Acute Hemorrhagic Necrotizing Enteritis

Acute hemorrhagic necrotizing enteritis is an acute intestinal phlegmon characterized by extensive hemorrhage and necrosis of the small intestine, mainly affecting the jejunum and ileum, and may also involve the duodenum and colon. Its main clinical manifestations are abdominal pain, bloody stool, fever, vomiting, and abdominal distension; severe cases may develop shock, intestinal paralysis, and complications such as intestinal perforation. It is a common acute fulminant disease clinically.

Common Symptoms

Abdominal pain with bloody stool; trauma; ...; diarrhea; tenesmus; peritoneal irritation signs; gelatinous stool; abdominal muscle rigidity; abdominal pain; ...; peritonitis

Causes and Pathogenesis

Visceral vasoconstriction and mesenteric hypoperfusion from various causes can lead to ischemic intestinal injury; the intestinal mucosa is most susceptible to ischemia. In experimental rats, small intestinal mucosal autolysis occurs 1 h after hemorrhagic shock. The principle of managing ischemic injury is early restoration of reperfusion to increase tissue oxygenation, but prolonged ischemia followed by reperfusion causes reperfusion injury due to calcium overload, oxygen free radical generation, activation of neutrophils releasing elastase and collagenase, and endothelial cell homeostasis imbalance. The intestine is the body's largest bacterial reservoir; the mucosal protective barrier prevents bacterial and toxin invasion. Shock, intestinal ischemia, asphyxia, and poor artificial feeding can disrupt the intestinal barrier, causing intestinal microecological imbalance and invasion by bacteria and toxins, triggering AHNE. The causative pathogen is not definitively known, but anaerobes, E. coli, specific Klebsiella, Clostridium or C. perfringens, and even viruses have been isolated from patient stools, causing intestinal wall infection, necrosis, and perforation. Type C C. perfringens (Welchii bacillus producing beta toxin) in stool readily causes pathogenic effects and intestinal microcirculatory disturbance, presenting as patchy gangrenous intestinal lesions. The intestinal barrier includes mechanical, immune, biological, chemical, and motor components. Intestinal epithelial cells, intercellular junctions, and the biofilm form the mechanical barrier; mucus and mucin form an elastin layer covering the mucosa preventing bacterial invasion. Secretory IgA secreted by the mucosa is critical for local mucosal immunity, forming a protective layer that blocks bacterial adhesion, agglutinates bacteria, inhibits bacterial activity, neutralizes bacterial toxins, and defends against viruses; sIgA deficiency allows bacterial adhesion and colony formation, leading to bacterial and endotoxin invasion into the systemic circulation via the portal vein and lymphatics, causing enteric endotoxemia and bacterial translocation. Recent research on AHNE pathogenesis has focused on inflammatory mediators; injury, enteric endotoxemia, and bacterial translocation trigger a cytokine and inflammatory mediator cascade under certain conditions. In animal models, platelet-activating factor (PAF), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and endothelin-1 (ET-1) may be important mediators. Although multiple causes have been proposed, some cases lack these predisposing factors; evidence links AHNE to viral infection and maternal cocaine use; cocaine's alpha-adrenergic effects reduce uterine blood flow and increase fetal mesenteric vasoconstriction, causing fetal hypoxia. Lesions mainly affect the distal jejunum or proximal ileum; only a few cases involve the entire small intestine and colon. Affected bowel is congested, edematous, thickened, and loses elasticity and peristalsis; focal necrosis is seen, with severe cases showing subserosal petechiae and patchy necrosis, bowel dilation, and the lumen filled with cloudy bloody fluid and necrotic material. Perforation and peritonitis may occur. The mesentery of affected segments may be involved with enlarged mesenteric lymph nodes. Lesions start in the submucosa, extend upward to the mucosa, and gradually reach the muscularis; mucosal lesions are generally more extensive than serosal surface changes. Microscopically, all layers show congestion, edema, and abundant lymphocyte, plasma cell, monocyte, eosinophil, and neutrophil infiltration; vascular wall collagen swelling and fibrinoid degeneration; myenteric ganglion cell degeneration; small vessel necrosis and thrombosis; and focal hemorrhage, necrosis, and ulcers in the bowel wall. Etiology: No satisfactory explanation exists, but consensus on predisposing factors includes intestinal ischemia, intestinal infection, impaired intestinal barrier function, respiratory distress syndrome, bleeding, asphyxia, congenital heart disease with heart failure, sepsis, shock, hypothermia, polycythemia and/or high blood viscosity, and artificial feeding. The disease is currently thought related to infection with Welchii bacillus (type C C. perfringens) producing beta toxin, which causes intestinal tissue necrosis and gangrenous enteritis. In the high-incidence highland of Papua New Guinea, local residents have low intraluminal protease levels related to a low-protein diet and heat-stable trypsin inhibitors in sweet potato, the staple food. In animal experiments, gastric instillation of Welchii bacillus alone does not cause disease, but simultaneous instillation of raw sweet potato or raw soybean powder containing trypsin inhibitors causes disease with the same histopathological changes as acute hemorrhagic necrotizing enteritis; canine pancreatic extract containing trypsin prevents and mitigates the disease. This suggests that besides eating contaminated meat, dietary factors such as sudden dietary change from vegetables to meat favor Welchii proliferation, or a sweet potato-based diet with abundant trypsin inhibitors reduces beta toxin degradation. The main pathological change is fibrinoid deposition and thrombosis in small intestinal arteries causing small intestinal hemorrhage and necrosis, most commonly and severely in the jejunum and ileum; sometimes involving the duodenum, colon, and stomach; rarely the entire gastrointestinal tract. Lesions are often segmental and may be multifocal. Lesions usually start in the mucosa, presenting as swelling, diffuse hemorrhage, and dirty-green pseudomembrane on fold crests, with clear demarcation from normal mucosa; they may extend to the muscularis mucosae and even serosa. The bowel wall is thickened and hardened; severe cases develop ulcers and perforation. Microscopically, affected mucosa shows varying degrees of necrosis, mild cases limited to villus tips and severe cases involving the full mucosal thickness. The submucosa shows extensive bleeding with severe edema and inflammatory cell infiltration; the muscularis and serosa may show minor bleeding. Intestinal smooth muscle shows swelling, fragmentation, hyaline degeneration, and necrosis; vascular walls show fibrinoid necrosis with thrombosis; myenteric plexus cells may show dystrophic changes. Besides intestinal lesions, there may be mesenteric lymph node enlargement and softening; hepatic fatty degeneration, acute splenitis, interstitial pneumonia, and pulmonary edema; individual cases may have adrenal focal necrosis. Acute calculous cholecystitis begins when stones obstruct the cystic duct, causing bile stasis and secondary bacterial infection; if inflammation is limited to the mucosal layer, it is acute simple cholecystitis; if inflammation involves the full wall with pus filling the gallbladder and purulent fibrinous exudate on the serosa, it is acute suppurative cholecystitis; if the gallbladder is distended with pus causing ischemia and gangrene, it is acute gangrenous cholecystitis; necrotic gallbladder wall may perforate causing biliary peritonitis, usually at the fundus or at the stone-impacted infundibulum or neck. Perforation into adjacent organs such as the duodenum, colon, or stomach can form internal biliary fistulas, relieving inflammation. Pus entering the common bile duct can cause acute cholangitis, and a few develop acute pancreatitis. Pathogens are mostly E. coli, Klebsiella, and fecal streptococci; anaerobes account for 10 to 15%, sometimes up to 45%. Acute acalculous cholecystitis usually has no cystic duct obstruction; the cause is unclear in most cases, often occurring after trauma or abdominal surgery unrelated to the biliary tract, and sometimes in children with non-hemolytic anemia. It is thought that dehydration, fasting, narcotic analgesic use, and severe stress-induced neuroendocrine changes reduce gallbladder contractility, cause bile stasis, and reduce mucosal resistance, with secondary bacterial infection causing acute inflammation. Some cases are thought due to acute embolism of gallbladder nutrient vessels. The pathology is similar to calculous cholecystitis but progresses rapidly, generally developing into gangrenous cholecystitis within 24 hours, with gangrene of the entire gallbladder.

Treatment

Drug therapy, surgical treatment, rehabilitation therapy

Preventive Measures

Pay attention to dietary hygiene and adequate rest during the high-incidence summer and autumn seasons; children should receive regular deworming per national immunization schedules, balancing work and rest. Dietary notes: 1. Avoid undercooked or spoiled meat, especially raw meat in high-incidence seasons. 2. Avoid large amounts of foods that inhibit intestinal proteases, such as sweet potatoes, especially when eating raw seafood or possibly undercooked grilled meats (such as grilled lamb skewers). 3. Maintain a balanced diet and avoid overeating.

Department to Visit

It is recommended to visit the General Surgery department; an appointment can be booked on this platform before the visit.

Warm reminder: The above information is for health science reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek medical attention at a regular hospital promptly.