageal perforation is suspected but who has a negative esophagogram. Prompt diagnosis and, therefore, a high index of suspicion are essential, as the frequency of complications and the mortality rate are directly dependent on the time elapsed between perforation and treatment. The differential diagnosis is broad and includes perforated ulcer, acute pancreatitis, myocardial infarction, pneumonia, aortic dissection, and pulmonary embolism.
Water-contrast esophagogram of a patient with Boerhaave syndrome. Note extensive extravasation of contrast and mediastinal emphysema.
Treatment should be instituted urgently and involves surgical debridement of necrotic tissue, secure closure of the perforation, correction of any distal obstruction, and wide drainage, usually performed through a left thoracotomy.10 Recent reports suggest favorable results in appropriately selected patients’ management with covered esophageal stents and image-directed drainage.11 Appropriate broad-spectrum antibiotics with anaerobic coverage and the maintenance of proper nutrition are also integral components of the management plan. Esophagectomy is occasionally required in the presence of a perforated, nondilatable stricture, a destroyed esophagus in which direct repair is not possible, or cancer. Nonoperative treatment is rarely appropriate but may be instituted in highly selected cases (i.e., contained, asymptomatic instrumental perforations) in which a significant interval has passed and the patient is clinically stable. Mortality is less than 10% if the perforation is recognized and repaired within 24 hours, whereas mortality increases to 30% to 40% if more than 24 hours have elapsed between perforation and repair. The mortality rises even higher with advanced age of the patient.
Tracheobronchial perforation is rare and is most commonly seen following trauma or instrumentation. Less common causes include anastomotic dehiscence after lung transplantation or airway surgery and necrotizing infections involving the airway. Severe mediastinitis is rare after tracheobronchial disruption, presumably due to the less noxious nature of its contents and better containment. Intubation is now the most frequent cause of tracheobronchial injury, but injury can be avoidable with gentle and proper technique. Blood in the airway, airway obstruction (infrequent), subcutaneous and mediastinal emphysema, and pneumothorax are the common presenting signs. Prompt recognition and operative repair are necessary and yield excellent results, although small tears in the cervical trachea may often be managed with antibiotics alone, without operation.
Descending Necrotizing Mediastinitis
Mediastinitis occasionally develops after severe deep head and neck infections that originate from the oropharynx or hypopharynx.12–18 Most patients present with a mixed aerobic and anaerobic infection. Previously these infections had a fulminant, often lethal course with mortality as high as 40%. Extension of the cervical infection down the layers of the deep cervical fascia into the mediastinum leads to this syndrome of descending necrotizing mediastinitis. Downward spread is aided by gravity, negative intrapleural pressure, and lytic dissolution of fascia and fat. The deep cervical fascia consists of three layers: the superficial (buccopharyngeal) layer, the middle (visceral) layer, and the deep layer that is further subdivided into the alar and prevertebral layers. All layers originate from the base of the skull. The superficial layer terminates at the superior chest. The visceral layer terminates as a continuation of the pericardium. The potential space between the superficial and middle layers, called the retropharyngeal space, allows infection to descend to the middle of the chest. The alar layer terminates at the diaphragm. The potential space between the middle and the alar layer confines infection above the diaphragm. Rare infections between the alar and prevertebral layers may allow the spread of infection below the diaphragm. Endo et al.15 classified descending necrotizing mediastinitis according to the extent of the infection to guide the surgical management according to this classification: Type 1, infection above the carina, Type IIA, infection to the level of the lower anterior mediastinum, and Type IIB, infection involving the lower anterior and posterior mediastinum.
The criteria for diagnosing descending necrotizing mediastinitis were established by Wheatley et al.14 in 1990 and include (1) severe head and/or neck infection, (2) radiographic evidence of mediastinitis, (3) evidence of necrotizing infection, and (4) establishment of a relationship between the cervical infection and necrotizing mediastinitis. Ridder et al.13 recently reported a large series and performed an updated meta-analysis of collected series that illustrate the cardinal features of this important clinical problem. Patients present with odyophagia (66%), neck swelling (41%), neck pain (21%), dyspnea (21%), and chest pain (5%). Signs include fever (100%) and swelling and redness of the oropharynx (69%). About 2/3 of patients have comorbidities that are associated with immunosuppression or chronic illnesses. Common causes include tooth abscesses, pharyngitis, peritonsillar abscess, epiglottis, and perforation of the pharynx. A period of delay of either presentation or diagnosis is common.
CT with intravenous contrast should be performed on all severe neck infections and suspected cases of descending necrotizing mediastinitis to identify radiologic signs of mediastinitis that may not be clinically apparent (Fig. 80-9). Streptococcus species are the most common aerobic organisms and Bacteroides species are the most common anaerobic organisms isolated. Antibiotics should be started upon clinical suspicion of this diagnosis. All patients require cervical incision, exploration, drainage, and treatment of the underlying condition. Many patients also require transthoracic drainage by a variety of routes, including thoracotomy, videothoracoscopy, transmediastinal, and subxyphoid. Many patients require several trips to the operating room for repeat debridements and drainage procedures. Tracheostomy is often required due to the severity of upper airway swelling. The mean length of stay is 36 days reflecting the severity of this illness. Recent series report an average mortality of 11%.
