Acute hemorrhagic necrotizing enteritis is an acute enteritis associated with infection by Clostridium perfringens type C. The disease primarily affects the small intestine, with pathological changes characterized by intestinal wall hemorrhage and necrosis. Its main clinical manifestations include abdominal pain, hematochezia, fever, vomiting, and abdominal distension and fullness. In severe cases, toxic symptoms such as shock and intestinal paralysis, as well as complications like intestinal perforation, may occur.

bubble_chart Epidemiology

The disease has experienced two major outbreaks: one occurred in Germany after World War II, and another in Papua New Guinea in the 1960s, both caused by consuming undercooked or spoiled meat. Apart from these two large outbreaks, the disease has been sporadic. It has been reported in countries such as Papua New Guinea, Uganda, Thailand, India, Singapore, and Sri Lanka. In China, cases have been documented in provinces including Sichuan, Yunnan, Guizhou, Hubei, Jiangsu, Zhejiang, Jiangxi, and Shandong, with the highest number of reported cases in Liaoning and Guangdong provinces. The incidence in rural areas is significantly higher than in urban areas. The disease can occur year-round but is most prevalent in summer and autumn. Children and adolescents are more commonly affected than adults. Among 733 cases reported in Guangdong and Liaoning, 463 were male and 270 were female, with a male-to-female ratio of 1.7:1. The age distribution ranged from 18 to 82 years, with those under 15 accounting for 60.5%.

bubble_chart Etiology

The disease cause of this illness has not yet been fully elucidated. It is currently believed that the onset of the disease is associated with infection by Welchii bacillus (Clostridium perfringens type C), which produces toxin B. Toxin B can cause necrosis of intestinal tissue, leading to necrotizing enteritis.

In the highland regions of Papua New Guinea, where the incidence of this disease is notably high, studies have found that the concentration of proteases in the intestinal lumen of local residents is low. This is related to a low-protein diet and the heat-stable trypsin inhibitors present in sweet potatoes, which are a staple food in the area. In animal experiments, administering Welchii bacillus solution via gastric tube did not cause illness in the animals. However, when raw sweet potato flour or raw soybean flour containing trypsin inhibitors was simultaneously administered, the animals became ill and exhibited histopathological changes identical to those of acute hemorrhagic necrotizing enteritis. Animal experiments also demonstrated that dog pancreatic extract containing trypsin could prevent and mitigate the occurrence and progression of this disease. The above evidence suggests that, in addition to consuming meat contaminated with pathogenic bacteria, other dietary factors contribute to the onset of this illness. For example, sudden changes in dietary habits may favor the proliferation of Welchii bacillus, or a diet predominantly based on sweet potatoes may lead to a high presence of trypsin inhibitors in the intestines, reducing the degradation of toxin B.

The main pathological changes of this disease are caused by fibrinoid deposition and embolism in the small blood vessels of the intestinal wall, leading to hemorrhage and necrosis of the small intestine. The lesions are most common and severe in the jejunum and ileum; sometimes they may also involve the duodenum, colon, and stomach; in a few cases, the entire gastrointestinal tract may be affected. The lesions often appear segmental, either confined to one section of the intestine or occurring as multiple foci. The lesions typically originate in the mucosa, manifesting as swelling and extensive hemorrhage, with the folds covered by a dirty green pseudomembrane, but the boundary between the lesions and normal mucosa remains clear. The lesions may extend to the muscularis mucosa and even involve the serosa. The affected intestinal wall becomes significantly thickened and hardened, and in severe cases, it may lead to intestinal ulcers and perforation. Microscopically, the affected mucosa shows varying degrees of necrotic changes, ranging from mild involvement limited to the tips of the villi to severe cases affecting the entire mucosal layer. In addition to extensive hemorrhage in the submucosa, there may also be severe edema and inflammatory cell infiltration. The muscularis and serosa layers may exhibit minor hemorrhage. Intestinal smooth muscle may appear swollen, fragmented, hyalinized, and necrotic. The blood vessel walls may show fibrinoid necrosis and often exhibit thrombosis. The neurons of the intestinal myenteric plexus may display dystrophic changes.

