Duodenal varicose veins

　　1. Etiology

　　Liver cirrhosis, portal hypertension, extrahepatic portal vein occlusion, vascular malformations, etc., are the causes of varicose veins in the duodenum. The course of varicose veins varies with the cause, and the incidence of extrahepatic portal vein occlusion is high in Europe and the United States.

　　2. Pathogenesis

　　When there is extrahepatic portal hypertension or occlusion of a branch of the portal vein, the blood flow of the portal vein can pass through the branches of the gastrocolic trunk and superior mesenteric vein to the portal of the pancreas and duodenum, and then return to the portal vein through the posterior superior venae cavae of the duodenum, the pylorus, or the right gastric epiploic vein. Therefore, varicose veins in the duodenum are prone to bleeding. Japan reported that the majority of patients with portal hypertension caused by liver cirrhosis. In liver cirrhosis, the blood flow of the superior mesenteric vein can flow into the inferior vena cava through the retroperitoneal veins. In patients with occlusion of the splenic vein, the gastric epiploic vein is often used as a collateral circulation for the portal of the duodenum and the portal of the pancreas and duodenum, so the above veins can often be seen to be dilated. In rare cases, there are serpentine varicose veins between the portal of the pancreas and duodenum and the abnormal vessels in the liver, and there is a shunt between the abnormal vessels and the venae umbilicales.

　　Once duodenal varices occur, due to the rich blood flow, it is difficult to stop bleeding, and it is easy to fall into shock, which can lead to death.

　　Shock is a clinical syndrome caused by insufficient tissue perfusion, which is a common complication in severe diseases in all clinical departments. The common feature of shock is insufficient effective blood volume, and although tissue and cell blood perfusion is compensated, it is still severely restricted, leading to poor blood perfusion of the whole body and organs, causing tissue hypoxia, stasis in the microcirculation, organ dysfunction, and abnormal cell metabolic function, and a series of pathophysiological changes. Therefore, the pathogenesis of shock generally develops from compensatory hypotension (reduction of tissue perfusion) to microcirculatory failure, and finally leads to membrane damage and cell death. The main clinical manifestations include blood pressure drop, systolic blood pressure below 12kPa (90mmHg), pulse pressure less than 2.67kPa (20mmHg), pale complexion, cold extremities and cyanosis of the extremities, superficial venous collapse, weak pulse, general weakness, decreased urine output, restlessness, drowsiness, confusion, and even coma, etc.

　　There are few characteristic symptoms. With the advancement of diagnostic techniques such as endoscopy, accidental findings are more common, and initial clinical manifestations may include variceal rupture and bleeding. In such cases, hematemesis and hematochezia are common, accounting for about 70%, due to the rich blood flow, it is easy to fall into shock.

　　Active treatment of the primary disease: liver cirrhosis, portal hypertension, vascular malformations, etc.

　　1. Liver cirrhosis:It is a common clinical chronic progressive liver disease, formed by the long-term or repeated action of one or more etiologies, resulting in diffuse liver damage. Pathologically, there are extensive liver cell necrosis, nodular regeneration of residual liver cells, proliferation of connective tissue, and formation of fibrous septa, leading to destruction of the lobular structure and formation of false lobules, gradual deformation and hardening of the liver, and eventually developing into liver cirrhosis.

　　2. Portal hypertension:It is a syndrome caused by persistent increase in portal vein pressure, with the vast majority of patients caused by liver cirrhosis, a few patients secondary to obstruction of the main portal vein or hepatic vein, and some unknown factors.

　　3. Vascular tumors:Also known as tubular tumors, or separately called angiomas, lymphangiomas; but some vascular malformations are not true tumors, so they can only be called vascular anomalies. They are tumors or anomalies originating from blood vessels or lymphatic vessels.

　　1. Laboratory examination

　　1. Changes in blood count

　　In the early stage of hemorrhage, there may be no change in the patient's hemoglobin, red blood cell count, and hematocrit, etc. Only when tissue fluid渗入血管内 or isotonic fluid is administered to expand blood volume, the blood becomes diluted and anemia manifests. Patients often present with normocytic normochromic anemia, and reticulocytes are often elevated. After a massive hemorrhage, the white blood cell count can reach 10,000 to 20,000, and it returns to normal 2 to 3 days after bleeding stops. In patients with liver cirrhosis and portal hypertension, the white blood cell count may not increase after bleeding, due to the common presence of splenic hyperfunction.

