Acute infection of the mediastinum is rare. The most common cause of acute mediastinitis is iatrogenic oesophageal perforation during diagnostic or therapeutic endoscopic procedures. Forceful vomiting may result in oesophageal perforation (Boerhaave's syndrome) and a leak into the mediastinum can result in acute mediastinitis. Such tears are almost invariably just above the gastro-oesophageal junction. Other causes of acute mediastinal infection are leakage from the oesophagus into the mediastinum through a necrotic neoplasm, and extension of infection from the neck, retroperitoneum or adjacent intrathoracic or chest wall structures into the mediastinum. Clinically, the patients are often very ill with an abrupt onset of high fever, tachycardia and chest pain. Diffuse mediastinitis has a very poor prognosis. The mortality associated with acute mediastinitis from oesophageal perforation is 5–30% even with appropriate treatment.
The CXR may show widening and ill-defined mediastinal outline adjacent to the oesophagus. Streaks or collections of air may be seen within the mediastinum, and there may even be mediastinal air–fluid levels. Air may also be seen in the soft tissues of the neck. Pleural effusions are frequent and are usually on the left. Lower lobe pneumonia or atelectasis often complicates the radiographic picture. Radiologically, detection of oesophageal perforation relies on the presence of indirect signs, including pneumomediastinum, left pleural effusion and pneumothorax. An oesophagram using water-soluble contrast medium may show the site of perforation, with extravasation into the mediastinum.
CT is optimal in evaluating suspected mediastinitis and mediastinal abscess. CT shows obliteration of the normal mediastinal fat planes, oesophageal thickening and extraluminal gas bubbles within the mediastinum. In advanced cases there may be walled-off discrete fluid or air–fluid collections indicating abscess formation (Fig.1). There may be an associated pleural effusion, empyema, subphrenic or pericardial collection. When acute mediastinitis is suspected following sternotomy, CT shows the extent of inflammation and any drainable mediastinal or pericardial fluid collections. Distinguishing a retrosternal haematoma from reactive granulation tissue or cellulitis is difficult, as is distinguishing osteomyelitis from the direct effects of the surgical incision. It should be remembered that substernal fluid collections and tiny pockets of air are normal in the first 20 days following sternotomy. Therefore, before gas-forming infections can be diagnosed, the air collections must appear de novo or must progressively increase in the absence of any other explanation. In descending necrotising mediastinitis, CT shows solitary or multiple fluid collections, which may be contiguous with other fluid collections in the cervical region and diffuse obliteration of normal fat planes related to fasciitis.
FIGURE 1 ■ Mediastinal abscess. An 83-year-old man had a contrast medium-enhanced CT of the chest (A–D) caused by persistent fever and chest pain following mitral valve replacement and ascending aortic graft repair. There is a large fluid collection with peripheral enhancement consistent with an abscess located posterior to the sternum and in close association with the aortic graft (A).
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