portal gas
Introduction
Introduction Portal venous gas (PVG) refers to the imaging signs of abnormal accumulation of gas in the portal vein and its intrahepatic portal vein due to various reasons, usually diagnosed by abdominal X-ray film. Common in neonatal necrotizing enterocolitis. Neonatal necrotic enterocolitis is the main clinical manifestation of abdominal distension, vomiting and blood in the stool. The cystic gas in the intestinal wall is a serious disease characterized by X-ray. 90% occurred in premature infants, with a mortality rate of up to 86% in the intestinal wall and portal vein.
Cause
Cause
(1) Causes of the disease
The cause of necrotizing enterocolitis has not been fully elucidated, but it is generally thought to be caused by a combination of causes, among which preterm birth and infection are the most important.
1. Premature delivery: Premature birth is an important pathogenic factor of NEC. Due to poor immune function, poor peristalsis, and suffocation at birth, causing hypoxia damage in the intestinal wall, causing bacterial invasion.
2. Infection: Infection is one of the main causes of NEC, mostly intestinal bacteria such as Klebsiella, Escherichia coli, and Pseudomonas aeruginosa.
3. Hypoxia and ischemia: In the neonatal asphyxia, respiratory disease, shock and other hypoxic-ischemic conditions, the intestinal wall vasoconstriction, resulting in intestinal mucosal ischemia and hypoxia, necrosis, with the recovery of oxygen supply, vasodilatation and congestion, Reperfusion during expansion increases tissue damage.
4. Feeding: Eating and exchanging blood transfusions can increase the reperfusion of the intestinal wall, which is the cause of the disease, which causes the intestinal tract to be attacked by bacteria. Once fed, it provides ample substrate for intestinal bacterial growth. Intestinal feeding has always been considered as a pathogenesis factor of NEC. Infected and asphyxiated premature infants prematurely and over-feeding milk can induce NEC. However, the opinion that feeding leads to NEC is still controversial. It is reported that the incidence of NEC in preterm infants who are delayed from feeding until 2 weeks is higher than that in early-feeders.
5. Others: When the umbilical artery or vein cannula, blood transfusion therapy, polycythemia, arterial catheter opening, hypothermia, etc., the incidence of NEC is higher.
(two) pathogenesis
In children with necrotizing enterocolitis, there are usually three factors in the small intestine: persistent intestinal ischemic damage, bacterial colonization, and intestinal lumen (eg, enteral feeding).
1. Intestinal wall hypoxia and inflammatory injury: premature infants with poor immune function, poor peristalsis, long food retention time, easy to make bacteria growth; high milk osmotic pressure, premature infants with infection and asphyxia prematurely overfeeding milk, can be aggravated Mucosal damage of the intestinal wall induces NEC. Asphyxiation at birth causes hypoxia damage to the intestinal wall, allowing bacteria to invade, excessive bacterial growth and its toxins can cause inflammation in the hypoxic intestinal wall. Cytokines released by tissues during inflammation, such as platelet activating factor, alpha tumor necrosis factor, prostaglandins, etc., aggravate the inflammatory response and promote the occurrence of NEC. Klebsiella has a strong fermentation effect on lactose in food, and the hydrogen produced causes cystic gas accumulation in the intestinal wall.
2. Hypoxia and reperfusion injury: ischemic damage can be caused by hypoxic damage, such as neonatal asphyxia, respiratory disease, triggered by the original diving reflex, caused by mesenteric artery spasm, resulting in a significant reduction in intestinal blood flow During the exchange of blood, during the period of sepsis or when fed with high-tension formula, intestinal blood flow is reduced, leading to intestinal ischemic damage. Similarly, in the case of ischemia, congenital heart disease and other ischemic conditions, can reduce systemic blood flow, or arterial oxygen saturation, resulting in intestinal mucosal ischemia and hypoxia, necrosis; recovery of oxygen, feeding and exchange of blood transfusion Reperfusion increases tissue damage.
3. Pathological changes: NEC can affect the entire small intestine and colon, but the most common sites are in the distal part of the ileum and proximal to the ascending colon. In mild cases, the necrotic intestine is only a few centimeters. In severe cases, it can extend to the jejunum and colon, but generally Does not affect the duodenum. Bacteria can penetrate the intestinal wall, produce hydrogen and accumulate, produce characteristic intestinal wall gas on the X-ray, gas can enter the portal vein, and can be seen through the abdominal X-ray film or liver B-ultrasound to the portal vein on the liver. Progression of the lesion can lead to necrosis, perforation, peritonitis, sepsis and death of the entire intestinal wall. Early lesions are mainly intestinal mucosa and submucosal congestion, edema, hemorrhage, necrosis. The extent of the disease in the advanced stage is enlarged, involving the muscular layer. In severe cases, the whole layer of the intestinal wall is necrotic, and intestinal perforation and peritonitis can be complicated.