　　2. Azotemia

　　After upper gastrointestinal bleeding, due to the entry of blood into the intestines, the protein digestion products are absorbed by the intestinal mucosa, so it can cause an increase in blood urea nitrogen concentration, known as intestinal origin of increased blood urea nitrogen. Urea nitrogen can increase within a few hours after bleeding, usually reaching a peak in 24-48 hours. If urea nitrogen continues to rise, it may be due to continued bleeding or due to renal urea nitrogen increase after a large hemorrhage, due to reduced effective blood volume, resulting in decreased renal blood flow and glomerular filtration rate. Therefore, after excluding the factors of renal urea nitrogen increase, monitoring the changes of blood urea nitrogen is a useful indicator for judging whether the bleeding has stopped.

　　Secondly, Imaging examinations

　　1. Upper gastrointestinal contrast

　　Upper gastrointestinal contrast is difficult to diagnose qualitatively, and it often appears as polypoid or giant pleated, and it must be differentiated from duodenal ulcer, duodenal polyps, and submucosal tumors of the duodenal mucosa.

　　2. Upper gastrointestinal endoscopy

　　Under endoscopy, varicosities of the duodenal wall can be seen, presenting as cystic or nodular protuberances, the color can be blue or consistent with the surrounding mucosa, the surface may have erosion, covered with a little grayish yellow fur or bloody matter. As with upper gastrointestinal contrast, it must be differentiated from polyps and submucosal tumors. Biopsy may cause massive bleeding, and special attention should be paid to this. To prevent biopsy bleeding, the protuberant part can be compressed with a biopsy forceps before biopsy to determine its elasticity. Diagnosis is difficult when there is active bleeding. Due to the large amount of blood accumulated in the duodenum, it is necessary to repeatedly flush and aspirate the blood clean and observe the mucosal surface in detail. The surface of the elevated lesions in the bleeding patients is often eroded and often manifests as effusive bleeding. It is difficult to immediately make a diagnosis of duodenal varices even at the time of bleeding. For those with a history of suspected variceal bleeding, endoscopic examination should consider this disease and try to insert the endoscope into the distal duodenum as much as possible.

　　3. Abdominal CT

　　It can determine the presence of liver cirrhosis, the degree of liver atrophy, and the presence or absence of ascites. Contrast CT examination can detect abnormal dilated vessels connected to the duodenal wall, and whether there is extravasation of contrast agent can be determined during the bleeding phase.

　　4. Abdominal angiography

　　Antegrade celiac artery and superior mesenteric artery angiography can determine that there is no extravasation of contrast agent outside the blood vessels during the arterial phase. In the venous phase, the gastric duodenal vein and pancreaticoduodenal vein can be seen to be thickened, with serpentine or nodular varicosities and contrast agent flowing into the inferior vena cava, which can be diagnosed. When bleeding is evident, contrast agent leakage outside the blood vessels can be seen. When there is a high suspicion of the disease, percutaneous transhepatic portal vein angiography is also valuable. Angiography through the gastric colonic branch can obtain very bright images of the portal vein. It is easy to obtain the cause of the blood vessel image through the usual celiac artery and superior mesenteric artery angiography, and embolization can be performed after the examination.

　　Gastric diverticulum food therapy recipe

　　It is recommended to eat easily digestible and less irritating foods, take anti-secretory drugs, gastric mucosal protective agents, and antibiotics.

　　(The above information is for reference only, please consult a doctor for details)

　　First, treatment

　　1. Surgical treatment:Duodenal varices are often treated with surgical operation. The rebleeding rate of simple variceal ligation is up to 57%, and about 40% of patients may experience rebleeding after gastrojejunal resection. The most effective surgical operation is portosystemic shunt, which reduces portal hypertension and the rebleeding rate to 10%. For cases with concurrent bleeding, due to underlying diseases such as liver cirrhosis, the condition is often severe or shock-like after bleeding. If surgical hemostasis is performed, a high number of deaths occur due to hepatic encephalopathy. Therefore, the selection of suitable surgical candidates should be cautious. For those who cannot tolerate surgery, other treatment methods can be chosen, and a scheduled operation can be considered after the initial hemostasis.