In addition to intestinal lesions, there may also be localized lymph node enlargement and softening in the mesentery; hepatic fatty degeneration, acute splenitis, interstitial pneumonia, and pulmonary edema; in rare cases, focal necrosis of the adrenal glands may also occur.

bubble_chart Type

1. Gastroenteritis type: Seen in the early stage of the disease with abdominal pain, watery stools, low-grade fever, and may be accompanied by nausea and vomiting.
2. Toxic shock: Manifested by high fever, shivering, mental apathy, drowsiness, delirious speech, shock, etc., usually occurring within 1-5 days of onset.
3. Peritonitis type: Presents with significant abdominal pain, nausea and vomiting, abdominal distension and fullness, and signs of acute peritonitis. The affected intestinal wall may become necrotic or perforated, with bloody effusion in the abdominal cavity.
4. Intestinal obstruction type: Characterized by abdominal distension and fullness, abdominal pain, frequent vomiting, cessation of defecation and flatus, disappearance of borborygmi, and development of tympanites.
5. Intestinal hemorrhage type: Mainly presents with bloody watery or dark red bloody stools, with a volume that may reach 1-2 liters, accompanied by significant anemia and dehydration.

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bubble_chart Clinical Manifestations

1. Medical history: The onset is acute, often with a history of unclean diet before the illness. Cold exposure, fatigue, intestinal ascariasis infection, and malnutrition are predisposing factors.
2. Abdominal pain: The onset is sudden, with abrupt abdominal pain, often the first symptom, mostly around the umbilicus. Initially, it often manifests as gradually worsening paroxysmal colicky pain around the umbilicus or in the mid-upper abdomen, which later progresses to persistent pain throughout the abdomen with paroxysmal exacerbations.
3. Diarrhea hematochezia: Diarrhea may occur immediately after the onset of abdominal pain. Initially, the stool is pasty with fecal matter, then gradually becomes watery yellow, followed by clear watery or red bean soup and jam-like, and may even appear bright red or dark red blood clots. The stool is scant and foul-smelling. There is no tenesmus. The amount of bleeding varies; mild cases may only have diarrhea or merely occult blood in the stool without hematochezia, while severe cases may lose several hundred milliliters of blood per day. The duration of diarrhea and hematochezia can be as short as 1–2 days or as long as over a month, and may present as intermittent or recurrent episodes. Severe diarrhea can lead to dehydration and metabolic acidosis.
4. Nausea vomiting: Often occurs simultaneously with abdominal pain and diarrhea. Vomitus may be watery yellow, coffee bean-like, bloody, or contain bile.
5. Systemic symptoms: General discomfort, weakness, and fever may appear shortly after onset. Fever is usually between 38–39°C, with a few cases reaching 41–42°C, but it typically subsides gradually within 4–7 days, rarely persisting beyond two weeks.
6. Abdominal signs: Relatively few. There may sometimes be abdominal distension and visible intestinal loops. Tenderness may be pronounced around the umbilicus and upper abdomen. Early borborygmi may be hyperactive but later weaken or disappear.

bubble_chart Auxiliary Examination

1. Blood picture: Peripheral blood leukocytosis, even up to 40,000/mm³ or more, predominantly neutrophilic, often with a left shift. Red blood cells and hemoglobin are often decreased.
2. Stool examination: Appearance is dark red or bright red, or occult blood test is strongly positive. Microscopy reveals a large number of red blood cells, occasionally with detached mesenteric membrane. A small or moderate amount of pus cells may be present.
3. X-ray examination: Abdominal plain films may show intestinal paralysis or mild to grade II intestinal dilatation. Barium enema examination may reveal thickened intestinal walls, significant edema, and disappearance of haustra. In some cases, gas between the intestinal walls may be observed, a sign caused by partial intestinal wall necrosis and bacterial invasion of the colon; or ulcers or polypoid lesions and rigidity may be seen. Some cases may also exhibit intestinal spasms, stenosis, and pneumatosis cystoides intestinalis.

bubble_chart Diagnosis

The diagnosis is primarily based on clinical symptoms. Sudden abdominal pain, diarrhea, hematochezia, and vomiting accompanied by moderate fever, or sudden abdominal pain followed by shock symptoms, should raise suspicion of this disease. Abdominal X-ray plain films aid in diagnosis.

