Pediatric acute hemorrhagic necrotizing enteritis

　　1. The etiology of the disease has not been fully understood and may be related to the following two factors

　　1. The presence of certain bacteria and their toxins. The possibility of Clostridium perfringens type C producing B toxin is high, as the anaerobic culture of the stool of patients with the disease shows that the detection rate of this bacterium and the positive rate of B toxin serum antibody are significantly higher than those in the normal population. Injecting the bacterial fluid into guinea pigs can cause hemorrhagic lesions in the intestines and lead to death.

　　2. The trypsin activity of children is reduced. The above B toxin can be hydrolyzed by intestinal trypsin and lose its pathogenic effect. Long-term protein malnutrition and/or frequent consumption of foods rich in trypsin inhibitors such as sweet potatoes and corn can significantly reduce the activity of intestinal trypsin, making children more susceptible to the disease. This explains why the disease is more prevalent in rural poverty-stricken areas.

　　The typical pathological change of necrotizing enteritis is necrotizing inflammation.

　　Starting from the submucosal layer, with the expansion of the lesion, it can develop into the muscular layer and mucosal layer, causing multiple intestinal wall full-thickness congestion, edema, and necrotic spots. After the necrotic mucosa falls off, ulcers form, and continue to develop into the muscular layer and serous layer, leading to perforation and peritonitis. The lesions are more common in the lower segment of the jejunum and the upper segment of the ileum, but they can also be seen in children with duodenum and colon. In severe cases, the entire small intestine can be affected. Generally, they are scattered and segmented, with some being 1 to 2 segments or more, each segment having different lengths, the shortest being over ten centimeters, and the longest reaching 100 cm, with clear boundaries. The damaged intestinal wall thickens, becomes brittle and loses elasticity, and expands. In severe cases, the serosal surface becomes rough with fibrin adhesion, and the intestinal lumen is filled with jam-like bloody stools. Under the microscope, inflammatory cells can be seen in all layers of the diseased intestinal wall, mainly lymphocytes, eosinophils, monocytes, and plasma cells. The mucosa can undergo necrosis or shedding, with large areas of hemorrhagic necrosis and edema in the submucosa, and dilated and congested capillaries. There may be turbid, purulent, or bloody exudate in the abdominal cavity. After the lesion recovers, there are no chronic granulomatous changes, and it is rare to cause abdominal adhesions.

　　1. Peritonitis:It is the inflammation of the parietal peritoneum and visceral peritoneum of the abdominal cavity, which can be caused by bacterial, chemical, and physical injuries, etc. It can be divided into primary peritonitis and secondary peritonitis according to the pathogenesis. Acute purulent peritonitis involving the entire abdominal cavity is called acute diffuse peritonitis.

　　2. Intestinal obstruction:(intestinal obstruction, ileus) refers to the obstruction of intestinal contents in the intestines. It is a common acute abdominal condition that can be caused by various factors. At the onset, the obstructed intestinal segment first experiences anatomical and functional changes, followed by the loss of body fluids and electrolytes, intestinal wall circulation disorders, necrosis, and secondary infection. Finally, it can lead to sepsis, shock, and death. Of course, if diagnosed and treated in time, most cases can reverse the progression of the disease and be cured.

　　3. Acidosis:Endocrine diseases refer to the accumulation of acidic substances in the blood and tissues of the body, which is essentially an increase in hydrogen ion concentration in the blood and a decrease in pH value. It is generally divided into metabolic acidosis and respiratory acidosis.

　　4. Jaundice:(jaundice) is a common symptom and sign, which is caused by the increase of serum bilirubin concentration due to the disorder of bilirubin metabolism. Clinically, it is manifested as the yellowing of the sclera, mucosa, skin and other tissues. Because the sclera contains more elastic protein (elastin) and has a strong affinity for bilirubin, the yellowing of the sclera in jaundice patients often appears before the mucosa and skin and is first noticed. When the total bilirubin in serum is between 17.1-34.2μmol/L, and jaundice cannot be seen with the naked eye, it is called隐性黄疸 or subclinical jaundice; when the total bilirubin concentration in blood exceeds 34.2μmol/L, jaundice can be found in clinical practice, which is also called 显性黄疸.

