portal vein stagnation
Introduction
Introduction Thrombosis often occurs in: 1 cirrhosis or extrahepatic compression caused by portal vein congestion and portal venous stasis; 2 intra-abdominal suppurative infection, such as gangrenous appendicitis, ulcerative colitis, strangulated sputum, etc.; Some blood abnormalities, such as polycythemia vera, hypercoagulable state caused by oral contraceptives; 4 trauma caused by trauma or surgery, such as mesenteric hematoma, splenectomy, right colon resection and so on. About 1/4 of patients have no obvious cause, called primary mesenteric venous thrombosis. After venous thrombosis, it can continue to spread to the proximal and distal ends. When the venous return of the affected bowel is completely blocked, the intestine is congested and edematous, and the subserosal bleeds first, then spreads into pieces. The intestinal wall and mesentery are thickened and edematous. In addition, hemorrhagic infarction occurred in the intestines, which was dark purple. A large amount of bloody fluid oozes from the intestinal wall and mesentery to the intestinal and abdominal cavities. Acute venous occlusion can also reflect the process of stenosis and thrombosis of visceral arteries and accelerate intestinal necrosis. Finally, it also leads to hypovolemia and toxic shock in infection.
Cause
Cause
The disease has two primary and secondary, but secondary is more common. Often accompanied by hypercoagulable state (such as polycythemia and cancer), superior mesenteric vein injury (trauma, surgery, radiotherapy, portal-cavary shunt), abdominal infection and long-term use of contraceptives. Nearly half of the patients have a history of peripheral venous thromboembolic inflammation, which may be a special type of thrombophlebitis (visceral type).
Examine
an examination
Related inspection
Intravenous gallbladder, cholangiography, abdominal vascular ultrasound, laparoscopic central venous pressure measurement (CVP)
There are often causes of stagnation, hypercoagulability, or vascular damage in the portal vein. The onset is slower. It manifests as abdominal discomfort, constipation or diarrhea. After a few days or weeks, as the spread of thrombus expands, venous blood flow is blocked, and when the intestinal tract is affected, sudden abdominal pain, persistent vomiting, diarrhea and bloody water are more common than arterial embolism. Abdominal distension, abdominal tenderness, rebound tenderness and abdominal muscle tension were observed during physical examination. The bowel sounds weaken or disappear. Abdominal puncture can draw bloody fluid. Frequent fever and white blood cell count, increased hematocrit. Abdominal X-ray film can show the expansion of the affected small intestine, accompanied by a gas-liquid plane. Intestinal peristalsis disappears during fluoroscopy.
Abdominal distension, abdominal tenderness, rebound tenderness and abdominal muscle tension were observed during physical examination. The bowel sounds weaken or disappear. Abdominal puncture can draw bloody fluid. Frequent fever and white blood cell count, increased hematocrit. Abdominal X-ray film can show the expansion of the affected small intestine, accompanied by a gas-liquid plane. Intestinal peristalsis disappears during fluoroscopy.
Diagnosis
Differential diagnosis
Portal hypertension is a group of syndromes caused by a persistent increase in portal pressure. The vast majority of patients are caused by cirrhosis, and a small number of patients are secondary to portal vein or hepatic vein obstruction and some unexplained factors. When the portal vein blood does not flow smoothly through the liver into the inferior vena cava, it will cause an increase in portal pressure. The performance of the portal-to-venous communication is open. A large amount of portal vein blood enters the systemic circulation directly through the traffic branch before entering the liver, resulting in abdominal wall and esophageal vein dilatation; splenomegaly and hypersplenism; liver function decompensation and ascites .
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.
When hardened, the portal pressure increases. When the water exceeds 200 mm, the blood flow to the normal digestive organs and spleen is blocked by the liver, resulting in a portal-body collateral circulation between many parts of the portal system and the vena cava.
There are often causes of stagnation, hypercoagulability, or vascular damage in the portal vein. The onset is slower. It manifests as abdominal discomfort, constipation or diarrhea. After a few days or weeks, as the spread of thrombus expands, venous blood flow is blocked, and when the intestinal tract is affected, sudden abdominal pain, persistent vomiting, diarrhea and bloody water are more common than arterial embolism. Abdominal distension, abdominal tenderness, rebound tenderness and abdominal muscle tension were observed during physical examination. The bowel sounds weaken or disappear. Abdominal puncture can draw bloody fluid. Frequent fever and white blood cell count, increased hematocrit. Abdominal X-ray film can show the expansion of the affected small intestine, accompanied by a gas-liquid plane. Intestinal peristalsis disappears during fluoroscopy.
Abdominal distension, abdominal tenderness, rebound tenderness and abdominal muscle tension were observed during physical examination. The bowel sounds weaken or disappear. Abdominal puncture can draw bloody fluid. Frequent fever and white blood cell count, increased hematocrit. Abdominal X-ray film can show the expansion of the affected small intestine, accompanied by a gas-liquid plane. Intestinal peristalsis disappears during fluoroscopy.
