Mediastinitis

Definition, Etiology, PathogenesisTop

Mediastinitis involves an infection in the mediastinum. The infection occurs through inoculation of organisms into the mediastinal space—typically through contiguous spread from nearby tissue spaces—and the subsequent inflammatory response.

Etiology:

1) Acute esophageal perforation: This may be a consequence of spontaneous rupture or due to complications from esophageal or gastric surgery. Organisms typically involved include oral aerobes and anaerobes and Candida spp.

2) Inoculation from the neck: Typically due to an odontogenic infection. Organisms include oral flora (as above).

3) Cardiac surgery: This is a consequence of inoculation of organisms due to contamination of the surgical bed or infection of the wound. Organisms include skin flora, such as staphylococci, streptococci, as well as a significant prevalence of gram-negative bacilliEvidence 1Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to indirectness. Wojnarski CM, Elgudin Y, Rubelowsky JJ, Wilson BM, Donskey CJ, Cmolik BL. Emerging trends in mediastinitis: National Veterans Health Administration experience with methicillin-resistant Staphylococcus aureus prevention. J Thorac Cardiovasc Surg. 2021 Oct;162(4):1125-1130.e1. doi: 10.1016/j.jtcvs.2020.02.116. Epub 2020 Apr 6. PMID: 32386766. and occasionally Candida spp.

4) Other organisms through extension from the lung: Inhalational anthrax leads to hemorrhagic mediastinitis after inoculation of pulmonary lymph nodes. Actinomyces and fungal agents causing mucormycosis may invade through pulmonary tissue planes into the mediastinal space.

5) Chronic fibrosing mediastinitis: A long-term inflammatory response to pulmonary histoplasmosis leading to complications from extrinsic compression of local structures.

Symptoms:

1) Acute mediastinitis presents as severe retrosternal chest pain that intensifies with breathing or coughing; tenderness around the sternum and sternocostal joints; symptoms of pneumomediastinum and subcutaneous emphysema; and symptoms of inflammation (systemic inflammatory response syndrome) or sepsis. In post–cardiac surgery mediastinitis there is instability or inflammatory changes of the sternal wound. Hemorrhagic mediastinitis after anthrax exposure leads to acute respiratory failure and acute respiratory distress syndrome (ARDS).

2) Chronic mediastinitis may present with signs of extrinsic compression of the mediastinal structures from advanced (overwhelming) fibrosis. This may lead to airway obstruction, superior vena cava syndrome, esophageal compression, or constrictive pericarditis.

DiagnosisTop

Diagnosis is made by diagnostic imaging of the mediastinum. Chest radiography may show air in the mediastinum, subcutaneous emphysema, or other complications from esophageal perforation. Computed tomography (CT) is typically used for confirmation. The presence of air, fluid, or distinct collections in the mediastinum is suggestive of acute mediastinitis. In chronic mediastinitis CT scans may show evidence of fibrosis of the mediastinum with compression of nearby anatomic structures.

TreatmentTop

In patients with acute esophageal rupture or after cardiac surgery, debridement of the mediastinal space along with repair of any perforated viscus is needed. Given that there are often different organisms involved, broad-spectrum antimicrobial therapy directed against gram-positive, gram-negative, and anerobic organisms, and occasionally against yeast, is required. A regimen such as vancomycin and piperacillin/tazobactam could be considered while waiting for cultures. Antimicrobial therapy should be subsequently tailored to the results of bacterial cultures. Antifungal therapy could be considered in critically ill patients or those where yeast are isolated from blood or sterile tissues.

Anthrax requires a combination treatment including ciprofloxacin, meropenem, linezolid, and monoclonal antibody therapy.

In chronic fibrosing mediastinitis the disease is mainly due to fibrosis as a consequence of inflammation derived from histoplasmosis. However, at this stage of mediastinitis, treatment has not been shown to alter its course and management is directed at reducing compression of the anatomic structures.