Mediastinitis Due to Esophageal Perforation

The esophagus is a thin-walled organ, and esophageal perforation is the most common cause of acute mediastinitis. Perforation usually occurs at one of the three sites of anatomic narrowing of the esophagus: (1) the proximal end, at the level of the cricopharyngeal muscle; (2) the midthoracic segment where the aortic arch and left main stem bronchus indent the esophagus; or (3) the transdiaphragmatic segment. Proximal perforations usually are caused by instrumentation or ingestion of a foreign body. The proximal segment is narrow, and perforations generally are located in the posterior wall, adjacent to the prevertebral and retrovisceral spaces. Perforations at the aortic arch usually are caused by ingested foreign objects. Transdiaphragmatic perforations usually are spontaneous. In most such cases, a longitudinal tear occurs on the left posterolateral wall just above the cardia, where the esophagus has little connective tissue support and the intrinsic musculature is weak.

Retching or vomiting can generate sufficient force to cause esophageal perforation, also known as Boerhaave syndrome. Traumatic perforation can occur after blunt trauma, from ingestion of a foreign body, or as a complication of endoscopic or open surgical procedures. Ingestion of coins, teeth, and food particles such as corn chips as well as objects such as a toy soldier or the spring from a clothespin have caused mediastinitis. Children with mediastinitis from erosion of the esophagus caused by a foreign body tend to have small and well-contained perforations. Sharp objects, such as pins and bone fragments, can cause immediate transmural penetration. More commonly, and especially when a blunt object is ingested, the foreign body becomes impacted in the esophagus. Eventually, suppurative necrosis of the wall occurs, with symptoms occurring days, weeks, or months after the ingestion.

Perforations from instrumentation can produce precipitous clinical deterioration from transmural laceration. A superficial tear can occur from which infection subsequently extends, and hours or days can elapse between instrumentation and onset of symptoms. Repair of esophageal atresia is a common condition associated with a tear of the esophagus in childhood. In one review, 7 of 41 infants had a clinically significant esophageal disruption requiring reoperation 1 to 18 days after repair of esophageal atresia. Postoperative perforations of the esophagus usually represent infectious complications of anastomotic leaks occurring after esophageal resection or of esophageal-pleural fistulas that develop after thoracic surgery. Most of these infections do not become apparent until weeks or months after surgery.

Presenting findings of acute mediastinitis after perforation of the esophagus include neck and chest pain, respiratory distress, and dysphagia. Chills, a temperature of 37.8°C to 39°C (100°F to 102°F), and leukocytosis are common. Infants can present with tachypnea, tachycardia, stridor, or a supplemental oxygen requirement. Some patients have a staccato breathing pattern characterized by an inspiratory halt with resumption of inspiration after a brief rest. The onset of symptoms usually is abrupt, and the course is fulminant. Physical findings include cervical tenderness and subcutaneous emphysema in patients with proximal perforations, whereas patients with perforations of the lower esophagus are more likely to have signs suggesting an abdominal catastrophe. Examination of the lung fields often shows nonspecific abnormalities. Children with chronically retained foreign bodies can present with signs suggestive of asthma or reflux.

The principal findings on chest radiographs are a widened mediastinum, subcutaneous and mediastinal emphysema, and pleural effusion. Pleural effusions occur more commonly with perforations of the lower than the upper esophagus and usually involve the left side. Basilar or retrocardiac infiltrates attributed to chemical pneumonitis can occur in the pulmonary segment adjacent to the site of perforation. Additional changes include basilar atelectasis, pneumothorax, or hydropneumothorax. Radiopaque foreign bodies can be detected with plain radiographs, but they are better visualized with mediastinal computed tomography (CT) or magnetic resonance imaging (MRI).

Gas in the soft tissues is highly suggestive of perforation of the esophagus if interpreted in the context of a compatible clinical presentation. Gas in the prevertebral tissue or superior mediastinum occurs most commonly with perforation of the upper esophagus. Other conditions, such as chest wall trauma or perforation of the trachea, also can cause mediastinal emphysema.