　　Generally without prodromal symptoms, sudden onset, mainly manifested as abdominal distension, abdominal pain, vomiting, diarrhea, bloody stool, fever. Many children appear severe toxic symptoms within 1 to 2 days, even shock. Abdominal pain is persistent, accompanied by intermittent exacerbation, often generalized abdominal pain, can also be localized to the lesion site. Vomiting and diarrhea appear soon after onset, feces are initially watery, containing mucus, and then turn into bloody stool. Some children have no diarrhea, and blood in stool starts 1 to 2 days after abdominal pain. The amount of blood in stool varies, the dark red blood in large amounts has an odor of decay and fishiness,呈洗肉水或红果酱样. Some children appear bloody stool several hours after onset, fever is about 38℃, severe toxicosis can cause body temperature to rise to 39-40℃ or lower than normal. The symptoms of infants and young children are often atypical, with obvious dehydration and acidosis symptoms, some may appear extraintestinal symptoms first, such as jaundice, cough and asthma, enlargement of liver and spleen, and convulsions, etc. Due to the different degrees of intestinal wall lesions, clinical symptoms can vary in severity, and are manifested in the following types:

　　1. Diarrhea with blood in stool type:主要以黏膜渗出性病变为主, abdomen is soft without tenderness, should be treated conservatively by internal medicine.

　　2. Intestinal obstruction type:The muscular layer of the intestinal tract is severely damaged and swells, the intestinal tract becomes rigid, loses peristalsis, and clinical symptoms of mechanical intestinal obstruction appear.

　　3. Peritonitis type:The serous layer has a large number of inflammatory cells infiltrating and exuding, there is a large amount of inflammatory exudate in the abdominal cavity, or due to necrosis, it becomes bloody fluid, and the clinical manifestations are symptoms of peritonitis.

　　4. Toxic shock type:This type of child has severe systemic toxic symptoms, with pale complexion, listlessness, weakness, cold extremities, weak pulse, low blood pressure, even undetectable, red tongue with slight purple hue, yellow greasy fur, sometimes accompanied by a small amount of bloody stool, dehydration and electrolyte imbalance, slight abdominal distension and muscle tension, mostly suspected of strangulated intestinal obstruction.

　　First, prevention

　　1. Regular physical examination:In order to achieve early detection, early diagnosis, and early treatment.

　　2. Do a good job of follow-up:Prevent the deterioration of the disease.

　　3. Strengthen physical fitness:Enhance immunity: Pay attention to a balance between work and rest, participate in physical exercises more often, and eat more fresh fruits and vegetables rich in vitamins.

　　2. Before treatment

　　It is necessary to have a detailed understanding of the symptoms and related taboos of the disease.

　　1. Blood routine examination:The total number of white blood cells and neutrophils increases, with left shift, toxic granules, and vacuoles; platelets are often reduced, and the reduction is more obvious in severe cases.

　　2. Stool routine examination:A large number of red blood cells, a small number of white blood cells, and a strong positive occult blood test can be seen. Gram staining shows a large number of Gram-positive short rods, and sometimes necrotic intestinal mucosa and pseudomembrane can be seen.

　　3. Stool culture:Most can be isolated Clostridium perfringens, and there may also be pathogenic Escherichia coli, Shigella, Salmonella, etc.

　　4. Coagulation mechanism examination:Coagulation time is often prolonged, prothrombin time is prolonged, and plasma protamine paracoagulation test is often positive. There is a decrease in coagulation factors to varying degrees.

