Meconium peritonitis

　　Because meconium peritonitis is mainly caused by intestinal perforation in utero, and there are many reasons for fetal intestinal perforation, such as intestinal atresia, intestinal stenosis, intussusception, intussusception, internal hernia, etc. Some cases may be due to local blood supply disorders of the intestinal wall, such as fetal necrotizing enterocolitis, muscular layer defect of the intestinal wall, mesenteric vascular occlusion, and secondary intestinal perforation (fetal appendicitis, diverticulitis, intestinal duplication anomaly, or ulcer perforation), etc. In other words, the above diseases indirectly lead to meconium peritonitis.

　　Under normal circumstances, by the fourth month of pregnancy, meconium has accumulated in the ileum at the end of the fetal intestine, and reaches the rectum by the fifth month. Intestinal perforation that occurs at this time or later can cause the leakage of meconium and lead to the disease. If the intestinal perforation occurs in the early stage, it may heal spontaneously. The peritonitis reaction caused by digestive enzymes, with a large amount of fibrin exudation, causes widespread adhesions of the peritoneum, blocking the perforation, and the peritoneal effusion and necrotic tissue can be absorbed in large part. Subsequently, due to the production and action of pancreatic enzymes, the meconium in the intestinal lumen can be dissolved, and the intestines become unobstructed. However, the calcium salts accumulated around the perforation react chemically with the inflammatory exudate of peritonitis and precipitate, forming calcified plaques. Since the liver is relatively large and occupies most of the peritoneal cavity at 4-5 months of fetal development, the intestinal perforation is often adherent to the liver. As the peritoneal cavity develops, the liver moves to the right upper abdomen, so the adherent part is also pulled to the right upper abdomen below the liver. Therefore, calcified shadows are often found in the right upper abdomen on X-ray films. If the intestinal perforation is not sealed or sealed after a long period of leakage, there may be a membranous tissue enveloping part of the intestinal loops, forming a pseudocyst. If the leakage continues, the cyst cavity can gradually enlarge and fill the peritoneal cavity. If the intestinal perforation occurs within a few days before delivery, the perforation is still open, and the peritoneal cavity is filled with peritoneal fluid contaminated with meconium, forming a diffuse peritonitis, which quickly evolves into a bacterial peritonitis.

　　Perforated meconium peritonitis is an aseptic peritonitis caused by the leakage of meconium into the peritoneal cavity due to intestinal perforation during fetal development. Although the leakage of meconium into the peritoneal cavity after intestinal perforation causes an aseptic inflammatory reaction, a large amount of fibrin is exuded, causing widespread adhesions in the peritoneal cavity, forming calcified masses around the perforation, completely blocking the perforation. The child may have no symptoms after birth, but there is a possibility of adhesive intestinal obstruction at any time. If the intestinal perforation does not heal, the contents of the intestines continue to flow into the peritoneal cavity, causing the intestines to adhere to each other and form a mass, fixed on the posterior abdominal wall. After birth, if the child swallows air while drinking milk, an abdominal pneumocele may occur, followed by suppurative peritonitis caused by bacterial invasion, or localized liquid-air peritoneum or peritoneal abscess may also occur.

　　Therefore, fetal meconium peritonitis may be complicated with purulent peritonitis, abdominal cysts, and other diseases.

　　Different types have different symptoms:

　　(1) Neonatal intestinal obstruction type The intestinal perforation at birth has healed, and there are adhesions and calcification, but due to the presence of intestinal atresia or stenosis, neonatal intestinal obstruction symptoms occur, with bile vomiting and abdominal distension. X-ray film shows intestinal dilation and multiple liquid levels, and there are obvious calcified plaques.

　　(2) Localized gas abdomen type The intestinal perforation at birth has not healed yet, but it is wrapped by fibrinous adhesions to form a pseudocyst, containing liquid and gas. In fact, it quickly develops into a localized peritoneal abscess. The clinical symptoms are related to the size of the abscess, the degree of infection, and the communication of the intestines. It is manifested as fever, abdominal distension, and vomiting, but it can still take milk and defecate. Symptoms of intestinal obstruction or sepsis may occur, with signs of infection such as redness and edema of the abdominal wall. Abdominal X-ray shows localized pneumoperitoneum, no gas under the diaphragm, and sometimes calcified plaques scattered on the pseudocyst wall or other parts of the abdominal cavity.