This condition needs to be differentiated from toxic dysentery, allergic purpura, acute Crohn's disease, strangulated intestinal obstruction, intussusception, amoebic intestinal disease, and intestinal tumors.

bubble_chart Treatment Measures

The treatment of this disease is mainly non-surgical therapy, with emphasis on strengthening systemic supportive therapy, correcting typical edema electrolyte imbalances, relieving toxic symptoms, and actively preventing and treating toxic shock and other complications. Surgical treatment is only considered when necessary.

(1) Non-surgical treatment

1. General treatment: Rest and fasting. During periods of abdominal pain, hematochezia, and fever, complete bed rest and fasting are required. Only when vomiting stops, hematochezia decreases, and abdominal pain alleviates can a liquid diet be introduced, gradually increasing the amount. During fasting, intravenous infusion of high-nutrient solutions such as 10% glucose, compound formula amino acids, and hydrolyzed protein should be administered. Premature ingestion of food may lead to disease recurrence, while delayed resumption of eating may affect nutritional status and delay recovery. For severe abdominal distension and fullness and vomiting, gastrointestinal decompression may be performed. Antispasmodics can be given for abdominal pain.
2. Correct typical edema electrolyte imbalances: Dehydration, sodium loss, and potassium loss are common in this disease. The total volume and composition of fluid replacement can be determined based on the condition. For children, the daily fluid replacement is about 80–100 ml/kg, and for adults, 2000–3000 ml/day, of which 5–10% glucose solution accounts for about 2/3–3/4, and normal saline accounts for about 1/3–1/4, with an appropriate amount of potassium chloride added.
3. Anti-shock: Rapidly replenish effective circulating blood volume. In addition to crystalloid solutions, plasma, fresh whole blood, or human serum albumin should be appropriately administered. For patients with unresponsive blood pressure, vasoactive drugs such as α-receptor blockers, β-receptor agonists, or tangut anisodus alkaloids can be selected as needed.
4. Antibiotics: Controlling intestinal infections can alleviate clinical symptoms. Commonly used antibiotics include ampicillin (4–8 g/day), chloramphenicol (2 g/day), gentamicin (160,000–240,000 units/day), kanamycin (1 g/day), sulbactam/ampicillin (6.0 g/day), ceftazidime (4 g/day), or polymyxin and cephalosporins, usually administered in combination of two drugs.
5. Adrenocortical hormones: These can alleviate toxic symptoms, suppress allergic reactions, and help correct shock, but they carry the risk of aggravating intestinal bleeding and inducing intestinal perforation. Generally, they should not be used for more than 3–5 days. For children, hydrocortisone is administered at 4–8 mg/kg/day or dexamethasone at 1–2.5 mg/day; for adults, hydrocortisone is given at 200–300 mg/day or dexamethasone at 5–20 mg/day, all via intravenous drip.
6. Symptomatic treatment: Severe abdominal pain may be treated with pethidine; for high fever and dysphoria, oxygen therapy, antipyretics, sedatives, or physical cooling may be administered.
7. Antitoxin serum: Intravenous drip of Welchii bacillus antitoxin serum (42,000–85,000 units) has shown good efficacy.

(2) Surgical treatment

The following conditions may warrant surgical intervention:

1. Intestinal perforation;
2. Severe intestinal necrosis with purulent or bloody effusion in the abdominal cavity;
3. Repeated massive intestinal hemorrhage complicated by hemorrhagic shock;
4. Intestinal obstruction or paralysis.
5. Other acute abdominal conditions requiring urgent surgical treatment cannot be ruled out.

Surgical methods:

1. For cases without intestinal necrosis or perforation, procaine mesenteric block can be performed to improve blood circulation in the affected segment;
2. For severe but localized lesions, segmental resection and anastomosis may be performed;
3. For intestinal necrosis or perforation, segmental resection, perforation repair, or intestinal exteriorization may be performed.