Spontaneous esophageal rupture (Boerhaaves syndrome) is an acute and dangerous thoracic disease with low incidence, easy misdiagnosis, rapid progression, and high mortality rate. Etiology, pathology and pathophysiology of spontaneous esophageal rupture The esophagus has no plasma membrane layer and the collagen and elastic fibers between the plasma membrane and submucosa are more prone to rupture than other digestive tracts under the same pressure. The vast majority of patients with spontaneous esophageal rupture have experienced alcohol consumption and vomiting after a full meal. Vomiting is a complex activity involving both random and non-random muscles, and spontaneous esophageal rupture is mostly due to uncoordinated vomiting movements and strong esophageal spasm causing obstruction of the esophageal lumen, increasing the risk of esophageal rupture. The normal resting pressure in the esophagus is consistent, below atmospheric pressure by 5-10 c mH2O (1 cmH2O= 0.098 kPa), while the intra-abdominal pressure is higher than atmospheric pressure by 5-10 cmH2O. Therefore, there is a physiological pressure difference of 10-20 c mH2O between the thoracic and abdominal cavities. Due to the existence of a “high pressure band” of 8-20 cmH2O in the LES, it is kept closed, not only to prevent gastric reflux, but also to regulate and maintain the balance of thoracoabdominal pressure. When vomiting or other reasons to increase intra-abdominal pressure to break through the resistance of the “high-pressure band”, the pressure difference between the esophagus and the stomach can increase by tens or even hundreds of times, and when the instantaneous pressure in the esophagus rises up to 5-10 pounds (1 pound = 0.45 kg) / cm2 can cause the normal esophagus to rupture. The health of the esophageal mucosa is also associated with morbidity, and patients with ulcerative esophagitis and esophageal stress ulcers are at greater risk. A sudden increase in the pressure gradient between the stomach and esophagus is the real risk factor for esophageal rupture. The inability to vomit out the stomach contents causes a sudden increase in pressure in the lumen of the esophagus, resulting in rupture of the entire esophageal wall. The most common rupture site is the lower 1/3 of the esophagus in the thoracic segment, with the left wall being the most common, accounting for 80%, because the lower part of the esophagus is mainly smooth muscle and the muscle layer is weaker than the upper part of the esophagus, and the nerves and blood vessels entering and exiting the esophagus wall also form certain weak points, because the right wall of the esophagus is supported by the mediastinal pleura and the middle part of the esophagus is supported by the aorta, so it is less likely to rupture than the left wall and the lower part of the esophagus. After the spontaneous esophageal rupture occurs, the integrity of the esophagus and the pressure balance inside and outside the esophageal cavity are destroyed, and not only the saliva, air and food swallowed by the mouth gush into the mediastinum and the pleural cavity with negative pressure; at the same time, because of the positive pressure in the abdominal cavity, a large amount of chyme and digestive juices in the gastrointestinal tract also enter the mediastinum and pleural cavity through the ruptured esophagus with the gastrointestinal tract reflux. When the pleura is subjected to strong chemical stimulation by gastric (acidic) and intestinal (alkaline) fluids, chemical pleurisy immediately arises. Samson calculates that the fluid exuded from the pleural cavity is about 1L per hour. spontaneous rupture of esophagus usually breaks into the pleural cavity directly, or it may break into the mediastinum only, if it breaks into the mediastinum only, the mediastinal pleura is intact and the contents of the digestive tract are confined to the mediastinum, if it is not diagnosed and treated in time, it may break into the pleural cavity only after several small swellings or several days. The spontaneous rupture of the esophagus into the pleural cavity forms a tense liquid pneumothorax, compressing the lung to make it atrophy, compressing the mediastinum to shift to the healthy side, compressing the upper and lower vena cava, blocking the venous blood return, and reducing the return heart blood flow. The heart beat volume decreases, and the patient develops rapid heartbeat and difficulty in breathing. The patient felt thirsty due to the large amount of chest fluid exudation, but the painful swallowing and the increase of pleural fluid caused by drinking water made the patient’s dyspnea increased, and he dared not drink water, and even spit out saliva. The patient quickly goes into shock. Patients who are not treated die quickly. Patients who enter the hospital without proper treatment hardly survive more than a week, and the majority of patients die of respiratory and circulatory failure. The vast majority of patients who are delayed in diagnosis but treated correctly die from uncontrollable infection and toxic shock. This is because the flora and microorganisms in the lumen of the esophagus enter the mediastinum and pleura and then spread quickly with the patient’s change in position and respiratory movements. It is difficult to control such severe contamination with antibiotics. With the increased awareness of this disease and the importance of its treatment in recent years, better progress has been made in its diagnosis and surgical treatment methods.