Mediastinitis

Etiology

Mediastinitis can be caused by various pathologies that breach the integrity of the mediastinal structures, including iatrogenic, traumatic, or infectious causes. Iatrogenic causes are common and typically involve complications from medical procedures, such as cardiac surgery, esophageal dilation, or endoscopic interventions, where inadvertent injury to the mediastinal tissues can introduce infection. Traumatic causes include direct physical injuries to the chest from accidents or penetrating wounds, which can disrupt the trachea or esophagus, leading to contamination of the mediastinum. Infectious causes often arise from nearby infections spreading to the mediastinum, such as in descending necrotizing mediastinitis, where infections from the oropharynx extend into the mediastinal space. Additionally, infections from other areas, such as pulmonary infections or complications from pancreatitis, can occasionally spread and cause mediastinitis.

Mediastinitis due to esophageal perforation can occur regardless of the perforation's cause, as the rupture allows gastric fluid to contaminate the mediastinum with digestive flora. This condition is often iatrogenic, accounting for 50% of cases, although it can also be spontaneous or traumatic.[7] Common causes include tracheal and/or esophageal rupture from endoscopic procedures, Boerhaave syndrome, and foreign body aspiration. Other rarer causes include direct traumatic injury, spread of pulmonary infection, and pancreatitis.[3][2][8]

Poststernotomy mediastinitis is an uncommon condition, occurring in 0.5% to 2.5% of cases.[9] Despite advances in surgical techniques, perioperative antibiotics, and guidelines aimed at preventing poststernotomy infections, the incidence of poststernotomy mediastinitis has remained consistent over the years. Notably, it is thought to be caused by the intraoperative introduction of infection or from infection of the surgical wound that seeds the mediastinum. Poststernotomy mediastinitis has also been referred to as deep sternal wound infection.[1][10]

Descending necrotizing mediastinitis, originating from oropharyngeal infections, occurs when the infection spreads from the cervical area to the mediastinum. This condition affects approximately 2% to 5% of deep neck infections, such as neck abscesses, Ludwig's angina, and other dental infections. Commonly, odontogenic or pharyngeal sources cause inflammation via the fascial planes, impacting the posterior mediastinum.[4][11]

Fibrosing mediastinitis, although believed to be idiopathic, has been associated with both infectious and noninfectious processes. Potential infectious causes include histoplasmosis and tuberculosis, linked to an immune-mediated hypersensitivity reaction.[12] Noninfectious causes include sarcoidosis, retroperitoneal fibrosis, and Riedel thyroiditis.[13]

Epidemiology

The exact incidence and prevalence of mediastinitis cases are not well documented. Postoperative mediastinitis has a relatively low incidence, ranging from 0.3% to 5%, with an average of 1% to 2% at most facilities.[14][15] Higher incidence rates have been associated with cardiac transplant surgeries, coronary artery bypass graft (CABG) with thoracic aortic surgery, and CABG with valvular surgery. Lower incidence rates have been found with isolated CABG, valvular repairs, and thoracic repairs.[14][16] 

Previously, descending necrotizing mediastinitis comprised 70% of mediastinitis cases; however, a significant decrease in incidence is observed due to advancements in imaging and antibiotics.[17] Regarding fibrosing mediastinitis, associations with a granulomatous subtype are observed, which is more frequently found in North America, where there is a higher prevalence of Histoplasma capsulatum.[13][18]

Pathophysiology

Mediastinitis is due to a breach in the mediastinal structures from an inciting incident, including a direct injury or secondary to an acute infectious process. Postoperative mediastinitis is often linked to intraoperative contamination, although infection can also spread postoperatively from an infected surgical wound into the mediastinum. Most cases are caused by gram-positive bacteria, particularly Staphylococcus aureus and coagulase-negative Staphylococcus, accounting for 60% to 80% of cases. Infections linked to S aureus frequently result from intraoperative contamination by the surgeon or surgical staff who are carriers or from the patient’s own nares. Coagulase-negative Staphylococcus, commonly found in skin flora, frequently infects surgical wounds due to its ubiquitous presence on the skin. Although S aureus and coagulase-negative Staphylococcus are the most common causes, other gram-positive and gram-negative bacteria and fungi (rarely) can also be causative agents.[10][14][19]

