Normal portal pressure is 5-10mmHg, when the portal system blood flow is blocked and/or blood flow increases, resulting in increased pressure in the portal vein and its branches, its pressure continues to rise (> 10mmHg) is called portal hypertension, resulting in a series of clinical syndromes called portal hypertension (PH), the most common cause of which is cirrhosis of the liver caused by various causes. A few days ago, Zhu Weibing, director of the Second Department of Medical Medicine of Guangzhou Fuda Cancer Hospital, shared with you the relevant contents of portal hypertension, esophageal and gastric varices at the 30th lecture of "Fuda New Vision Xu Kecheng Lecture Hall".
The portal vein system is formed by the confluence of the superior mesenteric vein and the splenic vein, starting from the capillary network of the stomach, intestine, pancreas, and spleen and ending in the hepatic sinusoidal space. The main trunk of the portal vein and the larger genus branch have no valve structure, blood can flow reversibly, there are communication branches with the hepatic artery, and there are many communication branches with the vena cava (systemic circulation), which is the main blood supply channel of the liver.
Portal hypertension is often caused by increased resistance to portal blood flow, and its initiating factors can be varied. Portal hypertension may cause a range of complications, such as ascites, esophageal and gastric varices (GOV), oesophagogastric variceal bleeding (EVB), and hepatic encephalopathy, among which EVB has a high mortality rate and is one of the most common digestive emergencies.
· How to diagnose portal hypertension –
1. Hepatic venous pressure gradient (HVPG)
At present, hepatic venous pressure gradient (HVPG) is commonly used to represent portal vein pressure, namely: HVPG = WHVP (hepatic vein wedge pressure) - FHVP (free hepatic vein pressure)
- >5mmHg is portal hypertension;
- ≥10 mmHg is the gold standard for diagnosing clinical portal hypertension;
- ≥ 12 mmHg is the threshold for varicose bleeding;
- ≥ 16mmHg is prone to uncontrollable complications and increases the risk of short-term death after non-liver surgery;
- ≥ 20 mmHg suggests poor hemostasis after varicose venous bleeding.
▲The relationship between HVPG and different stages of portal hypertension in cirrhosis
2. Laboratory examinations
In patients with portal hypertension whose initial cause is ascites, splenomegaly, liver shrinkage, or hematemesis, targeted laboratory tests are useful to confirm the diagnosis.
It is not only valuable for patients with cirrhosis, but also necessary for patients with tumors and bone marrow dysplasia. It is necessary to determine liver reserve function and the degree of damage. and other tests are essential to identify the cause of cirrhosis. For patients with suspected inherited metabolic disorders or hematologic disorders, etc. are also performed to make differential diagnosis.
3. Imaging examination
Ascites, liver density and texture, portal vein dilation, vascular openness, and blood flow can be determined. PH is present when the main portal trunk diameter is ≥ 1.3 cm and the splenic vein is ≥ 1.0 cm in diameter.
Risk of bleeding (presence, severity, presence or absence of red signs) of oesophageal varices in patients with cirrhosis portal hypertension can be assessed. For example, portal hypertensive gastropathy, when the stomach wall is bruised, edema → the arteriovenous branch of the submucosa of the gastric mucosa is widely opened→ gastric mucosal microcirculation disorder→ gastric mucosal defense barrier is destroyed→ portal hypertensive gastropathy (mucosal erosion, hemorrhage). This can be confirmed by gastroscopy.
· How to treat portal hypertension –
Because portal hypertension can lead to a variety of complications, patients should actively evaluate portal hypertension, treat the cause and necessary primary and secondary prevention under the guidance of professional doctors, so as to improve the quality of life and delay the progression of the disease.
First, the treatment of esophageal and gastric varices
✍ For primary prevention of drugs for variceal bleeding:
Nonselective β receptor blockers (NSBBs) are preferred for the prevention of oesophagogastric variceal bleeding, and their main mechanisms for reducing portal pressure include reducing the effective output of the heart (blocking the beta1 effect) and constricting the splanchnic blood vessels (blocking the beta2 effect), reducing portal blood flow. It is important to note that NSBB is similar in efficacy to endoscopic varicose vein ligation (EVL) in primary prevention, and the incidence of serious adverse effects is low.
For pharmacological secondary prevention of variceal bleeding: propranolol plus endoscopic therapy is the preferred treatment regimen for secondary prevention of variceal bleeding.
✍ Medical therapy for variceal bleeding:
Terlipressin and somatostatin and their analogues (octreotide) are preferred first-line regimens. Both agents are similar in controlling acute variceal bleeding. If one of these drugs fails to control bleeding, another drug may be switched or combined with.
Proton pump inhibitors (PPIs) can inhibit gastric acid secretion, make gastric juice pH > 5, and improve the success rate of hemostasis. Prophylactic use of antibiotics during acute bleeding can reduce the risk of infection such as bacteremia and spontaneous bacterial peritonitis, can reduce the rate of rebleeding and overall mortality, is an essential step for the treatment of acute variceal bleeding, generally recommended the use of third-generation cephalosporin antibiotics or quinolones, the treatment cycle is usually 5~7d.
In addition, drug combination with endoscopic therapy can significantly improve the success rate of hemostasis in acute bleeding and is the preferred method for controlling acute bleeding.
When variceal bleeding occurs, the emergency treatment is:
Three-chamber two-capsule duct compression to stop bleeding:
- The inflatable balloon is used to compress the varicose veins of the fundus and the lower esophagus respectively to achieve hemostasis;
- Balloon compression is only used for major bleeding as a temporary "bridge" (within 24 hours, preferably in intensive care) to buy time for endoscopic and other treatments;
- 80%~90% of the bleeding can be controlled by three-chamber two-capsule duct compression, but the rebleeding rate is as high as more than 50%, and the patient is in great pain, which is easy to cause complications such as aspiration pneumonia and tracheal obstruction;
- It is safe and effective to carry out three-chamber two-capsule tube compression to stop bleeding, and then endoscopic intensive ligation treatment within 24 hours.
2. Endoscopic treatment
It is the first-line endoscopic treatment of esophageal varices. It is usually used for acute variceal bleeding of the esophagus and to prevent rebleeding, and is used clinically earlier than EVL, but has a higher complication rate. EIS is currently primarily used as an alternative when EVL is technically difficult to complete. In addition, it is mainly used for gastric variceal bleeding.
Endoscopic treatment is the time when:
- Patients with cirrhosis of the liver with acute upper gastrointestinal bleeding should undergo endoscopy to confirm the source of bleeding;
- Before endoscopic therapy, fluid resuscitation and medication are required;
- Patients with stable vital signs but active bleeding should undergo emergency endoscopic therapy;
- Patients with medical therapy can control bleeding, can undergo endoscopy electively, and after hemodynamic resuscitation, endoscopy and treatment should generally be performed within 12 hours.
3. Interventional therapy
Mainly. When the combination of drugs and endoscopic therapy fails to treat variceal bleeding, PTFE-coated stent TIPS is recommended as a salvage treatment.
4. Surgical treatment
Such as.
Liver disease is very common in the mainland, and cirrhosis after hepatitis has brought a heavy medical burden to the mainland. About 50% of people with cirrhosis will eventually develop portal hypertension, so early detection and treatment of portal hypertension is essential to help reduce symptoms and prevent complications.
Diagnosis and differentiation of portal hypertension requires a detailed history and thorough physical examination, as well as targeted laboratory, imaging, and pathologic studies. In addition, rich professional knowledge, skilled clinical skills and rigorous clinical thinking are required to make accurate comprehensive judgments.