Abdominal cleft

　　1. Etiology

　　The timing of the occurrence of abdominal cleft, whether it is a developmental disorder that occurs in the early embryonic stage or shortly before birth, is still controversial at present.

　　1. Deficient development of lateral folds (the right lateral fold is more common): Most scholars believe that abdominal cleft is caused by the incomplete development of the two lateral folds (the right lateral fold is more common) during the early embryonic formation of the abdominal wall. The abdominal wall is formed by 4 mesodermal ridges in the early embryonic stage, namely the head fold, tail fold, and two lateral folds. The four ridges develop simultaneously and finally converge in the center to form the umbilical ring. If, during the formation of the abdominal wall, due to the influence of certain factors, the head and tail folds have already converged in the center, and one of the lateral folds is underdeveloped, it will cause abdominal cleft on the side of the umbilicus. Some authors believe that this part of the abdominal wall is weak, with the umbilical artery passing through, which is easy to be damaged.

　　2. The umbilical vein blood supply obstruction theory: Some authors believe that abdominal cleft is caused by blood circulation obstruction during the internal rotation of the right umbilical vein; Hoyme (1981) proposed that the occurrence of abdominal cleft may be due to the early degeneration of 1 to 2 umbilical mesenteric arteries, leading to ischemia of the abdominal wall and causing defects in the abdominal wall.

　　The Pathogenesis of the Disease

　　Children with abdominal wall defects have normal umbilicus and umbilical cord. The abdominal wall defect can be located on the left or right side of the umbilicus, with the vast majority (about 80%) located on the right side. Some believe that this may be related to the atrophy of the right umbilical vein. The defect is longitudinal, generally 2 to 3 cm in length, with a neat edge. In some cases, the defect is larger, and some skin strips are very narrow, even difficult to identify. The muscles and peritoneum at the site of the abdominal wall defect are absent. The abdominal cavity volume of children with abdominal wall defects is significantly reduced, the extent of which is related to the amount of organ prolapse. The protruding part is the primitive gut, from the stomach to the sigmoid colon, without other visceral organs such as the liver. In some female patients, the internal reproductive organs and bladder may also prolapse. The duodenum and transverse colon are connected as the pedicle, and are connected to the posterior abdominal wall. Between the two intestines is the superior mesenteric artery and vein, with the mesentery free and ending in dots. The intestines have not rotated, with the colon located on the left side of the abdomen. The protruding gastrointestinal tract is not encapsulated by amniotic sac and peritoneum, and there are no traces of the amniotic sac at the edge of the defect. The protruding intestinal tubes, having been long immersed in amniotic fluid, are stimulated by substances such as urea, uric acid, inorganic salts, and sebum, resulting in chemical inflammation, causing edema and thickening of the intestinal wall with a gelatinous substance covering the surface. Sometimes, a fibrous pseudomembrane of meconium color can be seen. This anomaly is easily confused with umbilical hernia due to vesicle rupture. Some authors have conducted histological examinations on the protruding intestinal tubes of abdominal wall defect animal models and found that under light microscopy, the intestinal mucosa and villi are basically normal; under electron microscopy, the microvilli are significantly edematous and unevenly thickened, with wide and deep clefts between microvilli, submucosal hemorrhage, and no obvious abnormalities in the muscular layer; the serosa is thickened, with subserosal edema, more obvious near the mesentery, and there are foci of granulation tissue hyperplasia outside the serosa. The degree of injury to this intestinal tube depends on the duration of immersion in amniotic fluid. At 30 weeks of gestation, the levels of urea and creatinine in amniotic fluid are significantly increased, sodium levels are decreased, and osmotic pressure is decreased, leading to inflammatory changes in the intestines. The longer the intestines are immersed in amniotic fluid, the more severe the pathological changes. The entire intestinal tube is significantly shortened, sometimes only 1/4 of the normal length, with intestinal absorption disorders and weakened peristalsis. It is believed that the intestinal absorption disorders and weakened peristalsis may be related to the significantly increased activity of nitric oxide synthase (NOS) in the small intestine. These changes in the intestinal tubes are reversible. After the intestines are returned to the abdominal cavity, not only can the intestinal function be restored, but the shape and length of the intestines can sometimes also return to normal.

　　Children with abdominal wall defects often have digestive tract anomalies, such as malrotation of the intestines, short bowel syndrome, common mesentery of the small and large intestines, or Meckel's diverticulum, etc. Gillbert measured the total length of the intestinal tubes in 17 cases of abdominal wall defects to be between 35 to 130 cm, with an average of 70 cm, and all had midgut atresia. Therefore, the protruding intestinal tubes with this anomaly are prone to become incarcerated, twisted, or necrotic. Abdominal wall defects may sometimes be accompanied by other systemic organ anomalies, such as congenital heart disease (such as atrial septal defect, ventricular septal defect, patent ductus arteriosus), urinary system anomalies, etc. Some authors report that 10% to 15% of children with abdominal wall defects may have associated small bowel atresia or stenosis; Fonkalsrud (1993) reported that all 52 cases of abdominal wall defects had malrotation of the intestines, 15 cases (29%) had associated anomalies, including 4 cases of duodenal incomplete obstruction, 4 cases of intestinal atresia, 3 cases of congenital heart disease, and 9 cases of urinary system anomalies.

