Abdominal cocoon

　　One: Causes of Onset

　　The etiology of abdominal cocoon is unknown and may be related to the following factors.

　　1. Secondary to some intra-abdominal inflammation Foo et al. believe that the disease is more common in women, and the onset time is often within 2 years of the first menstrual period. It is speculated that this may be due to menstrual blood refluxing through the fallopian tubes into the abdomen, triggering subclinical primary peritonitis, fibrosis, and organization. Sieck et al., based on the regional characteristics and the fact that it is more common in adolescent women, speculate that it may be due to retrograde infection caused by pathogens entering through the reproductive tract, leading to the sequelae of peritonitis. However, these speculations have not been confirmed, and they cannot explain the onset of the disease in male patients. The adhesion between the intestines found in surgery is also different from the general peritoneal adhesion caused by infection.

　　2. The etiology of abdominal cocoon is considered to be congenital developmental abnormality combined with postnatal factors by most scholars. The reasons are that the capsule is very complete and smooth, without adhesion to the parietal peritoneum, and some pathological examinations of the capsule confirm it as peritoneal tissue. The incidence of associated abdominal malformations is relatively high (54.3%), often with the absence of the omentum. It is speculated that this may be due to abnormal development of the omentum or biconical development of the mesentery, causing intestinal adhesion within the capsule, which may be related to postnatal factors. Some scholars also believe that abdominal cocoon is a congenital duodenal paraequivalent hernia or mesocolic hernia.

　　3. In the cases reported by Seng, there was a history of taking propranolol (Propranolol) (80mg/d), and it is believed that propranolol, a class of beta-receptor blockers, reduces the proportion of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) involved in the control of normal cell proliferation, leading to excessive collagen proliferation and abdominal fibrosis.

　　17. Primary peritonitis Francis noted that abdominal cocoon syndrome has a higher incidence in patients with liver cirrhosis, nephritis, malignant tumors, and heart failure with ascites, especially in patients with liver cirrhosis who undergo LeVeen shunt surgery. Wang Ronghua reported a high incidence in patients with tuberculous peritonitis.

　　Second, pathogenesis

　　The small intestine is wrapped in an abnormal fibrous membrane in the shape of a cocoon, with varying degrees. The entire or part of the small intestine from the Treitz ligament to the terminal ileum is wrapped into a mass, horseshoe shape, or U shape. The membrane is not adherent to the adjacent parietal peritoneum, and a few are fused with the pelvic wall or lateral peritoneum. Some may involve the colon, stomach, gallbladder, uterus, and its accessories. The membrane is uneven in thickness, with thickened areas appearing milky white. There may be loose adhesions between the small intestine within the membrane or between the membranes, stomach separation, and the membrane may locally thicken, forming a stenosis ring or a band that compresses the intestinal tract to form an obstruction. The incidence rate of intestinal obstruction is about 57%. Abdominal cocoon syndrome has a high rate of intra-abdominal malformations, about 54.3%, commonly including the absence or underdevelopment of the omentum, absence of the left lobe of the liver, free cecum, etc. The pathological examination results of the abdominal cocoon syndrome membrane may have two situations: ① Chronic inflammatory changes of fibrous and collagen tissue. ② The pathological changes of peritoneal tissue are varied, and the membrane may originate from peritoneal tissue.

　　Intestinal obstruction is the main complication of this disease and also the main reason for patients to seek medical attention. It is secondary to some intra-abdominal inflammation. Foo et al. believe that the disease is more common in women, and the onset time is often within two years of the first menstrual period, suggesting that menstrual blood may reflux into the peritoneal cavity through the fallopian tubes, triggering subclinical primary peritonitis, fibrosis, exudation, and organization. Sieck et al. suggest that the disease may be caused by retrograde infection of pathogens easily entering through the reproductive tract, leading to post-peritonitis sequelae. However, these speculations have not been confirmed and cannot explain the onset of the disease in male patients. The discovery of intra-peritoneal intestinal adhesions during surgery is also different from that caused by general infection.

　　The majority of patients experience symptom relief after surgery, while a small number of patients with residual symptoms can alleviate their condition through non-surgical treatment.

　　1, Develop good living habits, quit smoking and limit alcohol. The World Health Organization predicts that if people stop smoking, cancer in the world will decrease by one-third after 5 years; secondly, do not overindulge in alcohol. Smoking and alcohol are extremely acidic substances, and people who smoke and drink for a long time are prone to acidic体质.

　　2, Do not eat too much salty and spicy food, do not eat overcooked, cold, expired, or deteriorated food; the elderly, the weak, or those with certain genetic predispositions to diseases should eat some cancer-preventive foods and alkaline foods with high alkalinity in moderation to maintain a good mental state.

    Patients should avoid consuming foods high in protein and calcium, such as milk, dairy products, lean meats, fish, shrimp shells, egg yolks, salted eggs, preserved eggs, animal cartilage, beans, bean products, kelp, and seaweed, as they all contain a large amount of protein or calcium. If consumed excessively, it will make the stool alkaline, dry, and in small quantities, making it difficult to pass. Therefore, consumption should be reduced.

　　Surgical Treatment:

　　The treatment of abdominal cocoon syndrome is mainly surgical, and the pericapsule is excised or opened and fixed to the lateral abdominal wall 1 cm from the base of the pericapsule, with full relaxation of adhesions, stenotic rings, and complete relief of obstruction to anatomically reset the small intestine or add intestinal alignment, etc. The symptoms of the vast majority of patients disappear after surgery, and a few patients may have residual symptoms, which can be relieved by continuing to take prednisone and vitamin B1. During the operation, attention should be paid to the relationship between the intestinal tract and the mass, and it is strictly forbidden to excise the entire small intestine within the pericapsule or mistake it for a tumor, which may lead to short bowel syndrome.