Acute hemorrhagic necrotizing enteritis
Acute hemorrhagic necrotizing enteritis (AHNE) is a life-threatening fulminant disease of unclear etiology, the onset of which is related to intestinal ischemia and infection. The lesions mainly involve the small intestine and are segmental in nature, but in a few cases, the entire small intestine and colon may be involved, characterized by hemorrhage and necrosis. The main clinical manifestations are abdominal pain, abdominal distension, vomiting, diarrhea, blood in stool, and in severe cases, sepsis and toxic shock.
The etiology has not been completely elucidated. It is now believed that the pathogenesis of the disease is associated with infection with Bacillus welchii (C aerogenes), which produces B toxin that causes necrosis of intestinal tissues and gangrenous enteritis. In the highlands of Papua New Guinea, where the incidence of this disease is high, studies have found that the low concentration of proteases in the intestinal lumen of the local population is associated with a low-protein diet and heatstable trypsininhibitors contained in sweet potatoes, a local staple food.
In animal experiments, the animals were not diseased when Welchii bacillus liquid was instilled through the gastric tube; however, if raw sweet potato flour or raw soybean flour containing trypsin inhibitors were also instilled, they were diseased and produced the same histopathological changes as in acute hemorrhagic necrotizing enteritis. Animal experiments have also demonstrated that dog pancreas extracts containing trypsin can prevent and reduce the onset and progression of the disease.
The above facts suggest that the development of this disease is not only the result of eating meat food contaminated with pathogenic bacteria, but also other dietary factors, such as a sudden change in dietary habits from a diet rich in vegetables to one rich in meat, which changes the intestinal ecology and favors the multiplication of Welchii bacilli; or, if the diet is based on sweet potatoes, the high presence of intestinal trypsin inhibitory factors, which reduces the destruction of B toxin.
Pathology Small intestinal hemorrhage and necrosis due to fibrin-like deposits and embolism in the small arteries of the intestinal wall. The lesions are more common and severe in the jejunum and ileum; sometimes they can also involve the duodenum, colon and stomach; in a few cases, the entire gastrointestinal tract can be involved. The lesions are often segmental and can be confined to one section of the intestine or multiple.
The lesions often begin in the mucosa and show swelling, extensive hemorrhage, and a greenish pseudomembrane covering the top of the folds, but the lesions are clearly demarcated from the normal mucosa. The lesions may extend to the mucosal muscle layer and even involve the plasma membrane. The intestinal wall of the lesion is obviously thickened and hardened, and in severe cases, it may lead to intestinal ulceration and intestinal perforation. Microscopically, the mucosa of the lesion shows necrotic changes of varying depths, from the tip of the villi in mild cases to the entire mucosa in severe cases.
In addition to extensive hemorrhage, the submucosa may also have severe edema and inflammatory cell infiltration. There may be slight hemorrhage in the muscularis and plasma layer. Swelling, fracture, glassy changes and necrosis of the intestinal smooth muscle are seen. The vascular wall is fibrinoid necrotic and may often have thrombosis. The myenteric plexus cells of the intestinal wall may have dystrophic changes.
In addition to intestinal lesions, there may be localized lymph node enlargement and softening of the mesentery, hepatic steatosis, acute splenitis, interstitial pneumonia, pulmonary edema, and in some cases, focal necrosis of the adrenal glands.
Classification
1, gastroenteritis type is seen in the early stage of the disease with abdominal pain, watery stools, low fever, may be accompanied by nausea, vomiting.
2, toxic shock appears with high fever, chills, apathy, drowsiness, delirium, shock and other manifestations, often occurring within 1-5 days of onset.
3, peritonitis type has obvious abdominal pain, nausea and vomiting, abdominal distension and signs of acute peritonitis, necrosis or perforation of the affected intestinal wall, and bloody exudate in the abdominal cavity.
4, intestinal obstruction type has abdominal distension, abdominal pain, vomiting frequently, defecation and exhaustion stop, intestinal sounds disappear, appear bulging intestine.
5, intestinal bleeding type is mainly blood watery or dark red blood stool, the amount can be as much as 1 to 2L, obvious anemia and dehydration.
Clinical manifestations
1, history of the onset of the disease is rapid, before the onset of most of the unclean diet history. Cold, exertion, intestinal roundworm infection and malnutrition are the precipitating factors.
2, abdominal pain starts abruptly, abdominal pain appears suddenly, and it is often the first symptom, mostly around the umbilicus. At the beginning of the disease, it is often manifested as gradually increasing paroxysmal colic around the umbilicus or in the upper middle abdomen, and then gradually turns into continuous pain in the whole abdomen with paroxysmal increase.
3, diarrhea and blood in stool Diarrhea can occur after the onset of abdominal pain. The stool is initially paste-like with fecal matter, and then gradually becomes yellow water-like, followed by white-water-like or adzuki bean soup and jam-like, or even fresh blood-like or dark red blood clots, with little stool and foul smell. There is no urgency. The amount of bleeding is variable. In mild cases, there may be only diarrhea, or only positive fecal occult blood without blood in stool; in severe cases, the amount of bleeding may reach hundreds of milliliters a day. The duration of diarrhea and blood in stool is only 1 to 2 days in short cases, but can be more than a month in long cases, and can be intermittent, or repeatedly multiple episodes. Serious diarrhea can appear dehydration and metabolic acidosis, etc.
4, nausea and vomiting often occur simultaneously with abdominal pain, diarrhea. Vomit can be yellow water-like, coffee-like or blood-like, or vomit bile.