　　1, Intestinal ischemia and necrosis:Due to the prolonged compression of the mesentery, there is a disturbance in lymph and blood circulation, which can lead to intestinal necrosis or perforation in severe cases with poor blood circulation.

　　2, Abdominal wall defect with hardening of the skin:Most children are premature infants and low birth weight infants, with more heat dissipation than normal infants, and less brown adipose tissue in the body, so it is prone to the inhibition of brown adipose tissue heat production process, leading to hypothermia. In addition, newborns naturally have a high proportion of saturated fatty acids in the subcutaneous fat tissue, with a high melting point, which is easy to solidify and cause skin hardening.

　　At this time, the body temperature of the child

　　Prognosis:

　　In the past, the mortality rate of abdominal wall defect children was as high as 50% or more. It is generally believed that the cure rate is related to the child's birth weight and associated malformations, that is, the lower the baby's weight, the more serious the associated malformations, the higher the mortality rate. In recent years, due to early diagnosis (including prenatal) and the rapid development of perioperative treatment theory and technology, especially the extensive application of respiratory and body temperature regulation management and nutritional support therapy, the survival rate of abdominal wall defect children after surgery has increased to over 90%.

　　Abdominal wall defect children often are premature, with lower birth weight, and the recovery of intestinal function is slow after surgery. Therefore, they grow slower than normal children in infancy, and their intelligence and physical development gradually become normal. King et al. followed up 29 children with abdominal wall defect after surgery, except for 1 case of hydrocephalus and 1 case of cerebral palsy, the other 27 cases had good growth and development, could participate in daily activities normally, and had no long-term complications.

　　1, Blood gas analysis: Mainly manifested as hypoxemia and metabolic acidosis.

　　2, Blood biochemistry test: Often with hypoglycemia, increased blood urea nitrogen.

　　In recent years, through ultrasonic examination, abdominal wall defect malformation can be diagnosed before birth. During the examination, the fetus's intestinal tract can be seen to protrude, floating outside the abdominal wall in amniotic fluid, and the degree of intestinal expansion and wall thickening can also be observed.

　　First, postoperative abdominal wall defect dietary therapy

　　1, Jujube and Bamboo Rice Porridge: Jujube, white adzuki bean, polygonatum, Poria, coix seed, Chinese yam, lotus seed, and euryale seed each 10g, glutinous rice 250g. Cook together to make porridge. After the porridge becomes thick, add some rock sugar for flavoring and eat once in the morning and once in the evening.

　　2, Coix Seed and Lily Bulb Stewed with Angelica: Angelica 10g, Ophiopogon 12g, Lily Bulb 300g. Cut the lily bulb into segments, chop the angelica and ophiopogon, and place them in a pot with ginger, pepper, scallion whites, and lard. Boil until tender, season with salt and monosodium glutamate, and eat once a day for 3-7 days.

　　Second, what foods are good for the body with abdominal hernia

　　1. In the middle stage after surgery, it is advisable to eat some liquid or semi-liquid foods such as rice porridge, noodle soup, green vegetable soup, etc.

　　2. In the late stage of surgery, easily digestible and absorbable protein foods such as eggs, fish, and soy products can be provided.

　　3. During the period of body recovery, it is advisable to focus on nourishing the Qi and blood, and can choose radishes, loofah seeds, lotus root, etc.

　　4. It is advisable to eat more fish, eels, shrimps, white snake, crucian carp, mulberries, figs, lychees, walnuts, loquats, horse chestnuts, mung bean sprouts, black bean paste, olives, almonds, luffa, etc. to enhance the body's immunity.

　　Third, what foods should be avoided for abdominal hernia

　　1. Foods that are not conducive to wound healing, such as deer meat, preserved bean curd, scallions, chili, chives, etc., should be avoided as they are prone to cause infection and are not conducive to wound healing.

　　2. Avoid smoking, drinking, greasy, fried, moldy, and preserved foods.

　　3. Avoid eating chicken, geese, and other irritants after surgery to prevent inflammation.

　　4. It is advisable to avoid or eat less spicy foods such as alcohol, chili, ginger, garlic, cinnamon, etc., as they can stimulate wounds and are not conducive to the recovery of the condition.

　　Preoperative preparation and care are important, including the prevention of infection and the correction of water and electrolyte imbalances.

　　1. Temperature managementCover the prolapsed intestinal tract with sterile saline gauze immediately after birth, wrap it with dry gauze outside, and pay attention to prevent the intestinal tract from twisting and strangulation. Apply a layer of plastic film over the dressing or place the child's body in a plastic bag to prevent water evaporation and heat loss. In cases with late consultation, accompanied by low body temperature and organ contamination, the warm normal saline antibiotic solution can be used to rinse repeatedly to slowly restore body temperature and remove the contamination on the surface of the organs.

　　2. Gastrointestinal decompressionLeave a gastric tube in place and frequently aspirate to prevent vomiting and reduce gastrointestinal gas.

　　3. Rapid fluid replacement to correct water and electrolyte imbalanceSome people advocate that 2 times the normal required amount of fluid should be administered intravenously before surgery, and 20-40ml of plasma, 50mg of gamma globulin, and broad-spectrum antibiotics should be given at the same time. Surgery can be performed as soon as the child's condition improves.