　　(3) Free gas abdomen type The intestinal perforation at birth still exists and has not been wrapped by adhesions, and the newborn's swallowed gas, milk, and gastrointestinal secretions enter the abdominal cavity, rapidly causing bacterial peritonitis and a large amount of ascites. The condition is serious and critical, with vomiting, refusal to eat, constipation, low body temperature, and toxic shock. In severe cases, it affects respiration and causes symptoms such as dyspnea and cyanosis. The abdomen is distended like a ball, and it has a sensation of a gas-filled balloon when touched. Percussion produces dull sounds. The abdominal X-ray shows a large gas-liquid level spanning the entire abdomen, a large amount of gas under the diaphragm, the liver is prolapsed, the entire abdomen is opaque, and only a small amount of intestinal gas is seen. Calcified plaques can be found in any part of the abdominal cavity. In those with an unclosed peritoneal processus, there may be scrotal or labial edema, and even calcified plaques.

　　(4) Intestinal adhesion - may be accompanied by intestinal obstruction type The intestinal perforation at birth has healed, although calcified adhesions remain in the abdominal cavity, but there is no intestinal obstruction. Some cases can be asymptomatic throughout life, and sometimes calcified plaques in the abdominal cavity are found during X-ray examination when diagnosing other diseases. Some cases may develop adhesive intestinal obstruction later, caused by adhesion bands, most occurring between 2 and 6 months of age, and some developing at the age of 2 to 3 years.

　　Ultrasonic manifestations: If fetal meconium peritonitis is caused by intestinal atresia perforation, typical signs of intestinal obstruction can be displayed before the perforation, such as intestinal dilation and active peristalsis. Once perforation occurs, the previously dilated intestines disappear, and a free fluid shadow appears in the abdominal cavity.

　　Ascites signs can also appear in fetal meconium peritonitis not caused by intestinal obstruction perforation. Later, the free ascites gradually decreases or becomes thick, with fine and dense light spots and strip-like light bands appearing in the dark area of ascites, adhering to the surrounding intestinal tubes and omentum to form an irregular hyperechoic mass. Echo of calcification focus may appear inside.

　　Another condition is the gradual formation of encapsulated effusion from free ascites, which is shown as a cystic structure in ultrasound images, fixed together with the surrounding intestinal loops. At the same time, scattered calcification spots may be displayed on the surface of the pelvis and abdomen, the surface of the intestines, the surface of the liver, and even the surface of the diaphragm.

　　Patients with meconium peritonitis need to check for abdominal calcification spots: During the diagnosis of meconium peritonitis, calcification shadows are often in the form of masses, adhering to a certain part of the abdominal wall. Calcification shadows are often in the form of wider rings or scattered small plaques. A few are in the form of thin strips or small dots, surrounding the encapsulated hydropneumoperitoneum with wider large ring shadows. In the intestinal obstruction type, calcification is more common in localized masses, mainly distributed in the right middle and lower abdomen and lower abdomen.

　　Fasting and fluid replacement are required..

　　Western medicine treatment should be divided into two situations:

　　2. Clinical manifestations after birth are incomplete intestinal obstruction. In principle, non-surgical treatment should be adopted as much as possible. Therefore, after the prenatal diagnosis is clear, postnatal gastrointestinal decompression and enema can be performed, and the symptoms can be relieved after the meconium is excreted. For severe children, Gastrografin (a contrast agent) can be infused into the rectum under fluoroscopy to reach the intestine, which is more effective for relieving stubborn constipation than general enema. However, this agent has a high osmotic pressure, which can reduce blood volume and even endanger life. Therefore, intravenous fluid supplementation and maintenance of electrolyte balance are needed during treatment to prevent osmotic pressure from rising.

　　1. Clinical manifestations include peritonitis or complete intestinal obstruction. Early surgical treatment should be performed. After birth, the intestinal gas is full and can cause peritonitis. If there is severe abdominal distension with peritonitis, immediate peritoneal puncture should be performed, and thick green fluid and a large amount of gas can often be aspirated to relieve abdominal distension and improve respiratory distress. At the same time, sufficient preoperative preparations should be made. The surgical method should be different according to the local pathology and the overall situation of the patient. If the perforation site can be found, suture is the most ideal. Appropriate treatment should be given for complications such as intestinal atresia. If the perforation site is not found, only simple peritoneal drainage surgery can be performed. If it is a localized pneumoperitoneum type, peritoneal drainage is the main method. If it is adhesive intestinal obstruction, the principle should be to simply separate and relax the adhesions, and relieve the obstruction. It is not advisable to forcibly remove calcified plaques, as this may cause recurrence of perforation. If the site of obstruction is not found, a short-circuit anastomosis can be performed. In cases where the intestinal adhesions are localized and compact, intestinal resection can be performed if the condition permits. Intestinal fistulization can also be performed according to the local and systemic conditions of the lesion.