　　5. Electrolyte testing:Hyponatremia, hypokalemia, hypochlorhydria, and acidosis, etc.

　　6. Stool:The activity of trypsin is significantly reduced.

　　7. X-ray examination:The X-ray manifestations of acute necrotizing enteritis are various. Different clinical types and pathological changes at different stages lead to different X-ray manifestations. Abdominal supine and upright X-ray films are the main methods for diagnosing the disease. Since there is a risk of intestinal perforation, barium meal and barium enema examination are prohibited. In the acute stage, X-rays are taken every 6 hours to observe changes in the condition. In the early stage, small intestinal distension is the main symptom, and the widening of the intestinal wall is due to edema, congestion, and necrosis of the intestinal mucosa and submucosa. In mild to moderate cases, the intestinal wall can be seen to have cystic air accumulation, an increase in intestinal fluid, and widening of the intestinal spaces (if the intestinal space is wider than 5 cm, it has diagnostic significance). The intestinal mucosal folds become thick or blurred, and even the edges become deeply serrated. Some patients may have intestinal tubes arranged in a large span arch or step-like arrangement. In severe cases, the intestinal tubes may have large areas or segmental necrosis or perforation, showing dynamic intestinal obstruction, intestinal paralysis, local intestinal stricture, rigidity, and loss of normal soft curvature. The air-liquid level is obvious, and the intra-abdominal exudate increases or increases progressively. The intestinal loops gather towards the central abdomen, and the distance between the intestinal tubes and the abdominal wall becomes wider and blurred. The entire abdomen has increased density. If a segment of the intestine is completely necrotic, it can be seen that the intestinal loops are dilated, the motility is lost, and the position and shape are fixed, indicating severe lesions and potential or actual perforation. Free air is the X-ray feature of intestinal perforation, and free gas appears as an inverted triangular radiolucent shadow between the anterior abdominal wall and the aerated intestinal tubes.

　　What is good for children with acute hemorrhagic necrotizing enteritis?

　　6. Diet should be light.

　　5. Pay attention to the proportion of sugar, fat, and protein in food, and the content of vitamins and other essential nutrients for the body.

　　What should children with acute hemorrhagic necrotizing enteritis avoid eating?

　　1. Avoid smoking, drinking, and spicy刺激性 food.

　　2. Avoid irregular eating habits.

　　3. Avoid unclean diet: Gastritis patients should pay special attention to dietary hygiene, especially in summer. Unwashed fruits and vegetables should not be eaten, and spoiled food should not be consumed. Foods stored in the refrigerator must be thoroughly cooked before eating. If spoilage is found, it should be discarded immediately and not consumed.

　　4. Avoid cold, hot, and hard foods: such as, cold or hot food and drinks.

　　5. Avoid刺激性 foods, such as chili, mustard, pepper, strong tea, coffee, cocoa, and other food or beverage or drinks.

　　1. Fasting. Fasting is an important treatment measure for this disease. During the period of hematochezia and abdominal distension, if clinical consideration suggests the possibility of necrotizing enterocolitis, fasting should be initiated immediately. For moderate to severe abdominal distension, gastrointestinal decompression should be performed as soon as possible, with a nasogastric tube inserted through the nose to perform gastrointestinal decompression.

　　2. Correction and maintenance of water and electrolyte, acid-base balance. In severe cases, water and electrolyte imbalance is more prominent, with hyponatremia and hypokalemia being more common. Due to the longer fasting period, it is necessary to accurately calculate the intake and output of calories, and provide the maintenance amount required for physiological needs according to the child's age, and make up for cumulative and continuing losses.

