Acute necrotizing enteritis is a sudden-onset acute inflammation of the small intestine, characterized by extensive hemorrhage, hence also referred to as acute hemorrhagic enteritis. Children of all ages can be affected, with the majority being school-aged children, particularly those between 4 and 10 years old. The incidence is higher in spring and summer (neonatal necrotizing enterocolitis is discussed separately in another section). Over the past decade, the incidence of this disease has significantly declined.

bubble_chart Etiology

The exact cause is not fully understood, but it appears to be related to nonspecific intestinal infections and allergic reactions in the body. Stool cultures often show no pathogenic bacteria, though sometimes gas-forming spore-bearing bacilli and disease-causing large intestine bacilli may be isolated.

bubble_chart Pathological Changes

The typical pathological changes of necrotizing small intestine inflammation are necrotizing inflammatory alterations. Starting from the submucosal layer, as the lesion expands, it can extend to the muscular layer and mucosal layer, causing widespread congestion, edema, and even ulcer perforation in multiple areas of the intestinal wall, leading to peritonitis. Lesions are commonly found in the distal jejunum and proximal ileum, and in severe cases, the entire small intestine may be affected. Generally, the lesions are scattered and segmentally arranged, with some involving 1-2 segments or more, each varying in length—ranging from as short as over 10 cm to as long as 100 cm—with clear boundaries. The affected intestinal wall thickens, becomes brittle, loses elasticity, and dilates. In severe cases, the serosal surface appears rough with fibrin deposits, and the intestinal lumen is filled with jam-like bloody stool. Microscopically, inflammatory cell infiltration is observed in all layers of the affected intestinal wall, predominantly lymphocytes, eosinophils, monocytes, and plasma cells. The mucosa may undergo necrosis or sloughing, with extensive hemorrhage, necrosis, and edema in the submucosal layer, along with dilated and congested capillaries. The peritoneal cavity may contain turbid, purulent, or bloody exudate. After recovery, chronic granulomatous changes are not left behind, and intraperitoneal adhesions are rare.

Generally, there are no prodromal symptoms, and the onset is sudden. The main manifestations include abdominal distension and fullness, abdominal pain, vomiting, diarrhea, hematochezia, and fever. Many children develop severe toxic symptoms, even shock, within 1–2 days. The abdominal pain is persistent, accompanied by paroxysmal exacerbations. It is often generalized but can also be localized to the affected area. Vomiting and diarrhea appear shortly after onset. Initially, the stool is watery with mucus, later turning into hematochezia. Some children do not experience diarrhea; hematochezia begins 1–2 days after the onset of abdominal pain. The amount of hematochezia varies, with large amounts appearing dark red, accompanied by a foul, fishy odor, resembling meat-washing water or red fruit jam. Some children develop hematochezia within hours of onset. Fever is around 38°C; in severe cases, the temperature may rise above 39–49°C or fall below normal. Symptoms in infants and young children are often atypical, with pronounced dehydration and acidosis. Some may exhibit extraintestinal symptoms such as jaundice, cough, wheezing, hepatosplenomegaly, and convulsions.

Due to varying degrees of pathological changes in the intestinal wall layers, clinical symptoms can range from mild to severe, manifesting in the following types:

1. Diarrhea-hematochezia type: Primarily characterized by mucous membrane exudation and sexually transmitted disease-like changes, with a soft abdomen and no tenderness. Conservative medical treatment is recommended.
2. Intestinal obstruction type: Severe damage and swelling of the intestinal muscle layer lead to rigid intestines and loss of peristalsis, presenting with mechanical intestinal obstruction symptoms.
3. Peritonitis type: Massive inflammatory cell infiltration and exudation in the serous layer result in a large amount of inflammatory effusion in the abdominal cavity, or bloody fluid due to necrosis. Clinical manifestations resemble peritonitis symptoms.
4. Toxic shock type: Children with this type exhibit severe systemic toxic symptoms, including early-onset pallor, lethargy, weakness, cold extremities, weak pulse, low blood pressure (or even unmeasurable), red tongue texture with slight dark purple hue, and yellow, greasy tongue coating. Sometimes accompanied by minor hematochezia, dehydration, and electrolyte imbalance. The abdomen is slightly distended and tense, often suspected as strangulated intestinal obstruction.

bubble_chart Diagnosis

When a child suddenly presents with abdominal pain, vomiting, diarrhea, hematochezia accompanied by high fever and toxic symptoms, the possibility of this disease should be considered. X-ray examination aids in diagnosis, with abdominal plain films showing small intestine gas accumulation, rigid intestinal contours, thickened intestinal walls, blurred outlines, coarse mucosal folds, and widened intestinal spaces. Some cases may exhibit intestinal wall pneumatosis and portal venous gas.

bubble_chart Treatment Measures

Generally, non-surgical treatments and symptomatic management are adopted.

