ACG Clinical Guideline: disorders of the hepatic and mesenteric circulation

Disorders of the mesenteric, portal, and hepatic veins and mesenteric and hepatic arteries have important clinical consequences and may lead to acute liver failure, chronic liver disease, noncirrhotic portal hypertension, cirrhosis, and hepatocellular carcinoma. Although literature in the field of vascular liver disorders is scant, these disorders are common in clinical practice, and general practitioners, gastroenterologists, and hepatologists may benefit from expert guidance and recommendations for management of these conditions. These guidelines represent the official practice recommendations of the American College of Gastroenterology. Key concept statements based on author expert opinion and review of literature and specific recommendations based on PICO/GRADE analysis have been developed to aid in the management of vascular liver disorders. These recommendations and guidelines should be tailored to individual patients and circumstances in routine clinical practice.

Tratamiento farmacológico de la hipertensión portal

Variceal bleeding is the most lethal complication of portal hypertension. Recent estimates have shown worldwide 50 million people with this entity, of which 60 percent have varices at the time of diagnosis and 20 percent bleeds each year. The mortality of each bleeding episode approaches 50 percent, the rate of recurrence in the first year after the initial hemorrhage is 60 percent and even higher in the first six weeks after bleeding. Treatment of portal hypertension must include the following aspects: 1)Treatment of active bleeding, 2)Prevention of recurrence and 3)Prevention of the first bleeding episode. Variceal bleeding never occurs with portal pressure below 12 mmHg, which means that although portal pressure is only one of the factors that determines the incidence of bleeding, reduction of portal pressure is the goal of the treatment. Pharmacologic treatment is based on vasoactive drugs that decrease portal pressure by a reduction of the blood flow that reaches the portal circulation (splanchnic vasoconstrictors), or through a reduction of the portal vein resistance (venodilators). Many drugs can reduce portal pressure, but few have received clinical evaluation. Vasopressin and somatostatin have been used successfully in the treatment of active variceal bleeding, the latter has shown absence of significant cardiovascular side effects commonly seen with the former. Addition of nitrates have increased the positive effects of vasopressin with a salutary reduction of side effects. Non selective batablockers such as propanolol and other compounds have been proved effective by several controlled studies and recent metaanalysis in the control of the recurrence of bleeding and the initial bleeding episode.

Ascitis. Fisiopatología y tratamiento

Cirrhosis of the liver is the main cause of ascitis. Recent studies have shown in compensated cirrhotics a 40 percent chance to develop ascitis after five years of follow up. The presence of ascitis is usually associated with advanced liver disease, and higher mortality than patients with compensated cirrhosis. Many theories have been proposed to explain ascitis formation being the most important the presence of portal hypertension and sodium retention. Extravascular fluid accumulation depends directly of a balance between hydrostatic and colloid-osmotic pressure (Starling law). Hepatic sinusoids differ from splanchnic ones in regard to the presence of fenestrae, that allows albumin and other substances to flow freely from the sinusoid to the extravascular space. For these reasons the sinusoids lacks colloid-osmotic pressure, and the hydrostatic pressure regulates the flow of fluids passing through them. In cirrhosis, diffuse fibrosis and nodule formation cause functional obstruction to the hepatic blood flow, and a secondary increase in the sinusoidal pressure, that leads to exit of fluids from the sinusoids to the hepatic lymphatics and the thoracic duct. When the amount of fluid that leaves the sinusoids exceeds the capacity of the thoracic duct, fluids accumulate in the abdominal cvity (ascitis). A new theory about ascitis formation states that the first event is a diffuse peripheral arterial vasodilation that cause ineffective plasma volume that triggers the production of humoral factors directed to retain sodium in the kidney...