bubble_chart Overview

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. Severe cases may present with toxic symptoms such as shock and intestinal paralysis, as well as complications like intestinal perforation.

bubble_chart Epidemiology

The disease has experienced two major outbreaks: one occurred in Germany after World War II, and another in the 1960s in Papua New Guinea, both caused by consuming undercooked or spoiled meat. Apart from these two major outbreaks, the disease has been sporadic. Cases have been reported in countries such as Papua New Guinea, Uganda, Thailand, India, Singapore, and Sri Lanka. In China, reports have come from provinces including Sichuan, Yunnan, Guizhou, Hubei, Jiangsu, Zhejiang, Jiangxi, and Shandong, with the highest number of cases documented 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 particularly 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% of cases.

bubble_chart Etiology

The disease cause of this illness has not yet been fully elucidated. It is currently believed that the onset of this disease is associated with infection by Welchii bacillus (type C Clostridium perfringens) producing B toxin, which 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 local population has low concentrations of proteases in their intestinal cavity. This is related to a low-protein diet and the heat-stable trypsin inhibitors present in sweet potatoes, a staple food in the area. In animal experiments, infusing Welchii bacillus solution via gastric tube did not cause illness in the animals; however, when raw sweet potato powder or raw soybean powder containing trypsin inhibitors was simultaneously infused, 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 findings suggest 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 destruction of B toxin.

bubble_chart Pathological Changes

The main pathological changes of this disease are characterized by fibrinoid deposition and embolism in the small stirred pulse of the intestinal wall, leading to small intestine hemorrhage and necrosis. The lesions predominantly and severely affect the jejunum and ileum; occasionally, the duodenum, colon, and stomach may also be involved; in rare cases, the entire gastrointestinal tract can be affected. The lesions often appear segmental, either confined to a single segment of the intestine or presenting as multiple foci. The lesions typically originate in the mucous membrane, manifesting as swelling and extensive hemorrhage, with the folds covered by a dirty green pseudomembrane, yet the boundary between the lesions and normal mucous membrane remains distinct. The lesions may extend to the muscular layer of the mucous membrane or even involve the serous membrane. The affected intestinal wall becomes significantly thickened and hardened, and in severe cases, intestinal ulcers and perforation may occur. Microscopically, the affected mucous membrane exhibits varying degrees of necrotic changes, ranging from superficial involvement at the villous tips to full-thickness necrosis of the mucous membrane. The submucosal layer shows extensive hemorrhage, along with severe edema and inflammatory cell infiltration. The muscular and serous layers may exhibit mild hemorrhage. Intestinal smooth muscle may display swelling, fragmentation, hyaline degeneration, and necrosis. The vascular walls exhibit fibrinoid necrosis and often show thrombus formation. The ganglion cells of the intestinal myenteric plexus may exhibit dystrophic changes.

In addition to intestinal lesions, localized lymphadenopathy and softening of the mesenteric membrane may occur, along with hepatic steatosis, acute splenitis, interstitial pneumonia, and pulmonary edema; in some cases, focal necrosis of the adrenal glands may also be observed.

bubble_chart Clinical Manifestations

1. Medical history The onset is acute, often preceded by a history of unclean diet. Cold exposure, fatigue, intestinal ascariasis infection, and malnutrition are predisposing factors.

2. Abdominal pain The onset is sudden, with abrupt abdominal pain, which can also often be the first symptom, mostly around the umbilicus. Initially, it often manifests as gradually worsening paroxysmal colicky pain around the umbilicus or in the upper-middle abdomen, which later progresses to persistent pain throughout the abdomen with paroxysmal exacerbations.

3. Diarrhea and hematochezia Diarrhea may occur immediately after the onset of abdominal pain. Initially, the stool is pasty with fecal matter, then gradually turns watery yellow, followed by clear water-like or red bean soup and jam-like consistency, and may even appear as bright red or dark red blood clots. The stool is scanty and foul-smelling. There is no tenesmus. The amount of bleeding varies; mild cases may only have diarrhea or 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 it may occur intermittently or recur multiple times. Severe diarrhea can lead to dehydration and metabolic acidosis.