Clinical presentation and plain radiographic findings form the basis for the diagnosis of acute mediastinitis caused by perforation of the esophagus. Contrast-enhanced CT or MRI can provide anatomic detail and confirmation of the diagnosis. Findings include esophageal thickening, fluid collections in the mediastinum adjacent to the perforation, and extraluminal air. Analysis of pleural fluid usually shows a sterile exudate early in the disease course. Pleural fluid amylase levels often are normal within the first 24 hours after perforation. After 24 hours, the pleural fluid amylase level is elevated disproportionately compared with serum levels. Esophagoscopy is unnecessary and is contraindicated except for removing a foreign body.

Surgical drainage and repair and antimicrobial therapy are indicated for large perforations, when there is communication with the pleural space or abdomen, when vascular erosion is a concern, and in the setting of underlying esophageal pathology. Nonsurgical management can be considered for children in whom the perforation is a small, well-contained lesion in the upper esophagus in the absence of an underlying esophageal pathologic process. Supportive measures include intravenous fluid support, maintenance of an adequate airway, esophageal rest, and careful monitoring of vital functions. Blood and pleural fluid cultures should be obtained, but they usually are sterile except late in the course. Antimicrobial agents provided empirically should be directed against streptococci, staphylococci, and oral anaerobic bacteria. Mortality rates can be high when recognition of the infection is delayed.

Mediastinitis Due to Extension of Infection From Adjacent Structures

The mediastinum is anatomically well situated for involvement when infection extends downward from the oropharynx. Fascial planes from the supraclavicular region and abdomen traverse the mediastinum, and the lymphatic duct is located in the mediastinum. The lung, situated laterally to the mediastinum, is a frequent locus of potentially serious infection. Despite its position as an anatomic crossroad, extension of infection to the mediastinum from adjacent structures occurs infrequently.

In the preantibiotic era, retropharyngeal or peritonsillar abscess, Ludwig angina, dental abscess, and other infections of the head and neck were common causes of acute descending mediastinitis. Since the advent of penicillin, infections of the head and neck usually are contained at the site of origin. The principal spaces that serve as conduits to the mediastinum are the visceral division of the deep cervical fascia that envelops the esophagus, trachea, larynx, and thyroid gland and the carotid sheath, which extends from the base of the skull, passes through the posterior pharyngomaxillary space along the prevertebral fascia, and enters the chest. Mediastinitis can occur as a complication of retropharyngeal abscess, peritonsillar and dental abscesses, as well as mastoiditis, laryngectomy, mediastinotomy, tracheostomy, and surgery or trauma of the oropharynx. Mediastinitis can complicate placement of airway stents for management of tracheal or bronchial stenoses in children.

Children have developed mediastinitis after incurring intraoral injuries caused by falling with an object such as a toothbrush in their mouths. Infection spreads to the mediastinum through the retropharyngeal space. Sharp objects, such as fish bones, can perforate the esophagus, with resultant infection. A penetrating wound to the oropharynx can be caused by falling on a sharp or pointed object such as a pencil. Mediastinitis rarely complicates suppurative pleuropulmonary infection, but multiple necrotic or abscessed lymph nodes can occur with coccidioidomycosis or atypical mycobacterial infections. Extension of infection from vertebrae, ribs, or sternum also is unusual. The main radiographic feature is widening of the mediastinum. Imaging by contrast-enhanced cervicothoracic CT or MRI is crucial for establishing the diagnosis and can reveal heterogeneous infiltration, gas in tissues, abscesses, and fluid collections ( Fig. 30.1 ).

Contrast-enhanced computed tomography scan shows a 3 × 3-cm heterogeneous enhancing abscess (arrow) in the anterior mediastinum of a child acutely ill with Streptococcus pneumoniae bacteremia and pneumonia with empyema. Cultures from the mediastinal abscess at the time of surgical drainage were sterile.

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