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. Under normal circumstances, when vomiting occurs, there is a sudden increase in gastric pressure and the esophagus is reflexively relaxed to expel gastric contents. If ataxia occurs during vomiting, the upper esophageal sphincter does not relax or a segment of the esophagus contracts restrictively, the gastric contents cannot be expelled and the pressure in the esophagus increases dramatically, leading to rupture of the entire esophageal wall, which had a weakened local resistance. Spontaneous esophageal injury in adults does not occur frequently. Once it occurs, it mostly involves the thoracic and abdominal segments of the esophagus, and spontaneous perforation of the cervical segment of the esophagus is less common. Spontaneous esophageal injuries are divided into three categories: 1) intermural hematoma (incomplete perforation); 2) mucosal laceration (MalloryWeiss syndrome); and 3) complete rupture (Boerhaave syndrome). In adults, increased intra-abdominal or intra-esophageal pressure can cause esophageal injury, such as rupture of the esophagus can occur by lifting heavy objects, forceful stooling or blows to the abdomen. Perforation can occur as a result of violent vomiting, esophageal spasm, or a sudden increase in intraesophageal pressure due to foreign bodies, including food masses obstructing the esophagus. Spontaneous esophageal rupture can also occur in neonates, but this is rare. Spontaneous esophageal rupture should be excluded in newborns with acute respiratory distress occurring within 48 h of birth. Esophageal rupture often involves the entire esophagus and in most cases extends into the right thoracic cavity, the exact mechanism of which is unknown. It may be caused by an obstruction at the upper end of the esophagus, which increases the pressure in the esophagus. The pressure is transmitted to the amniotic fluid-filled esophagus during delivery. Increased pressure in the lumen of the esophagus caused when the vocal cords and pharynx are closed. Intraesophageal hypertension may occur during reflux and vomiting when the cricopharyngeal muscles and the upper esophagus are not coordinated or in postnatal spasm, which may lead to esophageal perforation.