Descending necrotizing mediastinitis is characterized by the spread of infection from the pharynx, odontogenic sources, or cervical areas into the mediastinum. The disease can extend through the deep fascial planes and typically affects the posterior mediastinum. In addition, the disease presents with manifestations such as cellulitis, abscess formation, sepsis, and necrosis, marking a fulminant and severe course.[11] Polymicrobial infection accounts for approximately 58% of cases, with the remainder being solely gram-positive organisms, including Streptococcus and anaerobes. In patients with diabetes, Klebsiella and other gram-negative enterobacteria can be causative agents.[4]

Although the exact pathophysiology of fibrosing mediastinitis is unknown, it has been shown to have multiple variants, including a granulomatous and a non-granulomatous form, which can then be divided into either diffuse or focal distributions.[20] Some forms, especially those associated with histoplasmosis, are believed to be due to a delayed immune-mediated hypersensitivity response. Histoplasmosis and tuberculosis have been closely associated with the focal form, while the diffuse form is linked with autoimmune syndromes.[13]

History and Physical

Patients with acute mediastinitis typically appear ill and may report symptoms such as dysphagia, chest pain, fever, and respiratory distress. Obtaining a thorough history, including recent surgeries or infections, along with a comprehensive medical, travel, and social history, is crucial to assessing risk factors associated with the development of mediastinitis.

When evaluating a patient for postoperative mediastinitis, it is essential to document important risk factors such as diabetes, obesity, smoking, renal failure, and an immunocompromised state. Additionally, obtaining a detailed surgical history is critical, as patients with longer surgical times, repeated thoracic surgeries, or excessive cautery might have an increased predisposition to developing postoperative mediastinitis. Findings obtained during physical examination of patients suspected of mediastinitis often include sternal instability, wound discharge, tenderness, and pain. Mediastinitis should be considered in patients experiencing unexplained slow postoperative recovery. Although mediastinitis can present up to a year after surgery or longer, most cases occur within 30 days of the surgery.[14][15][16][19]

If descending necrotizing mediastinitis is suspected, it often indicates an inadequately treated head or neck infection that has subsequently spread to the mediastinum. In addition to the previously mentioned symptoms, these patients may present with dyspnea, and on physical examination, signs of cervical or thoracic pain with crepitus and erythema may be noted.

Fibrosing mediastinitis often progresses insidiously, leading many patients to be asymptomatic initially. When symptoms do appear, common presentations include cough, shortness of breath, pleuritic chest pain, hemoptysis, fever, or weight loss.[21] These individuals may have a history of recurrent lung infections. As the disease advances, an obstructive or compressive pattern may develop, affecting organs within the mediastinum. Patients may present with airway or vascular compromise, such as in superior vena cava syndrome. A comprehensive history, including travel history, is essential due to its association with conditions such as histoplasmosis and tuberculosis.[13]

Evaluation

In cases of suspected mediastinitis, patients should undergo a prompt primary assessment of the airway, breathing, and circulation. If necessary, resuscitative measures should be prioritized over laboratory workup and imaging. Once the patient is stabilized, obtaining critical imaging is crucial for diagnosis. While a chest radiograph may reveal signs of mediastinal widening or pneumomediastinum, it often lacks detail in showing the full extent of the disease process.[15] Comparatively, computed tomography (CT) and magnetic resonance imaging (MRI) are better diagnostic tools for evaluating mediastinitis.

Postoperative mediastinitis can be challenging to assess with imaging due to physiological changes observed postoperatively in radiographic studies. The sensitivity and specificity of CT will notably improve after 14 days following surgery.[22] Mediastinal aspiration can also be performed to aid in the diagnosis.[15][23] 

For descending necrotizing mediastinitis, imaging may reveal a widened mediastinum, increased fat density within the mediastinum, air-fluid levels indicating abscess formation, or pleural effusions often associated with mediastinitis. If the pericardium is affected, findings may include thickening, pericardial effusion, or pneumopericardium.[4] In addition, a CT of the cervical area should be obtained to identify the primary source of infection.[2]

