Chest pain after a full stomach is a major manifestation of spontaneous esophageal rupture. SpontaneousRuptureofEsophagus refers to a sudden increase in pressure in the lumen of the esophagus due to various causes, resulting in a full longitudinal tear of the left wall of the esophagus on the adjacent diaphragm. It is also known as Boerhaave’s syndrome, spontaneous esophageal tear syndrome, pressure rupture of esophagus, peptic perforation of esophagus, and non-traumatic esophageal perforation. Most occur after alcohol consumption and vomiting. Although not 100% of patients have vomiting at the onset, most patients (70%-80%) have vomiting followed by esophageal perforation, so vomiting is still the most important cause of morbidity. Associated with vomiting is alcohol consumption, and most patients who vomit do so after overeating or drinking alcohol. Other causes of spontaneous esophageal rupture are childbirth, car accidents, after cranial surgery, and epilepsy. Spontaneous esophageal rupture is mostly caused by increased abdominal pressure transmitted to the esophagus, which can be in the angular part of the distal esophagus, and the rupture is more common in the lower segment of the esophagus. Because the upper segment is mainly skeletal muscle, it is not easy to rupture, while the middle and lower segments are mainly smooth muscle, with gradually decreasing longitudinal muscle fibers, thin muscle layer, and few vascular nerves, so it is easy to rupture. The rupture is mostly longitudinal in shape, 4-7 cm long, and near the level of the inferior pulmonary vein. The pressure factor causing spontaneous esophageal rupture is not the absolute pressure in the stomach, but the pressure difference in the transmural wall of the gastroesophageal junction. After esophageal perforation, if there is no traffic with pleural cavity (mediastinal pleura is not broken), strongly acidic gastric juice, gastric contents and oral saliva containing a large number of bacteria swallowed, under the action of negative pressure in pleural cavity, overflow into mediastinum through perforation, mainly causing mediastinal infection and corrosion of tissue by digestive juice, but at a later stage, infected material can also penetrate mediastinal pleura into pleural cavity, causing thoracic infection. If the mediastinal pleura ruptures at the same time after the esophageal perforation, the thoracic cavity infection will be the main manifestation.