Acute hemorrhagic necrotizing enteritis

Introduction to acute hemorrhagic necrotic enteritis Acute hemorrhagic necrotic enteritis (acute hemorrhagicnecrotizingenteritis) is an acute enteritis associated with infection with C-type Bacillus capsulatum. The disease is mainly in the small intestine, and the pathological changes are characterized by hemorrhagic necrosis of the intestinal wall. The main clinical manifestations are abdominal pain, blood in the stool, fever, vomiting and bloating. In severe cases, there may be complications such as shock, intestinal paralysis and other symptoms such as intestinal perforation. basic knowledge The proportion of illness: 0.014% Susceptible people: no specific population Mode of infection: non-infectious Complications: intestinal obstruction, shock, pneumonia, pulmonary edema

Causes of acute hemorrhagic necrotic enteritis

Intestinal ischemia (19%):

The visceral vasoconstriction caused by various reasons, the insufficiency of mesenteric vascular insufficiency can cause intestinal ischemic damage, and the intestinal mucosa is most susceptible to ischemia. Experimental observation of the rat intestinal mucosa after hemorrhagic shock for 1 h Autolysis occurs.

The principle of clinical treatment of ischemic damage should be to restore blood reperfusion as soon as possible to increase tissue oxygen supply, but long-term ischemia will occur after reperfusion injury reperfusion injury (reperfusion injury), this damage is due to calcium Overloading, oxygen free radical generation, neutrophil activation caused by the release of various enzymes including elastase and collagenase and endothelial cell homeostasis.

Intestinal infection (25%):

The intestine is the largest bacterial reservoir in the human body. Due to the protective effect of the intestinal mucosa itself, bacteria and toxins cannot be invaded. This protective effect is called the defense barrier. Shock, intestinal ischemia, asphyxia, artificial feeding, etc. can cause the intestines. The destruction of the barrier, which in turn causes the imbalance of bacterial micro-ecology in the intestine and the invasion of bacteria and toxins induces AHNE.

There is no definitive understanding of AHNE pathogenic pathogens, but anaerobic bacteria, Escherichia coli, specific Klebsiella, fusiform spores or genus Aeromonas can be isolated from the patient's feces. Even viruses, etc., can cause intestinal wall infection, necrosis, perforation, C-type Clostridium perfringens (the beta-toxin-producing Welchii bacilli) in the stool is easy to cause pathogenic effects, causing intestinal microcirculation disturbance, and showing patchy Gangrenous intestinal lesions.

Intestinal barrier dysfunction (15%):

The intestinal barrier function includes mechanical, immune, biological, chemical and motor function barriers. Under normal conditions, intestinal mucosal epithelial cells, intercellular connections and bacterial membranes form a mechanical barrier, and intestinal mucus and mucin form a covering of the intestinal mucosa. The surface of the elastin layer prevents bacteria from invading and protects against chemical and mechanical stimuli. Normally, secretory immunoglobulin (sIgA) secreted by the intestinal mucosa is extremely important for mucosal local immune function and is an immune barrier. Its role is to form a protective layer on the surface of the mucous membrane, prevent bacterial adhesion, agglomerate bacteria, inhibit bacterial activity and neutralize bacterial toxins and protect against viruses. For the lack of various proteolytic enzymes, sIgA, bacteria adhere to the mucosal epithelium and form colonies. In turn, bacteria and endotoxins invade the systemic circulation through the portal vein and lymphatic system, forming intestinal endotoxemia and bacterial translocation (BT).

The role of inflammatory mediators (5%):

In recent years, the pathogenesis of AHNE has been concentrated on the study of inflammatory mediators. Injury, intestinal endotoxemia and bacterial translocation can trigger a chain reaction between cytokines and inflammatory mediators under certain conditions. Platelet activating factor (PAF), tumor necrosis factor alpha (TNF), interleukin-6 (IL-6) and endothelin-1 (ET-1) may be found in animal models of AHNE. Sexual medium.

Although the foregoing exemplifies a number of reasons for the occurrence of the disease, it is true that some cases do not have these susceptibility factors. Materials have confirmed that the occurrence of AHNE is associated with viral infection and cocaine addiction in pregnant women. Because cocaine has an -adrenergic effect, It can reduce the blood flow of the uterus and increase the contraction of the mesenteric blood vessels of the fetus, thereby causing a series of changes in the fetal hypoxia.

