Neonatal gastric perforation

　　1. Etiology

　　There is no unified view among experts on the etiology of this disease, and it is generally believed to be related to the following factors:

　　1. Defect in the muscular layer of the gastric wall

　　During the embryonic development period, the digestive tract originates from the endoderm and mesoderm. The endoderm forms the submucosal epithelium, and the mesoderm forms the muscular layer. When the embryo is 3-4 weeks old, the stomach is a fusiform part of esophageal expansion. When the embryo is 5-6 weeks old, the left end of the stomach begins to have the primitive basis of the mesodermal circular muscle, originating from the lower end of the esophagus. When the embryo is 6-7 weeks old, it gradually develops towards the greater curvature and the bottom of the stomach. By 9 weeks of gestation, the oblique muscle fibers of the stomach can develop from the circular muscle, finally forming the longitudinal muscle. Until 4 months of gestation, the development is still incomplete, but the longitudinal muscle develops rapidly in the later stage of embryogenesis, especially in the bottom of the stomach. The oblique muscle develops slowly, so the muscular layer below the cardia of the stomach is still very thin after birth. If there is a developmental disorder during the development period, it can form a defect in the muscular layer.

　　2. Uneven force of stomach contraction

　　When there is a defect in the muscular layer of the gastric wall, the force of stomach contraction is uneven, which can cause the stomach to rupture.

　　3. Excessive expansion of the fundus of the cardia

　　Some scholars believe that in the process of gastric formation, the excessive expansion of the fundus of the cardia (such as after a child swallows air), increases the intragastric pressure, causing the muscular layer to break and lead to perforation.

　　The defect in the muscular layer of the gastric wall is most common at the bottom of the stomach and the greater curvature. Kneisil proposed that this is a fragile gap that has not fully developed in the normal muscular layer, and this small piece of muscular layer weakness is likely due to the incomplete development of the muscular layer of the normal neonatal gastric wall, with some intertwining gaps between the muscle bundles. This is a normal development process, but it quickly continues to develop and perfect in the first few days after birth, and these gaps also disappear accordingly.

　　4. Local ischemia of the gastrointestinal wall

　　Many authors do not agree that the thinning of the gastrointestinal muscle layer is a congenital malformation. On the contrary, they believe that it may be the result of local ischemia of the gastrointestinal wall. They propose that local ischemia is a common cause of perforation. Under conditions such as asphyxia, hypoxemia, difficult labor, and hemorrhage, the body's blood flow compensatorily redistributes, reducing the blood supply to the gastrointestinal tract, kidneys, and peripheral vascular beds to ensure the blood supply to the heart and brain. If this compensatory protective local reaction is too strong, it can produce local ischemia of the gastrointestinal tract leading to perforation.

　　Secondly, pathogenesis

　　Gastric rupture is more common in the greater curvature of the stomach, with necrotic defects in the gastric wall at the rupture site, manifesting as linear rupture or muscularis mucosae tearing, and there may be submucosal tearing. The edges of the rupture are neat, but there are irregular necrotic areas, and the surrounding gastric wall gradually becomes thin. The muscular layer at the rupture site is broken, and oblique and longitudinal muscles are absent, leaving only the mucosa, submucosa, and muscularis mucosae to form the gastric wall. Occasionally, inflammatory cell infiltration can be seen.

　　Diffuse peritonitis is the main complication of neonatal gastric perforation and can lead to shock and multi-organ failure, which are the main causes of death in neonatal gastrointestinal perforation.

　　After the peritoneum is stimulated, it becomes congested and edematous, losing its inherent luster, and subsequently produces a large amount of serous exudate. On one hand, it can dilute the toxins and digestive juices in the abdominal cavity, thereby reducing the stimulation of the peritoneum. On the other hand, it can also lead to severe dehydration, protein loss, and electrolyte disorders. Large amounts of neutrophils and phagocytes gradually appear in the exudate, which can engulf bacteria and fine particles. With the addition of necrotic tissue, bacteria, and clotted fibrin, the exudate becomes turbid and then becomes pus. The pus, commonly dominated by Escherichia coli, is yellow-green, thick, and has a fecal smell.

　　This disease has no obvious prodromal symptoms. A few children may have vomiting, regurgitation, and refusal to eat. The vomit contains mucus and breast milk, and may be accompanied by a small amount of bloody fluid or coffee-like matter. Generally, there can be the passage of meconium, but as the condition progresses, paralytic ileus may occur, causing cessation of defecation and flatus, and occasionally, bloody stools may be passed.

　　After the stomach rupture, a large amount of gas enters the abdominal cavity, causing the diaphragm to rise and affecting respiration. The child may show cyanosis of the lips, difficulty breathing, and due to diffuse peritonitis, a large amount of toxins are absorbed by the peritoneum, which can lead to toxic shock with pallor, cyanosis, cold extremities, and skin mottling. The abdomen is highly distended, the abdominal wall veins are dilated, there may be peritoneal edema or accompanied by muscle tension, and a tympanic sound is heard on percussion of the entire abdomen, the liver dullness is absent, and there may be shifting dullness and the disappearance of bowel sounds.

　　Due to mood swings or overeating, patients with gastric ulcer are prone to develop gastric perforation. Once related symptoms occur, immediate consideration should be given to the possibility of gastric perforation. Before the ambulance arrives, the following points should be taken into account:

　　1. Do not roll around with your stomach, but lie on your left side in bed. The reason is that the perforation site is mostly located on the right side of the stomach. Lying on the left side can effectively prevent stomach acid and food from further flowing into the abdominal cavity, thereby aggravating the condition.

