Abdominal wall erythema

Introduction Infants with acute necrotic enteritis have atypical symptoms, and infants are more likely to develop 3 to 10 days after birth. Due to premature birth or low body weight, he was admitted to the intensive care unit. During artificial feeding or during the establishment of gastric tube nasal feeding due to incomplete establishment of swallowing reflexes in immature children, there was retention in the stomach, followed by bloating, vomiting, blood in the stool or fever. , heart rate is too fast or slow, abdominal muscle tension, abdominal flatulence, abdominal wall erythema and other signs.

Cause

There is no satisfactory explanation for the pathogenesis of the etiology, but the opinions are more consistent in some susceptibility factors and reasoning. These susceptibility factors include: intestinal ischemia, intestinal infection, impaired intestinal barrier function, respiratory distress syndrome, hemorrhage, asphyxia, congenital heart disease with heart failure, sepsis, shock, hypothermia, erythrocytosis and (or High blood viscosity, artificial feeding, etc.

1, intestinal ischemia

The visceral vasoconstriction caused by various reasons, the insufficiency of mesenteric vascular blood supply can cause intestinal ischemic damage, and the intestinal mucosa is most susceptible to ischemia. Experimental observation of the rat intestinal mucosa 1oc, hemolysis occurred in the small intestinal mucosa. The principle of clinical treatment of ischemic damage should be to restore blood reperfusion as soon as possible to increase tissue oxygen supply, but long-term ischemia will occur after reperfusion injury (reperfusion injury), this damage is due to calcium overload Oxygen free radicals are produced, and neutrophils are activated to cause the release of various enzymes including elastase and collagenase and the imbalance of endothelial cell homeostasis.

2, intestinal infection

The intestine is the largest bacterial reservoir in the human body. Because of the protective effect of the intestinal mucosa itself, bacteria and toxins cannot be invaded. This protection is called a defense barrier. Shock, intestinal ischemia, asphyxia, artificial feeding, etc. can cause damage to the intestinal barrier, which in turn causes imbalance of bacterial micro-ecology in the intestinal tract and invasion of bacteria and toxins to induce AHNE. There is no definitive understanding of AHNE pathogenic pathogens, but anaerobic bacteria, Escherichia coli, specific Klebsiella, fusiform spores, or genus Capsella can be isolated from the patient's feces. A virus, etc., which can cause intestinal wall infection, necrosis, and perforation. C-type Clostridium perfringens (the beta-toxin-producing Welchii bacterium) in the feces is susceptible to pathogenic effects, causing intestinal microcirculatory disorders and exhibiting patchy gangrenous intestinal lesions.

3, intestinal barrier dysfunction

The intestinal barrier function includes mechanical, immune, biological, chemical, and motor function barriers. Under normal conditions, intestinal mucosal epithelial cells, intercellular connections and bacterial membranes constitute a mechanical barrier, and intestinal mucus and mucin form an elastin layer covering the surface of the intestinal mucosa, preventing bacteria from invading and chemical and mechanical stimulation. Play a protective role. Under normal circumstances, secretory immunoglobulin (sIgA) secreted by intestinal mucosa is extremely important for mucosal local immune function. It is an immune barrier. Its role is to form a protective layer on the mucosal surface, prevent bacterial adhesion, agglutinate bacteria, and inhibit bacterial activity. And neutralize bacterial toxins and protect against viruses, against a variety of proteolytic enzymes. In the absence of sIgA, bacteria adhere to the mucosal epithelium and form colonies, which in turn cause bacteria and endotoxins to invade the system through the portal vein and lymphatic system, forming intestinal endotoxemia and bacterial translocation (BT).

4. The role of inflammatory mediators

The pathogenesis of AHNE has been more concentrated in recent years on the study of inflammatory mediators. Injury, intestinal endotoxemia and bacterial translocation can trigger a chain reaction between cytokines and inflammatory mediators under certain conditions. Platelet activating factor (PAF) and tumor necrosis factor alpha have been found in animal models of AHNE. TNF), interleukin-6 (IL-6) and endothelin 1 (ET-1) may be important inflammatory mediators that cause their disease.

an examination

Related inspection

Skin smear microscopy abdominal CT

Check the diagnosis:

The disease lacks specific diagnostic features, and the severity of the disease is different, especially in non-multi-incidence areas, which is more likely to be misdiagnosed, and the misdiagnosis rate is 50% to 60%. The main basis for clinical diagnosis is:

1 There is a history of unclean diet, in the summer and autumn, sudden onset of severe abdominal pain, diarrhea and stagnation of blood in the stool, nausea and vomiting and obvious symptoms of poisoning, should consider the possibility of this disease.

2 According to the stage of the disease and the patient's performance, distinguish different clinical types: diarrhea and bloody stool type, with diarrhea and blood in the stool as the main manifestation; peritonitis type, mainly showing signs of mesenteric inflammation; poisoning type, with shock as prominent or with DIC; intestinal obstruction The main manifestations of acute intestinal obstruction.

Differential diagnosis

Identification:

1, abdominal pain with hematuria: abdominal pain with hematuria is one of the clinical manifestations of kidney and ureteral stones.

2, abdominal obesity: apple-shaped body waist and abdomen is too fat, like apples, thin arms and thin legs, also known as abdominal obesity.

3, small abdomen tingling: common symptoms of gynecological diseases in the lower abdomen, which brings great pain to the patient, sometimes it feels painful, and there are many types of abdominal pain, which causes many reasons.

diagnosis:

The disease lacks specific diagnostic features, and the severity of the disease is different, especially in non-multi-incidence areas, which is more likely to be misdiagnosed, and the misdiagnosis rate is 50% to 60%. The main basis for clinical diagnosis is:

1 There is a history of unclean diet, in the summer and autumn, sudden onset of severe abdominal pain, diarrhea and stagnation of blood in the stool, nausea and vomiting and obvious symptoms of poisoning, should consider the possibility of this disease.

2 According to the stage of the disease and the patient's performance, distinguish different clinical types: diarrhea and bloody stool type, with diarrhea and blood in the stool as the main manifestation; peritonitis type, mainly showing signs of mesenteric inflammation; poisoning type, with shock as prominent or with DIC; intestinal obstruction The main manifestations of acute intestinal obstruction.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.