The lesions invade the lower part of the jejunum or the upper part of the ileum. In only a few cases, all the small intestine and colon are involved at the same time. The diseased bowel is generally characterized by congestion, edema, thickening of the intestinal wall, loss of elasticity and peristalsis, visible focal necrosis, severe subserosal Bleeding point and flaky necrosis, intestinal tube dilatation, intestinal cavity filled with turbid bloody fluid and necrotic substance, affected intestinal segment can also be all small intestine and invade the colon, perforation and peritonitis can occur, the mesentery of the diseased intestinal segment can also be affected, mesangial Lymph node enlargement, the lesion begins from the submucosal layer and gradually extends to the muscular layer after going up to the mucosa. Generally, the range of mucosal lesions is larger than that displayed on the surface of the serosa. The layers of the intestinal wall seen under the microscope are hyperemic and edematous. A large number of lymphocytes, plasma cells, monocytes, eosinophilic and neutrophil infiltration, vascular wall collagen fiber swelling and fibrosis, intermuscular ganglion cell degeneration, small blood vessel necrosis and thrombosis, intestinal wall Focal hemorrhage, necrosis and ulcers.

Causes

So far, there is no satisfactory explanation for the pathogenesis of AHNE, but the opinions are quite consistent in some susceptibility factors and reasoning. These susceptibility factors include: intestinal ischemia, intestinal infection, intestinal barrier function. Impaired, respiratory distress syndrome, hemorrhage, asphyxia, congenital heart disease with heart failure, sepsis, shock, hypothermia, erythrocytosis and/or high blood viscosity, artificial feeding, etc., is now considered to be the onset and infection of this disease Related to the B-toxin-producing Welchii bacillus (C-type Clostridium perfringens), B-toxin can cause intestinal tissue necrosis and produce gangrenous enteritis.

In the Papua New Guinea plateau where the incidence of this disease is high, the study found that the local residents have low levels of protease in the intestine, which is associated with a low-protein diet and a heat-resistant trypsin inhibitor (heatstable) contained in the local sweet potato. Trypsin inhibitors), in animal experiments, perfused with Welchii bacilli through the gastric tube, the animal is not pathogenic; but if the raw sweet potato powder or raw soy flour containing trypsin inhibitor is simultaneously infused, it can cause disease and produce acute The same histopathological changes of hemorrhagic necrotic enteritis, animal experiments have also proved that the dog pancreas extract containing trypsin can prevent and reduce the occurrence and development of this disease, the above facts suggest that the disease occurs in addition to eating contaminated meat with pathogenic bacteria In addition to food-like foods, there are other dietary factors, such as sudden changes in eating habits, from eating more vegetables to eating more meat, so that the ecology of the intestines changes, which is conducive to the reproduction of Welchii bacilli; The presence of a large amount of enteric trypsin inhibitor reduces the destruction of B toxin.

The main pathological changes of this disease are fibrin deposition in the small arteries of the intestinal wall, embolization and small intestinal bleeding and necrosis. The lesions are more common and severe in the jejunum and ileum; sometimes the duodenum, colon and stomach are involved; Cases of the gastrointestinal tract can be affected, the lesions are often segmental, can be limited to a segment of the intestine, can also be multiple, lesions often start in the mucosa, manifested as swelling, extensive bleeding, wrinkled top is covered with green Pseudomembrane, but the lesion and the normal mucosa are clearly defined. The lesion can extend to the mucosal muscle layer, even involving the serosa. The intestinal wall of the lesion is thickened and hardened. In severe cases, it can cause intestinal ulcer and intestinal perforation. Different shades of necrosis change, the light is only the top of the villi, the severe one can involve the whole layer of the mucosa, in addition to extensive bleeding in the submucosa, there may be severe edema and inflammatory cell infiltration, the muscle layer and the serosa layer may be slightly Hemorrhage, intestinal smooth muscle can be seen swelling, rupture, glassy and necrosis, the blood vessel wall is fibrin-like necrosis, and often thrombosis, intestinal muscle plexus cells can have dystrophic changes.

In addition to intestinal lesions, there may be local mesenteric lymphadenopathy, softening; liver steatosis, acute splenitis, interstitial pneumonia, pulmonary edema; individual cases may be accompanied by adrenal focal necrosis.