　　2. If medical personnel cannot arrive in time, but there are some simple medical equipment on the scene, the patient can insert a gastric tube himself. The specific method is to insert the gastric tube into the nostril, to the throat, and while blowing air and swallowing with force, the gastric tube is swallowed into the stomach. Then, use a syringe to withdraw the contents of the stomach, which can reduce the extent of abdominal infection and win treatment time for the patient. Remember that the patient must also lie on their left side at this time.

　　1. Abdominal X-ray examination

　　The erect chest radiograph shows that the diaphragm rises on both sides, the liver and spleen shadows are located on both sides of the spine in the middle abdomen, a large amount of free gas under the diaphragm, especially on the right side, which can occupy 2/3 of the abdomen, and a large amount of fluid is present in the lower abdomen, forming a transabdominal gas-liquid interface.

　　Many authors believe that there are no obvious clinical manifestations or X-ray signs in the early stage of spontaneous gastrointestinal perforation in low birth weight infants. Judy reported 6 cases of gastric perforation in extremely low birth weight infants, and X-ray abdominal examination in 5 cases did not show free gas under the diaphragm, making diagnosis somewhat difficult. However, repeated timed imaging and abdominal puncture can help with rapid diagnosis.

　　2. Experience with Kosloske and Lilly's abdominal puncture technique

　　After preparing the skin with a disinfectant on the lateral abdomen, insert a 22 or 25-gauge needle, then connect a syringe. If the needle core retracts, it indicates the presence of gas. This process is relatively safe, but attention must be paid to free abdominal gas, which does not necessarily indicate a gastrointestinal perforation. It may occur due to alveolar rupture, causing generalized or abdominal gas production from aerobic bacteria, or even no cause can be found.

　　Avoid stimulation, mainly too spicy foods, and it is best to stick to a liquid diet for a period of time. Pay attention to abdominal warmth, especially at night; eat more easily digestible foods and have small and frequent meals.
　　1. Regular meals should be taken, with small amounts taken multiple times, and rough, cold, hot, and highly刺激性 foods such as spicy foods, strong tea, and coffee should be avoided.
　　2. Quit smoking and limit alcohol intake.
　　3. Relieve mental tension.
　　4. Use medication as necessary to accelerate the healing of ulcers. Some medications can reduce stomach acid secretion, while others can apply a protective layer to the ulcer surface, such as aluminum salts or protein. Medications that can damage the gastric mucosa, such as aspirin, indomethacin, and phenylbutazone, should be avoided.
　　Secondly, recommended foods and methods of consumption
　　1. Spirulina. After consuming spirulina, it can quickly decompose into fine particles, adhere to the mucous membrane of the stomach and duodenum, forming a protective layer. This promotes mucosal regeneration, repairs damaged mucosa, and makes the stomach feel comfortable.
　　2. Lecithin. Lecithin can promote cell activation and tissue regeneration and repair.
　　3. High-quality protein. High-quality protein contains a comprehensive, rich, and balanced set of essential amino acids, which can effectively address the issue of stomach nutrition supplement.
　　Method of consumption:
　　1. Mild ulcers: Take 4 capsules of spirulina, 4 capsules of lecithin, and 1 packet of high-quality protein daily in the morning, and continue to consume these foods for 60 consecutive days.
　　2. Severe Ulcer: Take 5-10 particles of spirulina and 5-15 particles of phospholipids daily, divided into two doses, and consume these foods continuously for 90-180 days.

　　1. Treatment

　　Once diagnosed, emergency surgical treatment should be performed.

　　1. Preoperative Preparation

　　(1) Place a gastric tube to decompress and remove the contents of the stomach. Sometimes, the gastric tube can be inserted into the peritoneal cavity through the rupture hole in the stomach, and the gas and liquid in the peritoneal cavity can be aspirated, which can alleviate abdominal distension and improve respiratory function.

　　(2) Correct the disorder of water, electrolyte, and acid-base balance.

　　(3) Strengthen supportive therapy, such as blood transfusion and oxygen therapy. However, it is not advisable to administer positive pressure oxygen therapy to avoid increasing intraperitoneal pressure.

　　(4) Administer antibiotics and vitamin K.

　　(5) For children with severe abdominal distension, abdominal puncture decompression can be adopted to relieve respiratory distress.

　　2. Surgical Methods

　　On the basis of the above treatment, perform repair of gastric rupture. Under local anesthesia, take a median or para-medial incision, and aspirate the peritoneal fluid. Explore the lesion, resect necrotic tissue, and pay attention to avoid causing difficulty in suture. Then, perform two-layer invagination suture at the healthy gastric wall around the perforation edge, and cover the local area with omentum after repair. After the repair is complete, thoroughly rinse with normal saline, and at the same time, carefully check whether there is obstruction in the distal part of the gastrointestinal tract, and give treatment at the same time. Finally, place an abdominal drain tube.

　　Some scholars advocate performing a subtotal gastrectomy, wedge resection, or sleeve resection, but the surgical trauma is too great, and newborns are difficult to tolerate.

　　3. Postoperative Management

　　Postoperative fasting, strengthening supportive therapy, intravenous fluid and antibiotic administration, and early initiation of parenteral nutrition or jejunal distal tube feeding if possible. Continue gastrointestinal decompression until gastrointestinal function is restored.

　　2. Prognosis

　　The prognosis of this disease is affected by many factors, including the physiological characteristics of newborns and the course of the disease. Newborns, especially premature infants, have incomplete respiratory, circulatory, and immune functions, poor tolerance to infection, and it is not easy to localize after perforation, leading to diffuse peritonitis with a mortality rate as high as 62% to 78%. Bell believes that sepsis-induced shock and multiple organ failure are the main causes of death from neonatal gastrointestinal perforation. The high mortality rate is related to 'endotoxemia'. BenSon et al. believe that it can be used to evaluate prognosis and clinical course.