　　3. Nutritional support should provide basic calories during fasting, and small amounts of plasma or whole blood transfusions, as well as parenteral nutrition support therapy, are given when necessary to supplement the body's essential substances. This can allow the intestines to rest sufficiently, thereby improving the cure rate. The basic calorie supply should be 167.4 to 251.0 kJ/kg (40 to 60 kcal/kg) per day. To ensure that children receive adequate nutrition during fasting, enhance the body's immune function, ensure gastrointestinal rest, and reduce physical or chemical stimulation, total parenteral nutrition (TPN) or supplements such as compound amino acids and hydrolyzed protein can be provided to meet the protein needs. Vitamin B, C, K, and calcium supplements are also provided. In parenteral nutrient solutions, the proportion of carbohydrates is approximately 50% of the total energy, fats 40%, and proteins 10%. The ratio of non-protein to protein calories is 10:1. Generally, it is 10% fat emulsion, 0.5 to 3g/kg per day, compound crystalline amino acids, 0.5 to 2.5g/kg per day, and glucose concentration is 8% to 10%. Appropriate amounts of electrolytes, various vitamins, and trace elements are given, with the total fluid volume controlled at 120 to 160ml/kg per day. Heparin (50U) is added to prevent clotting. Fat emulsion and amino acids should be started with low doses to avoid adverse reactions. If infection or poisoning symptoms are severe, the child's liver function may be impaired, affecting fat metabolism. The administration of parenteral nutrient solutions should be temporarily suspended, and 1 to 3 days of glucose solution containing electrolytes should be administered first, or amino acids and fat emulsion should be supplemented step by step to prevent fat overload syndrome. Children's organs are not fully developed, especially newborns, and after 1 to 2 weeks of intravenous nutritional supplementation, regular monitoring of liver and kidney function, blood lipids, blood glucose, and bilirubin is required. Once the condition improves, abdominal distension disappears, occult blood test in stool turns negative, and there is a feeding reflex, sugar water or diluted milk can be added, gradually transitioning from total parenteral nutrition to partial parenteral nutrition, until all nutrition is supplied through the intestines. There are reports that necrotizing enterocolitis in infants is related to the inability to digest and utilize lactose and sucrose due to a deficiency in disaccharidase. Non-disaccharide diets (such as 100ml soy milk plus 5 to 10g glucose) can significantly improve efficacy.

　　4. Vasoactive drug therapy, anisodamine (654-2): Generally 2-3mg/kg per day, administered intravenously over 6-8 hours, for a course of 7-14 days. It is used to improve microcirculation and can significantly improve efficacy. Phentolamine (regitin): As an alpha-adrenergic blocker, it can relieve vasoconstriction of the microvasculature, improve microcirculation, help reduce intestinal wall edema, relieve abdominal distension, and has a good therapeutic effect on paralytic ileus. The dose is 0.5-1.0mg/kg, infused into a small bottle and administered every 2-4 hours. Phenoxymethylpenicillin (phenoxybenzamine) can also be used, 0.5-1.0mg/kg, administered intravenously every 4-8 hours.

　　5. Early discovery and timely rescue of toxic shock. Severe necrotizing enteritis often complicates with toxic shock and is often the main cause of death. Specific measures are the same as for septic shock treatment, starting with rapid blood volume expansion, improving tissue oxygenation, correcting acidosis, using vasoactive drugs, adopting the rescue plan mainly with dextran 40, injection of anisodamine (654-2), and artificial hibernation therapy, and preventing organ failure.

　　6. Anticoagulant therapy The probability of DIC in children with necrotizing enterocolitis is high. Some observations have found that about 2/3 of the cases of this disease have a positive DIC test. Therefore, anticoagulant treatment is very necessary for severe cases. Generally, heparin therapy is used, 1mg/kg (1mg ≈ 125U) each time, once every 4 to 6 hours, by intravenous infusion or intravenous injection. Pay attention to observe for signs of bleeding tendency, and maintain a clotting time (tub test) of 20 to 30 minutes.

　　7. Antibiotics should be selected broad-spectrum antibiotics sensitive to intestinal bacteria, such as ampicillin combined with ribostamycin, netilmicin, or second and third-generation cephalosporins. Also, metronidazole can be taken orally at a dose of 50mg/kg daily, divided into three doses, for about one week.