1. Fasting: During episodes of bloody stools and abdominal distension and fullness, fasting is necessary. If required, a nasogastric tube can be inserted into the duodenum for gastrointestinal decompression. Once bloody stools and abdominal distension and fullness subside, and the fecal occult blood test turns negative, gradual resumption of diet can begin. Premature oral intake may lead to symptom recurrence.
2. Treatment of toxic shock: Early detection and prompt intervention for shock are crucial. Initial measures should focus on rapid blood volume replenishment and improving tissue hypoxia, primarily using low-molecular-weight dextran, 654-2 injections, and artificial hibernation therapy.
3. Correction of dehydration and electrolyte imbalance: Severe cases often exhibit significant water and electrolyte imbalances, with hyponatremia and hypokalemia being common. Due to prolonged fasting, precise calculation of intake and output, as well as caloric needs, is essential. Maintenance fluids based on the child's age should be provided, along with correction of cumulative and ongoing losses. Small, frequent blood transfusions may be necessary. Parenteral nutrition should be considered if required.
4. Other therapies: Appropriate antibiotics should be selected to control and prevent secondary infections. Hemostatic and analgesic medications can also be used concurrently. Since this condition may be related to allergic reactions, adrenal corticosteroids can yield certain therapeutic effects. During the acute phase, hydrocortisone 5–10 mg/kg/day can be administered intravenously, switching to prednisone 1–2 mg/kg/day orally after improvement. Some practitioners do not advocate corticosteroid therapy and instead recommend scopolamine 0.03–0.05 mg/kg/day intravenously for 3–7 days, followed by oral administration for 3–5 days after symptom control. Others have tried the antiallergic drug sodium cromoglicate (capsules) 5–10 mg/dose, four times daily for 3–7 days, with some efficacy.
5. Chinese medicinals, acupuncture, and moxibustion therapy: Bloody stools and abdominal distension and fullness can be treated with Chinese medicinals, focusing on clearing heat and removing toxin, cooling blood and nourishing yin, supplemented by invigorating blood and resolving stasis. For abdominal pain, acupuncture can be applied to points such as Zusanli (ST36), Yanglingquan (GB34), Tianshu (ST25), and Hegu (LI4).
6. Surgical therapy: If symptoms of intestinal obstruction are evident, or if peritonitis, intestinal necrosis, or perforation is suspected, or if X-ray examination reveals atonic intestinal dilation, blurred and rough contours, or significant peritoneal effusion, emergency surgical intervention should be considered. Surgical methods may include resection and anastomosis, decompression and stoma creation, or peritoneal drainage, depending on the extent of intestinal involvement.

bubble_chart Prognosis

For mild cases, timely symptomatic treatment usually leads to gradual recovery within 7 to 14 days. In severe cases where toxic shock, intestinal perforation, and peritonitis occur, active rescue measures, including surgical exploration, are necessary. If the critical phase is overcome, shock symptoms typically disappear within 2 to 5 days, abdominal distension and fullness gradually subside, and bloody stools cease. The mortality rate for such patients is very high. The disease generally does not become chronic after recovery.

bubble_chart Differentiation

1. Bacterial dysentery: Characterized by purulent and bloody stools, excessive mucus, frequent bowel movements, tenesmus, and dysentery bacilli can be detected in stool culture.
2. Toxic dyspepsia: Occurs in infancy, with gradual rather than acute onset, no bloody stools, and disease-causing bacilli of the large intestine can be found in stool culture.
3. Abdominal allergic purpura: Presents with recurrent bleeding and skin purpura, without diarrhea.
4. Acute intussusception: More common in infants and young children, a palpable abdominal mass can be felt, and barium or air enema can confirm the diagnosis and perform reduction.
5. Strangulated mechanical intestinal obstruction: A complete intestinal obstruction, with upright abdominal X-ray showing high-tension intestinal gas-fluid levels and absence of gas in the colon, differing from the X-ray signs of enteritis.