The portal vein and its tributaries
|Classification and external resources|
Portal hypertension is hypertension (high blood pressure) in the hepatic portal system, which is composed of the portal vein and its branches and tributaries. Portal hypertension is defined as elevation of hepatic venous pressure gradient. In clinical practice the pressure is not measured directly until the decision to place a transjugular intrahepatic portosystemic shunt has been made. Part of the procedure, a hepatic vein wedge pressure is measured with the assumption of no pressure drop across the liver yielding portal vein pressure.[medical citation needed]
Signs and symptoms
Signs and symptoms of portal hypertension include:
- Ascites (free fluid in the peritoneal cavity).
- Dilated veins in the anterior abdominal wall 
- Abdominal tenderness (Spontaneous bacterial peritonitis. presents as complication)
- Jaundice (Hepatorenal syndrome. presents as complication)
- Portal hypertension does not increase the risk of hemorrhoids
- Oesophageal varices and haematemesis
- Prehepatic causes include portal vein thrombosis or congenital atresia.
- Intrahepatic causes include liver cirrhosis, hepatic fibrosis, and less commonly noncirrhotic causes such as schistosomiasis, massive fatty change and diffuse granulomatous diseases (e.g. sarcoidosis, miliary tuberculosis).
- Posthepatic obstruction occurs at any level between liver and right heart, including hepatic vein thrombosis, and constrictive pericarditis.
The pathophysiology of portal hypertension is indicated by increasing vascular resistance via different etiologies; additionally, stellate cells and myofibroblasts are activated. Increased endogenous vasodilators in turn promote more blood flow in the portal veins.
Nitric oxide is an endogenous vasodilator and it regulates intrahepatic vascular tone (it is produced from L-arginine). According to Maruyama, et al., in laboratory studies nitric oxide inhibition increases portal hypertension and hepatic response to norepinephrine is increased.
The diagnosis of portal hypertension can be done via HVPG (hepatic venous pressure gradient) measurement has been accepted as the gold standard for assessing the severity of portal hypertension. Portal hypertension is defined as HVPG greater than or equal to 5 mm Hg and is considered to be clinically significant when HVPG exceeds 10 to 12 mm Hg.
The treatment of portal hypertension is divided into:
Selective shunts select non-intestinal flow to be shunted to the systemic venous drainage while leaving the intestinal venous drainage to continue to pass through the liver. The most well known of this type is the splenorenal. This connects the splenic vein to the left renal vein thus reducing portal system pressure while minimizing any encephalopathy. In an H-shunt, which could be mesocaval (from the superior mesenteric vein to the inferior vena cava) or could be, portocaval (from the portal vein to the inferior vena cava) a graft, either synthetic or the preferred vein harvested from somewhere else on the patient's body, is connected between the superior mesenteric vein and the inferior vena cava. The size of this shunt will determine how selective it is.
It should be noted that with the advent of transjugular intrahepatic portosystemic shunting (TIPS), portosystemic shunts are less performed. TIPS has the advantage of being easier to perform and doesn't disrupt the liver's vascularity.
Prevention of bleeding
Both pharmacological (non-specific β-blockers, nitrate isosorbide mononitrate, vasopressin such as terlipressin) and endoscopic (banding ligation) treatment have similar results. TIPS (transjugular intrahepatic portosystemic shunting) is effective at reducing the rate of rebleeding.
This should be gradual to avoid sudden changes in systemic volume status which can precipitate hepatic encephalopathy, renal failure and death. The management includes salt restriction, diuretics (spironolactone), paracentesis, and transjugular intrahepatic portosystemic shunt.
A treatment plan may involve lactulose, enemas, and use of antibiotics such as rifaximin, neomycin, vancomycin, and the quinolones. Restriction of dietary protein was recommended but this is now refuted by a clinical trial which shows no benefit. Instead, the maintenance of adequate nutrition is now advocated.
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