Laboratory studies for acute mediastinitis may reveal leukocytosis, elevated C-reactive protein, and increased procalcitonin levels. Blood cultures should be obtained, especially in patients suspected of postoperative mediastinitis, as bacteremia is frequently associated with the disease.[15][23]

Fibrosis mediastinitis most commonly manifests as an infiltrative mass on CT, which distorts the mediastinal fat planes and extends into surrounding mediastinal structures. The condition can manifest as diffuse involvement or localized to a specific area. Additionally, it may present with calcifications on imaging, particularly when associated with histoplasmosis. Localized masses are often found in the hila, paratracheal, or subcarinal areas.[21] In addition, commonly present symptoms include narrowing of the tracheal, bronchial, pulmonary artery, and superior vena cava or esophagus, as well as pulmonary infiltrates, pulmonary volume loss, collapse, or hyperlucency.[24] Chest radiographs typically show abnormalities in these patients, although findings may be subtle. Mediastinal widening with distortion of the mediastinal interfaces is frequently noted. In cases where pulmonary vessel involvement leads to pulmonary hypertension, peribronchial cuffing and septal thickening may be present. Pleural effusions are less often seen.[21]

Treatment / Management

Treatment for acute mediastinitis usually focuses on the early initiation of antibiotics and surgical debridement as necessary.[3][14][25] Antibiotics should initially be broad-spectrum and subsequently tailored based on culture results.(B2)

Various surgical approaches exist for mediastinitis, ranging from minimally to maximally invasive, selected based on the extent and severity of the condition. Following surgical intervention, it is crucial to conduct repeat CT scans, closely monitor laboratory parameters, and frequently reassess the patient's clinical status to evaluate the need for further surgical intervention. Patients with mediastinitis necessitate ongoing evaluation and treatment in an intensive care unit.[2]

The exact pathogenesis of fibrosing mediastinitis remains unknown, leading to a lack of standardized treatment regimens.[13] Although evidence supporting successful medication therapies is limited, current strategies often involve immunosuppressants, corticosteroids, or antifungals due to the limited treatment options available for these patients.[20] Surgical interventions, such as decompressive procedures such as stent placement or bypasses of affected structures, should be considered for symptomatic patients.[13][26][27](B3)

Differential Diagnosis

When evaluating a patient suspected of having mediastinitis, it is crucial to consider a comprehensive differential diagnosis, as this condition can overlap with other thoracic and systemic disorders. Accurate and prompt differentiation among these conditions is essential to ensure appropriate and timely treatment.

The differential diagnoses of mediastinitis include, but are not limited to, the following conditions:

• Coronary artery disease
• Acute coronary syndrome
• Pulmonary embolism
• Pneumothorax
• Aortic dissection
• Cellulitis
• Localized infection in the head or neck
• Tumor or mass [8][13][15]

Prognosis

Postsurgical and descending necrotizing mediastinitis are both associated with high morbidity and mortality if not treated early. They are considered life-threatening conditions, with descending necrotizing mediastinitis having a mortality rate of 20% to 40% despite current treatments.[3][2] Advancements in surgical management techniques and improved evaluation and treatment regimes have led to a reported mortality rate for postsurgical mediastinitis of 1% to 14%, an improvement from past rates of 12% to 50%.[28]

Comparatively, fibrosing mediastinitis generally carries a better prognosis when unilateral involvement is present compared to bilateral involvement.[26] However, despite its relatively slow progression, patients often succumb to recurrent pneumonia or pulmonary heart disease associated with fibrosing mediastinitis.[13]

Complications

Mediastinitis can lead to severe and potentially life-threatening complications if not promptly diagnosed and treated. Immediate intervention is crucial to mitigate these risks and improve patient outcomes.

Complications of mediastinitis may include the following:

• Pericarditis
• Myocarditis
• Recurrent pneumonia
• Lung abscess
• Pleural effusion
• Sepsis
• Obstructed airway
• Severe bleeding or hemoptysis
• Cor pulmonale
• Multiorgan failure
• Scarring and fibrosis
• Chronic pain
• Complications from surgical treatment or debridement [14][4][21]