The clinical signs and symptoms of esophageal perforation are largely dependent upon the anatomic location of the defect. Fever, tachycardia, tachypnea, dyspnea, shock, and leukocytosis are frequently present regardless of the site of the injury. Crepitus, indicative of underlying subcutaneous emphysema, suggests a perforation in the neck or pyriform sinus. Additionally, these patients may describe neck pain of varying severity, vocal disturbances classically described as a prominent “nasal” tonality, dysphagia, or bleeding through the mouth. Perforations of the thoracic or abdominal esophagus often result in vomiting, chest and/or back pain, dyspnea, dysphagia, and bleeding. In addition, defects of the intra-abdominal esophagus commonly cause abdominal pain and distention. “Mackler’s Triad” denotes the classic presenting syndrome of patients with spontaneous esophageal rupture, and includes vomiting, lower chest pain, and subcutaneous emphysema. The Anderson Triad, likewise suggestive of spontaneous esophageal rupture, includes subcutaneous emphysema, rapid respirations, and abdominal rigidity.

Evaluation of the patient with suspected esophageal perforation begins with a detailed history and physical examination. Particular attention should be given to any recent history of instrumentation or trauma to the neck or torso, quantitative and qualitative assessment of recent food and liquid consumption, evidence of malignancy such as recent weight loss or dysphagia, or any signs of progressing sepsis. Hemodynamic instability should be immediately addressed with placement of large-bore intravenous catheters and fluid administration. Once esophageal perforation is suspected, antero-posterior and lateral upright chest and abdominal radiographs should be obtained without delay. Radiographic findings suspicious for perforation include subcutaneous emphysema, the ­presence of pleural effusions, pneumomediastinum, hydro/­pneumothorax, and pleural thickening. Radiographs are particularly useful in the setting of suspected iatrogenic perforation, as they may prove diagnostic in up to 80% of these patients. Furthermore, radiographs have utility in terms of localization of the defect; a right pleural effusion suggests a mid-esophageal perforation, while a left effusion portends a lower esophageal lesion.

The gold standard for diagnosis of perforation is a contrast swallow study, done in the presence of the treating surgeon. Performed fluoroscopically, the patient should be oriented obliquely relative to the source and remain in a standing, semierect position, which will facilitate the detection of small leaks (Fig. 14.1 through Fig. 14.5). Given the risk of severe pneumonitis associated with gastrograffin aspiration, angiography agents are preferred. Barium use can complicate future imaging in the patient due to persistence of the substance in the esophagus for several days, and should only be used if an obvious perforation is not detected on initial swallow evaluation with a water-soluble contrast agent. Although essential in the initial evaluation of suspected esophageal perforation, the false negative rate of contrast radiography approaches thirty percent.