　　8. The occurrence of lesions related to trypsin application is associated with decreased trypsin activity and reduced secretion. It is recommended to take trypsin regularly. The commonly used oral dose is 0.1mg/kg, three times a day. For shock and severe cases, intramuscular injection can be added once a day at a dose of 1000U. Trypsin can hydrolyze the B toxin produced by Welchii bacteria, reduce its absorption, and clear necrotic tissue in the intestines, which is conducive to the recovery of lesions.

　　9. Adrenal cortical hormones are used to suppress allergic reactions and alleviate toxic symptoms. They should be administered early in severe cases and patients with shock, and the duration of use should not exceed 3 to 5 days. Hydrocortisone is administered at a dose of 4 to 8mg/kg, or dexamethasone at a dose of 0.25 to 0.5mg/kg daily, by intravenous infusion. If the application time is too long (>1 week), there is a risk of promoting intestinal necrosis, triggering hemorrhage, and causing intestinal perforation.

　　10. It is common for children with acute necrotizing enterocolitis to develop toxic ileus. If there is no improvement after treatment with fasting, gastroenteric decompression, anal exhaust, and intravenous injection of neostigmine, phen妥拉明 can be administered intravenously to competitively block the binding of norepinephrine to α receptors, relieve the vasoconstrictive effect of norepinephrine, improve systemic and intestinal microcirculation, alleviate symptoms such as intestinal wall congestion and edema, and restore or enhance intestinal peristalsis. The dosage and method are the same as before. Abdominal pain is one of the main symptoms, and the effect of antispasmodic drugs is often not ideal. Scopolamine hydrobromide (654-2) can be used intradermally at a dose of 0.1 to 0.3mg/kg or atropine at a dose of 0.01mg/kg, repeated every 4 to 6 hours if necessary. For severe abdominal pain, dolantin can be administered intramuscularly at a dose of 0.5 to 1.0mg/kg, but it is not suitable for small infants; also, hypothermic therapy or unilateral or bilateral renal capsule closure with 0.25% procaine can be used. In case of serious complications such as pulmonary dysfunction, cerebral edema, respiratory distress syndrome, and microcirculatory disorders, appropriate treatment should be carried out in a timely manner. Other symptomatic treatments include fever reduction using subhypothermic therapy; sedation should be administered to those who are restless and anxious.

　　11. Traditional Chinese medicine and acupuncture therapy can be used to treat blood in the stool and abdominal distension. The main treatment is to clear heat and detoxify, cool blood and nourish yin, supplemented by promoting blood circulation and removing blood stasis. Abdominal pain can be treated by acupuncture at acupoints such as Stomach 36, Yanglingquan, Tianshu, Hegu, etc.

　　13. Other therapies should use appropriate antibiotics to control and prevent infection. Hemostatic and analgesic drugs can also be used simultaneously. It is generally recommended to take trypsin orally, 3 times a day, 0.5 to 1.0g each time, and for severe cases, 1000U can be injected intramuscularly once a day. Due to the possibility of an allergic reaction, the use of adrenal cortical hormones can achieve certain efficacy. In the acute stage, hydrocortisone can be administered intravenously at a dose of 5 to 10mg/(kg·d), and after improvement, prednisone can be taken orally at a dose of 1 to 2mg/(kg·d). Some people do not advocate the use of hormone therapy and instead use scopolamine 0.03 to 0.05mg/(kg·d) intravenously for 3 to 7 days, and after symptom control, oral administration for 3 to 5 days. Some people have tried sodium cromoglycate capsules for anti-allergic reactions, 5 to 10mg per dose, 4 times a day, for 3 to 5 days, with certain efficacy.

　　12. In cases where the symptoms of intestinal obstruction are obvious, there is a suspicion of peritonitis, intestinal necrosis, or intestinal perforation; or when the X-ray examination shows that the intestinal tract is dilated without tension, the contour is blurred and rough, and there is significant peritoneal effusion, emergency surgical treatment should be considered. The surgical method can be selected according to the degree of intestinal tract lesions, including intestinal resection and anastomosis, decompression fistula, and peritoneal drainage.