Examine
an examination
Related inspection
Angiographic vascular ultrasonography central venous pressure measurement (CVP)
Abdominal X-ray film is of great significance for the diagnosis of this disease. In the early stage, the main manifestations were paralytic ileus: the small intestine was disordered, the inflation was obvious, and multiple fluid levels were seen in the intestinal lumen, which was stepped. Progression of the disease, such as intestinal gas into the intestinal wall, occurs in the intestinal wall. The intestinal wall is widened, and a vesicular or beaded translucent area appears in the intestine wall. When the subserosal gas is accumulated, a line, an arc-shaped or a ring-shaped translucent area can be present. In the heavier case, the intestinal venous gas is visible due to intestinal gas entering the portal vein: The liver can see a strip or dendritic translucent shadow from the hepatic portal to the liver along the portal vein. In severe cases, intestinal fistula fixation (intestinal necrosis) pneumoperitoneum (intestinal perforation) and peritoneal effusion (peritonitis) can be seen. Intestinal cystic gas accumulation and portal vein inflation are characteristic features of this disease.
Severe cases are often accompanied by severe infection, metabolic acidosis and/or respiratory acidosis, platelet and neutropenia, DIC, etc., therefore blood gas analysis, fecal occult blood and culture, blood routine and culture, and DIC screening and The diagnosis laboratory is very important for the judgment of the condition.
With the following three items, you can confirm the diagnosis:
1 systemic poisoning performance: such as unstable body temperature, pale, irregular breathing and bradycardia.
2 Gastrointestinal manifestations: gastric retention, vomiting, gross bloody stools, abdominal distension and bowel sounds disappeared.
3 abdominal X-ray findings: intestinal obstruction and intestinal wall accumulation.
Diagnosis
Differential diagnosis
1. Toxic intestinal paralysis: When the primary disease is diarrhea or sepsis, it is easy to misdiagnose NEC as toxic intestinal paralysis. However, toxic intestinal paralysis has no blood in the stool, and there is no gas accumulation between the intestinal wall on the X-ray film.
2. Mechanical small bowel obstruction: On the X-ray web, the span of the liquid surface is larger, the intestinal wall is thinner, the intestinal gap is widened and blurred, and there is no gas accumulation in the intestinal wall.
3. Intestinal torsion: The symptoms of mechanical intestinal obstruction are severe when the torsion is reversed, and vomiting is frequent. The plain X-ray film shows the image of duodenal obstruction, the abdominal density is evenly deepened, and there is irregular polymorphic gas shadow, no obvious inflation expansion. Intestines.
4. Hirschsprung's disease: Early NEC should be differentiated from congenital megacolon when the small intestine is generally flatulent. The latter is mainly caused by abdominal distension and difficulty in defecation, and there is no bloody stool. X-ray dynamic observation of abdominal changes without intestinal wall gas accumulation, combined with clinical identification
5. Neonatal hemorrhagic disease: gastrointestinal bleeding can occur mainly 2 to 5 days after birth, and needs to be identified. Neonatal hemorrhagic disease has not been given vitamin K injection history after birth, abdominal distension, abdominal X-ray plain film without intestinal lumen inflation and intestinal wall accumulation, vitamin K treatment is effective.
6. Meconium peritonitis: In some cases, the abdominal X-ray film can be seen scattered in the small vesicle-like intestinal wall, but there may be typical abnormal calcification, and it is not difficult to identify with clinical combination.
7. Spontaneous gastric perforation: mostly due to congenital gastric wall muscle defect, often occurs in the stomach near the cardia, most of the children have a history of hypoxia. Sudden onset, sudden onset of abdominal distension 3 to 5 days after birth, accompanied by vomiting, difficulty breathing and cyanosis, X-ray plain abdomen only see pneumoperitoneum, no intestinal wall gas or intestinal tube flatulence.
Abdominal X-ray film is of great significance for the diagnosis of this disease. In the early stage, the main manifestations were paralytic ileus: the small intestine was disordered, the inflation was obvious, and multiple fluid levels were seen in the intestinal lumen, which was stepped. Progression of the disease, such as intestinal gas into the intestinal wall, occurs in the intestinal wall. The intestinal wall is widened, and a vesicular or beaded translucent area appears in the intestine wall. When the subserosal gas is accumulated, a line, an arc-shaped or a ring-shaped translucent area can be present. In the heavier case, the intestinal venous gas is visible due to intestinal gas entering the portal vein: The liver can see a strip or dendritic translucent shadow from the hepatic portal to the liver along the portal vein. In severe cases, intestinal fistula fixation (intestinal necrosis) pneumoperitoneum (intestinal perforation) and peritoneal effusion (peritonitis) can be seen. Intestinal cystic gas accumulation and portal vein inflation are characteristic features of this disease.
Severe cases are often accompanied by severe infection, metabolic acidosis and/or respiratory acidosis, platelet and neutropenia, DIC, etc., therefore blood gas analysis, fecal occult blood and culture, blood routine and culture, and DIC screening and The diagnosis laboratory is very important for the judgment of the condition.
With the following three items, you can confirm the diagnosis:
1 systemic poisoning performance: such as unstable body temperature, pale, irregular breathing and bradycardia.
2 Gastrointestinal manifestations: gastric retention, vomiting, gross bloody stools, abdominal distension and bowel sounds disappeared.
3 abdominal X-ray findings: intestinal obstruction and intestinal wall accumulation.