4. Nausea and vomiting These often occur simultaneously with abdominal pain and diarrhea. Vomitus may be yellow-watery, coffee-ground-like, bloody, or contain bile.

5. Systemic symptoms General discomfort, weakness, and fever may appear soon after onset. Fever typically ranges between 38–39°C, with a few cases reaching 41–42°C, but it usually subsides gradually within 4–7 days, and persistence beyond two weeks is rare.

6. Abdominal signs Relatively few. Sometimes, abdominal distension or visible intestinal loops may be observed. There may be significant tenderness around the umbilicus and upper abdomen. Early hyperactive bowel sounds may later weaken or disappear.

Clinical types

1. Gastroenteritis type Seen in the early stages of the disease, with abdominal pain, watery stools, low-grade fever, and possibly nausea and vomiting.

2. Toxic shock type Presents with high fever, chills, apathy, drowsiness, delirium, and shock, usually occurring within 1–5 days of onset.

3. Peritonitis type Features significant abdominal pain, nausea, vomiting, abdominal distension and fullness, and signs of acute peritonitis due to necrotic or perforated intestinal walls, 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, absent bowel sounds, and tympanites.

5. Intestinal hemorrhage type Dominated by bloody or dark red stools, with volumes up to 1–2L, accompanied by significant anemia and dehydration. {|111|}

bubble_chart Auxiliary Examination

1. Blood Picture Peripheral blood leukocytosis, even as high as 40,000/mm³ or more, with a predominance of neutrophilic granulocytes, often showing a left shift. Red blood cells and hemoglobin are often decreased.

2. Stool Examination The appearance is dark red or bright red, or the occult blood test is strongly positive. Microscopic examination 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 Plain abdominal 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 invasion by colonic bacteria; 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 the sudden onset of abdominal pain followed by shock symptoms, should raise suspicion of this disease. Abdominal X-ray plain films aid in the 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 thereafter. During fasting, intravenous infusion of high-nutrition solutions such as 10% glucose, compound formula amino acids, and hydrolyzed protein should be administered. Premature eating may lead to disease recurrence, but 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 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 and other colloid solutions should be appropriately transfused. 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, etc. Generally, two types are combined.

5. Adrenocortical hormones: These can alleviate toxic symptoms, suppress allergic reactions, and help correct shock, but they carry the risk of exacerbating intestinal bleeding and promoting intestinal perforation. Generally, they should not be used for more than 3–5 days. For children, hydrocortisone is used at 4–8 mg/kg/day or dexamethasone at 1–2.5 mg/day; for adults, hydrocortisone is used at 200–300 mg/day or dexamethasone at 5–20 mg/day, all administered intravenously.

6. Symptomatic treatment: For severe abdominal pain, pethidine can be given; for high fever and dysphoria, oxygen therapy, antipyretics, sedatives, or physical cooling can be administered.

7. Antitoxin serum: Intravenous infusion of Welchii bacillus antitoxin serum (42,000–85,000 units) has shown good efficacy.

(2) Surgical treatment

The following conditions may warrant surgical treatment: ① Intestinal perforation; ② Severe intestinal necrosis with purulent or bloody effusion in the abdominal cavity; ③ Repeated massive intestinal bleeding complicated by hemorrhagic shock; ④ Intestinal obstruction or paralysis; ⑤ Other acute abdominal conditions requiring urgent surgical intervention cannot be ruled out. Surgical methods include: ① For intestines without necrosis or perforation, procaine mesenteric block can be performed to improve blood circulation in the affected segment; ② For severe and localized lesions, segmental resection and anastomosis can be performed; ③ For intestinal necrosis or perforation, segmental resection, perforation repair, or intestinal exteriorization can be performed.