The onset of acute calculous cholecystitis is due to stones blocking the cystic duct, causing bile retention in the gallbladder, secondary bacterial infection causing acute inflammation, such as inflammation, congestion and edema in the gallbladder mucosa, called acute simple cholecystitis If the inflammation spreads to the whole layer of the gallbladder, the gallbladder is filled with pus, and the serosal surface also has purulent fibrinous exudation, it is called acute suppurative cholecystitis. The gallbladder is extremely swollen due to empyema, causing ischemia and gangrene of the gallbladder wall. Is acute gangrenous cholecystitis, necrosis of the gallbladder wall can be perforated, leading to biliary peritonitis, gallbladder perforation occurs in the gallbladder at the bottom of the gallbladder or stone incarcerated gallbladder ampulla or neck, such as gallbladder perforation to adjacent organs Such as duodenum, colon and stomach, etc., can cause biliary fistula, at this time the acute inflammation in the gallbladder can be drained through the internal fistula, the inflammation can quickly disappear, the symptoms are relieved, such as the discharge of pus in the gallbladder Common bile duct can cause acute cholangitis, a small number of people can also develop acute pancreatitis, most of the pathogenic bacteria are Escherichia coli, Klebsiella and Streptococcus faecalis, anaerobic bacteria account for 10 to 15%, but When up to 45%.

Acute acalculous cholecystitis, cystic duct often without obstruction, the cause of most patients is unclear, often occurs in trauma, or some abdominal surgery unrelated to the biliary system, sometimes can occur in some children with non-hemolytic anemia, generally It is believed that the effects of dehydration after surgery and trauma, fasting, application of anesthetic analgesics, and neuroendocrine caused by severe stress response lead to decreased gallbladder contractility, bile retention and decreased gallbladder mucosal resistance. On the basis of secondary bacterial infection, and finally caused acute inflammation of the gallbladder, it is also believed that some cases are caused by acute embolism of the gallbladder's nutrient vascular disease. The pathological evolution of such acute acalculous cholecystitis is similar to that of calculous cholecystitis, but the course of disease development Rapidly, it usually develops into gangrenous cholecystitis within 24 hours and manifests itself as gangrene of the entire gallbladder.

Acute hemorrhagic necrotic enteritis prevention

In the high-yielding summer and autumn seasons, attention should be paid to food hygiene and good rest. Children of school age should be dewormed according to the national immunization requirements, and work and rest should be combined. Pay attention to the following aspects of diet:

1. Avoid eating uncooked or spoiled meat, especially in the high seasons to avoid eating raw meat.

2. Avoid eating a lot of foods that damage proteolytic enzymes in the intestines, such as sweet potato foods, especially when eating raw seafood, barbecues that may not be fully cooked (such as kebabs, etc.), avoid eating large quantities of such foods at the same time. .

3. Balance the diet and avoid overeating.

Complications of acute hemorrhagic necrotic enteritis Complications, intestinal obstruction, pneumonia, pulmonary edema

There may be local mesenteric lymphadenopathy, softening; liver steatosis, acute splenitis, interstitial pneumonia, pulmonary edema; other cases may be accompanied by adrenal focal necrosis, severe cases may have shock, intestinal paralysis and other symptoms of poisoning and Complications such as intestinal perforation.

1. Intestinal obstruction: due to bacteria, endotoxin, intestinal wall congestion, edema, loss of elasticity and peristalsis, intestinal retention, small bowel obstruction symptoms, clinically misdiagnosed as mechanical intestinal obstruction.

2. Shock and disseminated intravascular coagulation (DIC) bacteria, endotoxin absorbed into the blood, causing systemic poisoning disorders and hemodynamic disorders, about a quarter of patients may develop toxic shock, or with DIC.

Acute hemorrhagic necrotic enteritis symptoms Common symptoms Abdominal pain with blood in the stool, abdominal distension, abdominal pain, jelly-like diarrhea, peritoneal irritation, peritonitis, high fever, abdominal muscle tension, acute and heavy

The onset of the disease is rapid, and 1/3 may have a history of unclean diet. Clinical manifestations of acute abdominal pain, bloating, vomiting, diarrhea, blood in the stool and systemic poisoning.

1. Abdominal pain, bloating: abdominal pain is mostly sudden, persistent and can be aggravated. The abdominal pain is mostly in the umbilical or upper abdomen. Some patients may have total abdominal pain, which may have mild bloating in the early stage and then worsen.

2. Vomiting and abdominal pain are accompanied by nausea and vomiting. The spit contains bile, coffee or blood.

3. Diarrhea and blood in the stool: the degree is different, more than 10 times a day. According to the lesion site, bleeding rate, in the intestinal retention time and intestinal peristalsis, the feces can be blood, broth, jam or black stool, and often mixed with rotten tissue and special odor. If the lesion is limited in the small intestine, there is no urgency after the phenomenon.