　　2. Endoscopic treatment:Endoscopic treatment of varicose veins includes sclerotherapy and ligation. Sclerotherapy is an established method with the advantage that sclerotherapy can be performed immediately during endoscopic examination, which is a widely used technique. The first report of sclerotherapy for duodenal varices was made by Sauerbruch et al. in 1982, and since then, reports have gradually increased. The most commonly used sclerosing agent is aethoxyskerol (AS) and ethanolamine oleate (EO), with an injection volume of up to 20-30ml. The side effects and complications of the drug are few, and it has a certain therapeutic effect. However, for the rupture of duodenal varices, only about 1/3 of patients achieve long-term hemostasis after sclerotherapy, and the overall efficacy is not good. The reason is that duodenal varices, like solitary gastric varices, have a large and fast分流, and with the anatomical characteristics of the duodenum, varices often occur in the descending part of the duodenum, making it difficult to apply balloon compression for hemostasis and to block blood flow. Even if endoscopic treatment is chosen, it is often difficult to perform endoscopic manipulation. There have been reports of increased bleeding after sclerotherapy, and due to the thin wall of the duodenum, it is difficult to perform the operation, and there have also been cases of perforation caused by puncture.

　　There have been reports of successful hemostasis using tissue adhesive (histoacryl). Tissue adhesive is a rapid curing agent that immediately undergoes polymerization when injected intravenously and comes into contact with blood, causing local hardening. There have been reports of embolic symptoms in other distant organs after intravascular injection. Since tissue adhesive is a rapid curing substance, to prevent rapid curing that may cause operational difficulties, it can be diluted with oily contrast agent lipiodol at a ratio of 0.5:1 or 1:1 with tissue adhesive. However, the curing time after contact with blood and the degree of dilution of the tissue adhesive are positively correlated, meaning the lower the concentration, the longer the curing time, the higher the chance of entering the systemic circulation, and the higher the chance of ectopic embolism. Therefore, there is an increasing number of scholars advocating for the use of undiluted tissue adhesive in recent years.

　　Endoscopic sclerotherapy is a mature treatment method for the treatment of esophageal and gastric fundus variceal bleeding, but it has certain limitations in the treatment of duodenal variceal bleeding. It is still difficult to say that it is a minimally invasive and reliable hemostatic method at present.

　　The endoscopic ligation treatment for variceal bleeding is simple, has good temporary hemostatic effects, and can be implemented even by those who are not very skilled in endoscopic operations, making it a good method for emergency hemostasis. However, the endoscopic variceal ligation is only a local treatment for varices and has no effect on deep varices and communicating branches, with a high recurrence rate of bleeding. It can be used as an emergency hemostatic method, but other treatment methods should be supplemented after the improvement of the overall condition.

　　3. Catheter-based Treatment:The reports of percutaneous transhepatic portal vein embolization, subballoon retrograde venous embolization, and embolization via the ileal vein are increasing. The reasons for choosing the above treatments are due to the poor general condition of the patients, most of whom cannot tolerate general anesthesia during surgical operations; or endoscopic treatment due to a large amount of bleeding, unclear vision, and difficulties in sclerosis treatment, as well as concerns about the damage to renal function caused by sclerosing agents. Regardless of the type of embolization treatment chosen, the tip of the catheter should enter the pancreaticoduodenal vein and other responsible vessels. Inject 99% ethanol or use stainless steel coils to form thrombi within the varices to control bleeding. Embolization treatment is a low-invasive treatment, and compared to endoscopic treatment, it not only achieves local treatment effects on varices but also blocks the blood flow of varices, making it a good treatment method. However, there have been reports of increased portal vein pressure after treatment, and cases of variceal recanalization and the formation of collateral circulation causing rebleeding. Postoperative observation of the disease course should be cautious.

　　II. Prognosis

　　The prognosis of successful hemostasis cases is good. As emergency treatment, the success rates of endoscopic treatment, embolization treatment, and surgical rescue are respectively about 70%, 80%, and 70%. The combination of endoscopic variceal sclerosis treatment with embolization of the retrocolonic vein and endoscopic ligation treatment with embolization of the retrocolonic vein also achieves good efficacy, but there is no significant difference in efficacy compared to the above treatment methods.