5, systemic symptoms can appear after the onset of general malaise, weakness and fever and other systemic symptoms. The fever is usually 38-39℃, and a few can reach 41-42℃, but the fever mostly subsides in 4-7 days, and it is rare for it to last for more than 2 weeks.
6. There are relatively few abdominal signs. Sometimes there may be abdominal fullness and see intestinal type. There may be obvious pressure pain around the umbilicus and in the upper abdomen. The bowel sounds may be hyperactive in the early stage, and then may diminish or disappear.
Ancillary tests
1.Blood picture of peripheral blood leukocytosis, even up to 40,000/mm3 or more, mainly neutrophilia, often with left shift of the nucleus. Red blood cells and hemoglobin are often reduced.
The stool examination is dark red or bright red in appearance, or the occult blood test is strongly positive, and a large number of red blood cells are seen microscopically, and occasionally detached intestinal mesentery. There may be a small or moderate amount of pus cells.
3.X-ray examination of abdominal plain film can show intestinal paralysis or mild or moderate intestinal dilatation. Barium enema examination can show thickening of the intestinal wall, significant edema, and disappearance of the colonic pouch. In some cases, gas between the intestinal wall can be seen, this sign is caused by partial necrosis of the intestinal wall and colon bacterial invasion; or ulcers or polyp-like lesions and rigidity can be seen. In some cases, intestinal spasm, stricture, and cystic pneumatization of the intestinal wall may also be seen.
Diagnosis
Diagnosis is mainly based on clinical symptoms. Sudden abdominal pain, diarrhea, blood in stool and vomiting with moderate fever, or sudden abdominal pain followed by symptoms of shock should be considered as a possibility of the disease. Abdominal radiographs can help in the diagnosis. The disease needs to be differentiated from toxic bacillary dysentery, allergic purpura, acute Crohn’s disease, strangulated intestinal obstruction, intussusception, amoebic enteropathy, and intestinal polyposis.
Treatment
The treatment of this disease is based on non-surgical therapy, strengthening systemic support therapy, correcting water-electrolyte imbalance, relieving toxic symptoms, and actively preventing toxic shock and other complications. Surgical treatment should be given only when necessary.
1.Non-surgical treatment
(1) General treatment: rest and fasting, complete bed rest and fasting during abdominal pain, blood in stool and fever. Until vomiting stops, blood in stool is reduced and abdominal pain is relieved, a liquid diet can be introduced, and the amount is gradually increased later. Highly nutritious fluids such as 10% glucose, compound amino acids and hydrolyzed protein should be given intravenously during the fasting period. Premature feeding may lead to relapse of the disease, but late resumption of feeding may affect the nutritional status and delay recovery. Gastrointestinal decompression may be given for severe abdominal distension and vomiting. Antispasmodics may be given for abdominal pain.
(2) Correction of water-electrolyte disorders Water loss, sodium loss and potassium loss are more common in this disease. The total amount and composition of the infusion can be determined according to the condition. The daily rehydration amount is about 80-100ml/kg for children and 2000-3000ml/d for adults, of which 5%-10% glucose solution accounts for about 2/3-3/4, saline accounts for about 1/3-1/4, and appropriate amount of potassium chloride is added.
(3) Anti-shock rapid replenishment of effective circulating blood volume. In addition to supplemental crystal solution, plasma, fresh whole blood or human serum albumin and other colloidal fluids should be appropriately transfused. Those whose blood pressure does not rise can be treated with vasoactive drugs, such as α-blockers, β-agonists or scopolamine, etc. can be used as appropriate.
(4) Antibiotics to control intestinal infection can alleviate clinical symptoms. Commonly used antibiotics include: aminobenzyl penicillin (4-8g/d), chloramphenicol (2g/d), gentamicin (16-24 million u/d), kanamycin (1g/d), sulforaphane (6.0g/d), fudaxin 4g/d or polymyxin and cephalosporin, etc., generally choose two kinds of combined application.
(5) Adrenocorticotropic hormone can reduce the symptoms of poisoning, inhibit allergic reactions, and help to correct shock, but there is a risk of aggravating intestinal bleeding and promoting the development of intestinal perforation. The general application does not exceed 3-5 days; children use hydrocortisone 4-8mg/kg/day or dexamethasone 1-2.5mg/d; adults use hydrocortisone 200-300mg/d or dexamethasone 5-20mg/d, both by intravenous drip.
(6) Symptomatic therapy can be given to those with severe abdominal pain; those with high fever and irritability can be given oxygen, antipyretics, sedatives or physical cooling.
(7) Anti-venom is used for Welchii bacillus anti-venom 42,000~85,000u intravenous drip, which has good efficacy.
2.Surgical treatment: The following cases can be considered for surgical treatment.
① intestinal perforation.
②severe intestinal necrosis with purulent or bloody exudate in the abdominal cavity.
(iii) repeated massive intestinal bleeding, complicated by hemorrhagic shock.
④ intestinal obstruction, intestinal paralysis.
⑤ other urgent surgical treatment of acute abdominal disease cannot be excluded.
Surgical methods.
①In cases without necrosis or perforation in the intestinal canal, procaine mesenteric closure can be given to improve the blood circulation of the lesioned segment;
②Severe and limited lesions can be resected and anastomosed;
(3) In cases of intestinal necrosis or intestinal perforation, intestinal segment resection, perforation repair or intestinal external placement can be performed.