4. Symptoms of poisoning around the body: due to the translocation of bacteria and endotoxin, the inflammatory reaction in the whole body may have fever or hypothermia, wilting or irritability. If sputum or coma is more likely to cause serious illness, multiple organ dysfunction (MODS) may occur. There may be cases of intestinal necrosis.

5. Infant and child symptoms: atypical, infants are more likely to develop 3 to 10 days after birth. Due to premature birth or low body weight, he was admitted to the intensive care unit. During artificial feeding or during the establishment of gastric tube nasal feeding due to incomplete establishment of swallowing reflexes in immature children, there was retention in the stomach, followed by bloating, vomiting, blood in the stool or fever. , heart rate is too fast or slow, abdominal muscle tension, abdominal flatulence, abdominal wall erythema and other signs. It is generally believed that the smaller the gestational age, the higher the incidence of AHNE. The incidence of low birth weight children was 12%.

6. Physical examination: abdominal distension, abdominal tenderness, due to inflammatory exudation can show different degrees of peritoneal irritation, intestinal and abdominal mass, such as intestinal necrosis, perforation can show typical signs of total abdominal peritonitis. For those with toxic shock, there are many unstable respiratory and circulatory systems, shortness of breath, low blood pressure, increased heart rate, mental disorders, and skin spots.

Examination of acute hemorrhagic necrotic enteritis

1. Blood routine: manifested as increased white blood cell count, smear classification with nuclear left shift phenomenon; red blood cell reduction, hemoglobin reduction; progressive platelet count reduction.

2. Blood biochemical examination: may have hypoproteinemia, electrolyte imbalance, metabolic acidosis, high or low blood sugar.

3. Liver, kidney and coagulation function: In some cases, liver, kidney function damage and DIC manifestations may occur.

4. Fecal occult blood test is positive.

5. Bacteriology of blood and feces: This test helps to judge the infected flora.

6. Abdominal X-ray film: X-ray performance is related to the severity of AHNE. Most of the early stage can have different degrees of intestinal lumen inflation, the intestinal gap is slightly widened, and the intestine due to intestinal edema mucosal inflammatory exudation The inner edge of the wall is blurred. As the disease progresses, the image of the gas in the intestinal wall can be found. It is generally believed that the gas in the intestinal cavity passes through the damaged mucous membrane and enters the submucosa or the subserosal. Wide and advanced, there are fixed and dilated intestinal fistulas, portal vein gas accumulation, ascites effusion, pneumoperitoneum, etc. Dynamic observation of X-ray changes in abdominal intestines is often helpful in judging the vitality of the intestines. In the acute phase, hemorrhage or perforation may be aggravated.

7. Fibrous colonoscopy: early detection of intestinal inflammation and bleeding.

8. B-ultrasound: The continuous accumulation of experience in imaging examination of the gastrointestinal tract is complementary to the X-ray examination. It is more convenient and quick to use this inspection method.

Diagnosis and diagnosis of acute hemorrhagic necrotic enteritis

diagnosis

Diagnosis is based primarily on clinical symptoms. Sudden abdominal pain, diarrhea, blood in the stool and vomiting, with moderate fever, or sudden onset of abdominal pain, especially after the patient has a scent of scented meat and no obvious urgency, the possibility of acute hemorrhagic necrotic enteritis should be considered. . Abdominal X-ray film is helpful for diagnosis.

Differential diagnosis

1. Intussusception: childhood onset is easily misdiagnosed as intussusception, but the general intussusception is paroxysmal abdominal cramps, intermittent episodes last for several minutes each time, remission period sick children play as usual, often in the onset of abdominal pain In the right lower abdomen, the intestine wall mass can be seen. The anus can be seen in the blood of the anus. There is no special odor in the blood. For the case of ileocele intussusception, jam-like stools often appear in the early stage, but small intestine-type incarceration occurs later in the blood.

2. Allergic purpura: allergic purpura allergic disease, mainly involving the capillary wall and bleeding symptoms, the intestinal response is caused by intestinal mucosal edema, hemorrhage, clinical manifestations of sudden onset of abdominal cramps, Mostly located in the umbilical cord and lower abdomen, sometimes very intense, but more often accompanied by skin purpura, joint swelling and pain, urine examination can find proteinuria, hematuria or tubular urine.

3. Others: AHNE needs to be differentiated from acute appendicitis, acute enteritis, bacillary dysentery, Mechel's diverticulitis, Crohn's disease, mesenteric vascular embolism, intestinal ascariasis, biliary ascariasis, strangulated intestinal obstruction.

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