Tuberculous intestinal obstruction is a common form of gastrointestinal tuberculosis, often caused by intestinal tuberculosis or intestinal adhesions of tuberculous peritonitis, with insidious onset and often misdiagnosed or missed. The conventional treatment principle is active anti-TB treatment, gastrointestinal decompression, intravenous nutrition therapy, etc. Most patients with mild cases are cured. However, in clinical practice, there are often some patients with severe tuberculosis intestinal obstruction who have repeatedly worsened after weeks of ineffective conventional treatment, especially some patients with serious abdominal adhesions that cannot be operated, and lack effective treatment plans, so what should we do? We try to introduce the concept of “early postoperative inflammatory bowel obstruction” into this treatment field, and start titrated enteral nutrition sequential treatment early on the basis of adequate anti-tuberculosis, and clinical treatment research shows that we have achieved very good clinical results. Most of the tuberculous intestinal obstruction is chronic incomplete intestinal obstruction, and we believe that tuberculous intestinal obstruction is a special kind of “inflammatory intestinal obstruction”. Based on adequate anti-tuberculosis treatment, early enteral nutrition plus glucocorticoid therapy is the key to this treatment method. Tuberculous intestinal obstruction is a state in which the contents of the intestine cannot function normally and pass through the intestine smoothly due to tuberculous peritonitis or intestinal tuberculosis, which often manifests as chronic incomplete intestinal obstruction. The proliferation of tuberculous granulomas thickens and adheres the intestinal wall, congestion and edema, healing of circular ulcers narrow the intestinal lumen, adhesion of intestinal loops, and entanglement and adhesion of intestinal loops with the thickened greater omentum binds the intestinal curvature, and these factors cause the final occurrence of tuberculous intestinal obstruction. The main pathophysiological changes of tuberculous intestinal obstruction are exudation, hyperplasia and mutual adhesions, which are only caused by tuberculous lesions rather than surgical trauma, and are a special kind of “inflammatory intestinal obstruction”. Based on the above basic understanding of the pathophysiology of tuberculosis intestinal obstruction, we believe that the primary key to the treatment of severe tuberculosis intestinal obstruction is early enteral nutrition and glucocorticoid application on the basis of adequate anti-tuberculosis treatment. By reducing the changes of edema and adhesions, the symptoms of intestinal obstruction will then be relieved, as in the management of early postoperative inflammatory bowel obstruction. At the same time, we believe that intestinal dysfunction/bowel failure is the inevitable outcome of severe tuberculous intestinal obstruction. All tissues and organs of the body receive nutrient requirements from the arterial blood supply, except for the intestinal mucosa, which receives only 30% of its total nutrient requirements from the blood supply and the remaining 70% directly from the intestinal lumen. Since enteral nutrition has a nourishing effect on intestinal mucosal tissues, intestinal mucosal cells can proliferate, repair and grow only when they are in contact with chyme, so early restoration of enteral nutrition is another important measure to maintain the function of intestinal mucosa. Enteral nutrition is an effective method to restore intestinal function. Therefore, early administration of titrated enteral nutrition therapy according to the patient’s tolerance of enteral nutrition is an effective method to treat intestinal dysfunction caused by severe tuberculous intestinal obstruction. Glucocorticoids have a rapid, potent and nonspecific anti-inflammatory effect. Moderate, short-term glucocorticoids are not absolutely contraindicated in the treatment of tuberculosis. Graeme Meintjes et al. showed that the release of inflammatory mediators such as TNF-a and IL-6 in the blood of patients with tuberculosis was reduced with prednisone, thereby reducing the inflammatory response in patients with tuberculosis, and no adverse effects were observed compared with controls. We believe that for severe tuberculous intestinal obstruction, the moderate use of glucocorticoids on the basis of adequate anti-tuberculosis treatment is safe, and is important for reducing exudation and edema, and reducing inflammatory sequelae such as scarring and adhesions, with controllable side effects. In conclusion, for severe tuberculosis intestinal obstruction without surgical indication, we should start enteral nutrition as early as possible on the basis of adequate anti-tuberculosis to open the road to recovery of gastrointestinal dysfunction, combine parenteral nutrition to supplement the nutritional deficiency, adjust the speed of nasal feeding and the type of gastrointestinal nutrition solution according to the patient’s tolerance to enteral nutrition, gradually transition to all enteral nutrition and resume normal diet. This strategy of “titrated enteral nutrition sequential treatment” not only provides another useful exploration for the treatment of severe tuberculous intestinal obstruction without surgical indication, but is also believed to have certain guiding significance for the treatment of non-severe tuberculous intestinal obstruction.