| disease | Acute Necrotizing Enteritis |
| alias | Acute Hemorrhagic Enteritis, Nonspecific Enteritis |
Acute necrotizing enteritis has a sudden onset and is an acute inflammation of the small intestine. Due to extensive bleeding, it is also known as acute hemorrhagic enteritis. Children of all ages can be affected, but it is most common in school-aged children, with the majority of cases occurring between 4 and 10 years old. The incidence is higher in spring and summer (neonatal necrotizing enterocolitis is discussed in a separate section). Over the past decade, the incidence of this disease has significantly decreased.
bubble_chart Etiology
The exact cause is not fully understood, but it appears to be related to non-specific intestinal infections and allergic reactions in the body. Stool cultures often show no pathogenic bacteria, but occasionally gas-producing spore-forming bacilli and other disease-causing bacteria of the large intestine may be cultured.
bubble_chart Pathological Changes
The typical pathological changes of necrotizing small intestine inflammation are characterized by 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 and edema throughout the intestinal wall, and even ulcer perforation leading to peritonitis. The lesions are commonly found in the lower segment of the jejunum and the upper segment of the ileum, and in severe cases, the entire small intestine can be affected. Generally, the lesions are scattered and segmentally arranged, with some involving 1-2 segments or more, each varying in length from as short as over 10 cm to as long as 100 cm, with clear boundaries. The affected intestinal wall thickens, becomes brittle and loses elasticity, and may dilate. In severe cases, the serosal surface becomes 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 intestinal wall, predominantly lymphocytes, eosinophils, monocytes, and plasma cells. The mucosa may undergo necrosis or detachment, with extensive hemorrhage, necrosis, and edema in the submucosal layer, and capillary dilation and congestion. The abdominal cavity may contain turbid, purulent, or bloody exudate. After recovery, chronic granulomatous changes are not left behind, and intra-abdominal adhesions are rare.
bubble_chart Clinical ManifestationsThe onset is usually sudden without precursor symptoms. The main manifestations include abdominal distension and fullness, abdominal pain, vomiting, diarrhea, bloody stools, and fever. Many children develop severe toxic symptoms, even shock, within 1 to 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 the onset. Initially, the stool is watery with mucus, then turns into bloody stools. Some children do not have diarrhea, and hematochezia begins 1 to 2 days after the onset of abdominal pain. The amount of hematochezia varies; large amounts are dark red with a foul, fishy odor, resembling meat wash or red jam. Some children develop bloody stools within hours of onset. Fever is around 38°C, and in severe cases, the temperature can rise above 39-49°C or fall below normal. Symptoms in infants and young children are often atypical, with marked dehydration and acidosis. Some may present with extraintestinal symptoms such as jaundice, cough, hepatosplenomegaly, and convulsions.
Due to varying degrees of pathology in different layers of the intestinal wall, clinical symptoms can range from mild to severe, presenting as the following types:
1. Diarrhea and hematochezia type: Mainly characterized by mucosal exudation and sexually transmitted disease changes, with a soft abdomen and no tenderness. Conservative medical treatment is recommended.
2. Intestinal obstruction type: Severe damage to the intestinal muscle layer causes swelling, rigidity, and loss of peristalsis, leading to symptoms of mechanical intestinal obstruction.
3. Peritonitis type: Significant inflammatory cell infiltration and exudation in the serosal layer, with a large amount of inflammatory exudate in the abdominal cavity, or bloody fluid due to necrosis. Clinical manifestations include peritonitis symptoms.
4. Toxic shock type: This type presents with severe systemic toxic symptoms, including early onset of pale complexion, lethargy, weakness, cold extremities, weak pulse, low blood pressure, or even unmeasurable blood pressure. The tongue texture is red with a slightly dark purple hue, and the tongue coating is yellow and greasy. Sometimes accompanied by a small amount of bloody stools, dehydration, and electrolyte imbalance. The abdomen is slightly distended and tense, often suspected as strangulated intestinal obstruction.
bubble_chart Auxiliary Examination
Increased white blood cells with a left shift. Platelets are slightly low. Coagulation time is normal, and prothrombin time is mostly prolonged. In early cases without diarrhea, stool occult blood tests are positive. Stool bacterial tests are generally negative.
When a child suddenly experiences 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, thickened mucosal folds, and widened intestinal spaces. Some cases may also show intestinal wall pneumatosis and portal venous gas.
bubble_chart Treatment Measures
Generally, non-surgical treatments and symptomatic management are adopted.
(2) Rescuing toxic shock: Early detection and timely rescue of shock are crucial. Initially, rapid replenishment of blood volume and improvement of tissue hypoxia should be prioritized, using a rescue protocol primarily consisting of low molecular weight dextran, 654-2 injections, and artificial hibernation therapy.
(3) Correcting dehydration and electrolyte imbalance: Severe cases often exhibit significant water and electrolyte imbalances, with hyponatremia and hypokalemia being common. Due to prolonged fasting, it is essential to accurately calculate intake and output volumes and caloric needs, providing the physiological maintenance requirements based on the child's age, and supplementing cumulative and ongoing losses. Small, frequent blood transfusions may be necessary. Parenteral intravenous nutrition should be administered 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 the disease may be related to allergic reactions, the use of adrenal corticosteroids can yield certain therapeutic effects. During the critical phase, hydrocortisone 5-10 mg/kg/day can be administered intravenously, switching to prednisone 1-2 mg/kg/day orally after improvement. Some do not advocate for hormone therapy, instead using scopolamine 0.03-0.05 mg/kg/day intravenously for 3-7 days, switching to oral administration for 3-5 days after symptom control. Some have tried using the antiallergic drug sodium cromoglicate (capsules) 5-10 mg per dose, four times daily, for 3-7 consecutive 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 toxins, cooling blood and nourishing yin, supplemented by invigorating blood and resolving stasis. Abdominal pain can be treated by acupuncture at points such as Zusanli, Yanglingquan, Tianshu, and Hegu.
(6) Surgical therapy: If symptoms of intestinal obstruction are evident, or if peritonitis, intestinal necrosis, or perforation is suspected, or if X-ray examinations show intestinal dilation without tension, blurred and rough contours, and significant peritoneal effusion, emergency surgical treatment should be considered. Surgical methods can be selected based on the extent of intestinal lesions, including resection and anastomosis, decompression and stoma creation, and peritoneal drainage.
Patients with mild conditions, if treated promptly with symptomatic therapy, usually recover gradually 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 period is overcome, shock symptoms typically disappear within 2 to 5 days, abdominal distension and fullness gradually subside, and bloody stools also disappear. The mortality rate for such children is very high. After recovery, the disease generally does not progress to a chronic condition.
1. Bacillary Dysentery: Characterized by purulent and bloody stools, excessive mucus, frequent bowel movements, tenesmus, and dysentery bacilli can be found in stool culture.
2. Toxic Dyspepsia: Occurs in infancy, with a gradual rather than acute onset, no bloody stools, and bacilli of the nature of disease large intestine can be found in stool culture.
3. Abdominal Allergic Purpura: Features recurrent bleeding and skin purpura, without diarrhea.
4. Acute Intussusception: More common in infants and young children, a mass can be palpated in the abdomen, and barium or air enema can confirm the diagnosis and achieve reduction.
5. Strangulated Mechanical Intestinal Obstruction: Presents as complete intestinal obstruction, with X-ray upright plain film showing high-tension intestinal gas-fluid levels and absence of gas in the colon, differing from the X-ray signs of enteritis. {|104|}
