Crohn’s disease is an inflammatory disease of the intestine of unknown origin that can occur anywhere in the gastrointestinal tract, but is more prevalent in the terminal ileum and right hemicolectum. The disease and chronic nonspecific ulcerative colitis are collectively referred to as inflammatory bowel disease (IBD). The clinical manifestations of this disease are abdominal pain, diarrhea, and intestinal obstruction, accompanied by fever, nutritional disorders, and other extraintestinal manifestations. The course of the disease is prolonged, recurrent and not easily curable. The disease is also known as limited enteritis, limited ileitis, segmental enteritis, and granulomatous enteritis. The cause of this disease is unknown and may be related to infection, genetics, humoral immunity and cellular immunity. Crohn’s disease is a proliferative lesion that penetrates all layers of the intestinal wall, invading the mesentery and local lymph nodes, and is confined to the small intestine (mainly the terminal ileum) and the colon, or both, often the ileum and the right hemicolectum. The lesions are segmental in distribution, with clear boundaries between normal intestinal segments, and are characterized by a skip area. The pathological changes are divided into acute inflammatory phase, ulcer formation phase, stricture phase, and fistula formation phase (perforation phase). The acute phase is characterized by edema and inflammation of the intestinal wall; in the chronic phase, the intestinal wall is thickened and stiffened, and the affected intestinal canal has a tubular shape with dilatation at its upper end. The typical lesions on the mucosal surface are: 1. ulcers Early shallow small ulcers, then become longitudinal or transverse ulcers, longitudinal ulcers deep into the intestinal wall that form a more typical cleavage furrow, distributed along the mesenteric side, the intestinal wall may have abscesses. 2, pebble nodules due to submucosal edema and cellular infiltration formation of small islands of protrusion, coupled with the contraction of fibrosis and scar after ulcer healing, so that the mucosal surface like pebbles. 3.Sarcoidosis No caseous changes, distinct from tuberculosis. 4.Fistula and abscess The fissure in the intestinal wall is essentially a penetrating ulcer, causing adhesions and abscesses between the intestinal tube and intestinal tube, intestinal tube and organs or tissues (such as bladder, vagina, mesenteric or retroperitoneal tissues, etc.), and forming an internal fistula. If the lesion penetrates the intestinal wall and passes outside the body through the abdominal wall or perianal tissues, an external fistula is formed. There is no cure, and many patients develop complications that require surgery and a high recurrence rate after surgery. The recurrence rate of the disease is related to the extent of the lesion, the strength of the disease invasion, the prolongation of the disease, and the increase in age, with a consequent increase in mortality.