Gastroschisis

Introduction to abdominal fissure Gastroschisis is a rare defect in abdominal wall development. In the past, some scholars combined this disease with uterine rupture and intrauterine rupture. In 1953, Moore et al. proposed different pathological features of abdominal fissure and umbilical rupture. Also named as a splitting and recognized. Abdominal fissure is a congenital abdominal wall hypoplasia, with a full-thickness abdominal wall defect at the navel and a visceral self-defect. It is a rare deformity. The incidence rate varies greatly from country to country, but it is more common in low birth weight children. After birth, the intestine can be found to be removed from the defect of the abdominal wall of the umbilicus. The mesentery is free, the intestine is congested, edematous, thickened, and the surface is covered with cellulosic exudate. The intestines adhere to each other. basic knowledge Sickness ratio: 0.0001% Susceptible people: no specific population Mode of infection: non-infectious Complications: scleredema

Cause of abdominal dissection

(1) Causes of the disease

The time of occurrence of abdominal fissure is a developmental disorder that occurs early in the embryo or shortly before birth. It is still controversial.

Lateral dysplasia (40%):

Most scholars believe that the abdominal fissure is caused by the dysplasia of the two lateral iliac crests (the right iliac crest is common) in the early stage of embryonic development. The abdominal wall is formed by four mesodermal folds in the early stage of the embryo, namely the head lice, the cercaria, and the ridges on both sides. 4 wrinkles develop at the same time, and finally form a umbilical ring at the central meeting. If during the formation of the abdominal wall, due to certain factors, the head and tail are joined at the center, and one of the two sides of the fold is underdeveloped, resulting in a split. Occurred in the side of the side of the umbilical, some authors believe that the abdominal wall is weak, there is umbilical artery passing, vulnerable to damage.

Umbilical venous blood supply disorder (20%):

Some authors believe that abdominal fissure is caused by blood circulation disorder in the right umbilical vein. Hoyme (1981) suggested that the occurrence of abdominal fissure may be due to premature degeneration of 1-2 umbilical mesenteric arteries, leading to abdominal wall ischemia. A defect has occurred.

(two) pathogenesis

Children with abdominal fissure have normal umbilical cord and umbilical cord. The abdominal wall rupture can be located on the left or right side of the umbilicus. The vast majority (about 80%) is on the right side. Some people think that this may be related to the right umbilical vein atrophy. Generally, it is 2~3cm, and its edge is neat. In some cases, the gap is larger, even ~2cm. The individual strips are narrow and even difficult to identify. The muscles and peritoneum of the abdominal fissure are absent. The abdominal cavity volume of children with abdominal fissure is significantly reduced. The degree of reduction is related to the amount of organ dislodgement. The intestine is the original intestine, from the stomach to the sigmoid colon, and there are no other internal organs such as the liver. Sometimes the female genital and bladder can also be prolapsed, duodenum and transverse colon. And behavioral pedicle, connected with the posterior wall of the abdomen, the mesenteric arteries and veins between the two intestines, the mesenteric detachment is point-like, the intestine is not rotated, the colon is located in the left abdomen, and the gastrointestinal tract without the amniotic sac and peritoneum is wrapped. There is no trace of amniotic sac at the edge of the rupture. The long-term immersion in the amniotic fluid is chemically irritated by the stimulation of urea, uric acid, inorganic salts, sebum, etc., causing edema of the intestinal wall. Thickened and covered with jelly on the surface, sometimes melitose cellulose film can be seen, which is easily confused with ruptured umbilical bulge.