Representative CT images from a patient with descending necrotizing mediastinitis from a retropharyngeal abscess. A. Low-density collection surrounding the trachea and retropharyngeal space. B. Right paratracheal collection. C. Collection surrounding the airway and esophagus with small loculated empyemas. D. Bilateral empyemas. This patient required transcervical and transthoracic drainage. (Reproduced with permission from Chen KC, Chen JS, Kuo SW. Descending necrotizing mediastinitis: a 10-year surgical experience in a single institution. J Thorac Cardiovasc Surg. 2008;136(1):191–198.)
Mediastinitis from Direct Extension
Necrotizing pneumonias may cause mediastinitis by direct extension, most often in immunocompromised patients. Aspergillosis of the posterior mediastinum has been reported with increasing frequency and is highly lethal. Treatment involves reversal of immunosuppression (if possible), appropriate antibiotic therapy, and surgical drainage and debridement.
Pancreatitis can extend from the retroperitoneum into the mediastinum and may present as a mediastinal process with evidence of mediastinitis. Pancreatic pseudocysts can also erode into the mediastinum and cause pleural effusions with increased levels of amylase. Treatment is directed at providing adequate drainage of the pseudocyst, usually by internal drainage into the stomach. The pleural effusion(s) may require tube thoracostomy drainage.
Sternal wound infection with resulting mediastinitis is a relatively new entity, which emerged in the era of modern cardiac surgery. The incidence remains low at 0.5% to 1% of all sternotomies, but such infection is a source of major morbidity, prolonged hospital stay, and significant mortality (0%–30%; average, 15%). Multivariate analysis has demonstrated that prolonged preoperative stay, advanced age, BMI >30 kg/m2, chronic obstructive pulmonary disease, diabetes, reoperation, blood transfusions, and reexploration for bleeding are significant risk factors.19,20 Staphylococcus aureus is the most common causative organism. Other organisms commonly isolated include Staphylococcus epidermidis, various gram-negative organisms, as well as Candida species and atypical mycobacteria. The etiology appears to be a combination of intraoperative contamination and hematogenous seeding of mediastinal clot in the early postoperative period. Most patients with poststernotomy mediastinitis have an insidious presentation with low-grade fever and leukocytosis, wound problems (erythema, drainage, sternal instability), and eventually bacteremia. Infections caused by gram-negative organisms tend to become manifest earlier than those caused by gram-positive organisms. Most infections occur within the first or second week following the operative procedure. A high index of suspicion must be maintained so that an early diagnosis can be made and appropriate treatment instituted. Wound aspiration, local wound exploration, and CT imaging aid in making the diagnosis. Exploration in the operating room remains the definitive diagnostic maneuver and material should be obtained for culture at that time if it has not been obtained before or has been unrevealing.
If the infection is relatively early and the bony sternum appears viable, debridement, drainage, and saline (or antibiotic) irrigation with reclosure are indicated.20 Although it may seemingly violate time-honored surgical principles (leaving contaminated wounds open, to close by secondary intention), primary closure of the early, infected sternum yields excellent results in many patients if adequate debridement is carried out. Of course, proper and prolonged antibiotic therapy is necessary. Reported mortality rates approach zero for these early infections if managed appropriately. Late sternal wound infections with mediastinitis present a more formidable challenge, in part due to the extensive sternal osteomyelitis and necrotic soft tissue which, when debrided, result in significant dead space, thereby creating a favorable environment for continued bacterial proliferation and persistent infection. The presence of prosthetic material, such as sutures, Teflon pledgets, or prosthetic grafts further complicates the problem and may lead to catastrophic hemorrhage with a fatal outcome. Mediastinitis in the presence of a prosthetic aortic graft is a particularly disastrous complication. Most surgeons favor extensive sternal debridement, usually with total sternal excision and rotation of pectoralis muscle flaps (bilateral) or transposition of gastrocolic omentum to fill the dead space with viable tissue. More recently successful outcomes have been reported with the use of negative pressure wound therapy (vacuum-assisted closure [VAC]).21 Caution is required to protect the right ventricle when using negative pressure wound therapy to prevent erosion of the ventricle against the sternum.22
Anthrax, caused by Bacillus anthracis, was previously found primarily in the Middle East, with farm animals as the primary reservoir.23,24 Following the advent of substantial immigration and bioterrorism, anthrax has been diagnosed in the United States and has been prominent in the mainstream media. An index case of fatal inhalational anthrax complicated by hemorrhagic mediastinitis due to bioterrorism in the United States has been reported in detail.25 The inhalation of anthrax spores allows entry into the lungs with subsequent transport to the mediastinal lymph nodes by alveolar macrophages. A hemorrhagic mediastinitis typically quickly ensues and death is common. Gram-positive bacilli are present in tissue specimens. The initial treatment involves the initial use of either ciprofloxacin or doxycycline plus one or two additional antimicrobial agents with activity against B. anthracis.