Portal Hypertension:     Introduction    

Introduction
 

 

Figure 1. Location of liver in the body.

As early as the 17th century, it was realized that structural changes in the portal circulation could cause gastrointestinal bleeding. In 1902, Gilbert and Carnot introduced the term "portal hypertension" to describe this condition. Portal hypertension is a pressure in the portal venous system that is at least 5 mm Hg higher than the pressure in the inferior vena cava. This increased pressure results from a functional obstruction to blood flow from any point in the portal system's origin (in the splanchnic bed) through the hepatic veins (exit into the systemic circulation) or from an increase in blood flow in the system.

Substantial progress has been made in understanding the pathophysiology of portal hypertension. This knowledge has led to the development of new therapeutic management approaches such as pharmacological therapies, endoscopic therapies, and surgical and radiological shunting procedures. Although many advances have been made in this field, the complications of portal hypertension (gastrointestinal hemorrhage, hepatic encephalopathy, hepatorenal syndrome, and ascites) continue to be the cause of significant morbidity and mortality. Portal hypertension remains one of the most serious sequelae of chronic liver disease. 

 


   
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General Info
 


What is Portal Hypertension?
Portal hypertension is a term used to describe elevated pressures in the portal venous system (a major vein that leads to the liver). Portal hypertension may be caused by intrinsic liver disease, obstruction, or structural changes that result in increased portal venous flow or increased hepatic resistance. Normally, vascular channels are smooth, but liver cirrhosis can cause them to become irregular and tortuous with accompanying increased resistance to flow. This resistance causes increased pressure, resulting in varices or dilations of the veins and tributaries. Pressure within the portal system is dependent upon both input from blood flow in the portal vein, and hepatic resistance to outflow. Normally, portal vein pressure ranges between 1–4 mm Hg higher than the hepatic vein free pressure, and not more than 6 mm Hg higher than right atrial pressure. Pressures that exceed these limits define portal hypertension.



  
Symptoms
Gastrointestinal hemorrhage may be the initial presenting symptom of patients with portal hypertension. Those patients with more advanced liver disease often present with ascites, hepatic encephalopathy , jaundice, coagulopathy, or spider angiomata. Patients who are hemodynamically stable may have warm skin, hyperdynamic pulses, and low systolic blood pressures in the range of 100–110 mm Hg. Additionally, splenomegaly and dilated abdominal wall veins are also indicative of portal hypertension. Splenomegaly can result in sequestration of platelets  from the systemic circulation, and low platelet counts may be the earliest abnormal laboratory finding. Hepatomegaly is variable and dependent upon the cause and stage of liver disease. Portal vein thrombosis may occur as a complication of portal hypertension but may also occur in cases of myeloproliferative or hypercoagulable disorders.


The clinical manifestations of portal hypertension may include caput medusae, splenomegaly, edema of the legs, and gynecomastia (less commonly) (Figure 2).

Figure 2. Clinical manifestations of portal hypertension

Caput medusae is a network of dilated veins surrounding the umbilicus. It is caused by increased blood flow in the umbilical and periumbilical veins and is often accompanied by an audible venous hum over the umbilical vein (Cruveilhier-Baumgarten murmur). Gynecomastia refers to the unilateral or bilateral abnormal enlargement of breast tissue behind the areola in males. It may be precipated by hormonal imbalance or hormone-secreting tumors, testicular or pituitary tumors, liver failure, and antihypertensive medications or medications containing estrogen or steroids. Edema, or swelling of the legs, is seen in portal hypertensive patients because of alterations in systemic hemodynamics.


 
 
Make an appointment today - call (410) 955-4166.
 

 

 
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