Some authors have performed histological examination of the intestines of the animal model of abdominal dissection. It is found that the intestinal mucosa and villi are basically normal under light microscope; the microvilli are obviously edematous and coarse and uneven under electron microscope, and the microvilli are wide and deep, submucosal hemorrhage, muscle There is no obvious abnormality in the layer; the serosa is thickened, the subserosal edema is obvious, the mesenteric membrane is obvious, and the focal granulation tissue is also visible outside the serosa. The degree of damage of the intestinal tube depends on the length of time the intestine is soaked in the amniotic fluid. At 30 weeks of embryo, urea in the amniotic fluid, creatinine content increased significantly, sodium content decreased, osmotic pressure decreased, resulting in intestinal inflammatory changes, the longer the intestine tube was soaked in amniotic fluid, the heavier the pathological changes, the entire intestinal tube was significantly shortened, sometimes only It is 1/4 of normal and has intestinal malabsorption and weakened peristalsis. The sick children are often accompanied by gastrointestinal malformations, such as poor intestinal rotation, short bowel malformation, common mesentery or Meckel diverticulum in the small intestine and colon, Gillbert measures the total length of the intestine in 17 cases of abdominal splitting disease is 35 ~ 130cm, an average of 70cm, and All the intestines have not turned, so the intestines with this deformity are prone to incarceration, torsion, intestinal necrosis, and abdominal dissection can sometimes be accompanied by other systemic organ deformities, such as congenital heart disease (such as atrial septal defect, ventricular septal defect). , patent ductus arteriosus, urinary malformations, etc., some authors reported that 10% to 15% of children with abdominal fissure can be associated with small intestine atresia or stenosis; Fonkalsrud (1993) reported 52 cases of abdominal fissure with intestinal malrotation, 15 cases (29%) had associated malformation, 4 cases of duodenal insufficiency, 4 cases of intestinal atresia, 3 cases of congenital heart disease, 9 cases of urinary malformation.

Abdominal crack prevention

Preoperative preparation and care are important to prevent infection and correct water and electrolyte imbalance.
(1) Body temperature management: Immediately after birth, the child is covered with sterile saline gauze to remove the intestines, and the outer gauze is wrapped with dry gauze, taking care to prevent the intestines from being twisted and twisted. Apply a plastic film to the outside of the dressing, or put the body of the child into a plastic bag to prevent evaporation and heat loss. Late treatment, accompanied by hypothermia and organ contamination, can be washed repeatedly with warm saline antibiotic solution, so that body temperature slowly recover, remove the contamination of the surface of the organs.
(2) Gastrointestinal decompression: Indwelling gastric tube, and often pumping to prevent vomiting and reduce gas in the gastrointestinal tract.
(3) rapid rehydration to correct water and electrolyte imbalance: Some people advocate that the body should be given 2 times the normal amount of liquid before surgery, and give plasma 20 ~ 40ml, -globulin 50mg, and give broad-spectrum antibiotics. After the child's condition improves, surgery can be performed.

Abdominal fissure complications Complications

1. Intestinal ischemia and intestinal necrosis: due to long-term compression of the mesentery, lymphatic and blood circulation disorders, necrosis or perforation of the intestinal tract of severe blood circulation disorders.
2. Scleritis: Most children with peritoneal fissure are premature and low birth weight infants. The heat dissipation is more than that of normal infants, and the body's brown fat is less. Therefore, the brown fat production process is inhibited and hypothermia occurs. In addition, the newborn's subcutaneous adipose tissue contains more saturated fatty acids, has a higher melting point, and is prone to coagulation, causing hard skin swelling.
At this time, the child's temperature is <35 °C, the crying is weak, the sucking is weak, the reaction is poor; the skin is cool, the subcutaneous fat becomes hard, the edema, the touch seems to be hard like a skin-like skin, and the limb is stiff in severe cases, and there may be depressed edema. The skin is pale or dark red.

Abdominal splitting symptoms common symptoms abdominal infections dehydrated umbilical cord abdominal wall defects sepsis scleredema

Partial performance

After the newborn is born, the stomach and intestines protrude beyond the abdominal wall at the umbilical rupture, without amniotic membrane covering, and there is no trace of amniotic membrane rupture. The intestine is located outside the abdominal wall. Because of the relationship between the stomach, small intestine and colon, it is stimulated by amniocentesis. Edema and thickening, the intestines are 2 to 3 times larger than the normal intestines. The intestinal fistulas are adhered to each other, and the jelly-like substances are covered. Sometimes the meconium of the meconium is visible, the intestines are stiff, tarnished, and the peristalsis is moved. Weakened or disappeared, sometimes there is hematoma under the serosa, edema and hypertrophy of the intestinal wall make the intestines shortened obviously, some are only 1/4 of the normal intestinal tube, the color of the contaminated intestinal tube is purple, the surface seems to be lifeless, and the intestinal peristalsis recovers slowly after treatment. The length of the intestine can still return to normal, the intestine can be dysfunctional, the intestinal tract of the severe blood circulation disorder can be necrotic or perforated, and the abdominal wall is mostly connected to the base of the umbilical cord on the right side, sometimes the skin of the abdominal fissure is separated from the umbilical cord by 1-2 cm. .

2. Whole body performance

(1) hypothermia: poor neonatal thermoregulatory function, especially premature infants and neonatal thermoregulatory center immature development, lack of control of vasomotor function, no normal heat production and heat regulation, body temperature is susceptible to external fluctuations The neonatal body surface area is relatively large, the subcutaneous fat is small, and it is easy to radiate heat to the surroundings; in addition, the heat-generating tissue in the neonatal body is brown adipose tissue, and the oxygen production process requires sufficient oxygen to participate in the abdominal fissure disease. Children often have hypoxemia and acidosis, and the heat production is seriously affected. In addition, the intestinal tube is directly exposed to the body, the calorie loss is very fast, and the hypothermia is prone to occur. Therefore, the child is often in a hypothermia state when the patient is treated, and the body temperature is severe. Can fall below 35 ° C, and even hard swelling.

(2) Dehydration: a large number of intestinal tubes are exposed to the air, and the amount of liquid evaporation is large, which may lead to different degrees of dehydration and electrolyte disturbance in the sick children. According to Bryat, the water loss is estimated to be 2-10 ml/(kg·h), and the loss of Na is 0.3~. 1mmoL / (kg · h), protein loss is 50 ~ 250mg / (kg · h) per hour.

(3) Acidosis: Because the child's body temperature is low, the respiratory center is poorly excitable, blood oxygen saturation may decrease, acidosis is prone to occur, cold stimulation, free adrenaline causes pulmonary vasospasm, and right-to-left shunt is added; On the one hand, low body temperature accompanied by low respiratory excitability, and decreased oxygen saturation, which can form a vicious circle.

(4) Intraperitoneal infection and sepsis: due to prolonged immersion in the amniotic fluid before birth, it is stimulated by urea, uric acid, inorganic salts, sebum, etc., and there is a chemical inflammatory change at birth; after the birth, the intestinal tube is exposed to In vitro, bacterial contamination is easy to occur; local and systemic resistance of the sick child is low, and the abdominal cavity disease is not prone to occur in the abdominal cavity and sepsis.

According to the gastrointestinal tract from the abdomen rupture, the diagnosis of abdominal fissure is not difficult.

Abdominal fissure examination

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

2. Blood biochemical examination: often have low blood sugar, elevated urea nitrogen.

In recent years, through ultrasound examination, the diagnosis of abdominal fissure deformity can be made before delivery. The fetal bowel can be seen in the examination, floating in the amniotic fluid outside the abdominal wall, and the degree of dilatation of the intestine and thickening of the intestinal wall can be observed.

Diagnosis and diagnosis of abdominal fracture

diagnosis

According to the gastrointestinal tract from the abdomen rupture, the diagnosis of abdominal fissure is not difficult.

Differential diagnosis

It should be differentiated from the umbilical bulge. The surface of the umbilical bulge is coated with a capsule, and there is no normal umbilical structure. However, the position and shape of the umbilical cord and the umbilical cord are normal, and the abdominal wall is left on one side of the umbilicus. The defect of the layer, the intra-abdominal organ protrudes from the ventral wall of the umbilicus, especially when the intestinal edema is removed, thickened, and the surface is covered with inflammatory exudate, which is easy to be confused with the rupture of the capsular rupture.

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