Table 12. Causes of portal hypertension according to site of abnormality. - Гастроэнтерология (анг,рус) - Конспект лекций
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Гастроэнтерология (анг,рус)

Table 12. Causes of portal hypertension according to site of abnormality.

Fig. 5. Classification of portal hypertension according to site of vascular obstruction

 

Cirrhosis causes 90% or more of portal hypertension in adults in Western countries. Schistosomiasis is the most common cause of portal hypertension world-wide but it is infrequent outside endemic areas. Increased portal vascular resistance leads to a gradual reduction in the flow of portal blood to the liver and simultaneously to the development of collateral vessels, allowing portal blood to bypass the liver and enter the systemic circulation directly. Collateral vessel formation is widespread but occurs particularly in the gastrointestinal tract, especially the oesophagus, stomach and rectum, in the anterior abdominal wall, and in the renal, lumbar, ovarian and testicular vasculature.

Clinical features

Splenomegaly is a cardinal finding, and a diagnosis of portal hypertension is unlikely when splenomegaly cannot be detected clinically or by ultrasonography. The spleen is rarely enlarged more than 5 cm below the left costal margin in adults. Hypersplenism is common and frequently results in thrombocytopenia. Platelet counts are usually around 100 × 109/l; values below 50 × 109/l are rare. Leucopenia occurs occasionally, but anaemia can hardly ever be attributed to hypersplenism. Collateral vessels may be visible on the anterior abdominal wall and occasionally several radiate from the umbilicus to form a caput medusae. The most important collateral vessels occur in the oesophagus and stomach, where they can cause severe bleeding. Rectal varices also cause bleeding and are often mistaken for haemorrhoids.

Complications

Gastrointestinal bleeding from varices or from congestive gastropathy is the main complication. Hypersplenism is rarely severe enough to be clinically significant and portal hypertension is only one factor contributing to the development of ascites, renal failure and hepatic encephalopathy.

Table 13. Complication of portal hypertension.

Variceal bleeding occurs from oesophageal that are usually located within 3-5 cm of the oesophago-gastric junction or from gastric varices. Variceal bleeding is often severe, and recurrent bleeding occurs if preventative treatment is not given. Bleeding from varices at other sites is comparatively uncommon but most often occurs from varices in the rectum.

 

Ascites refers to the accumulation of free fluid in the peritoneal cavity. While cirrhosis is a common cause of ascites, there are many other causes.

 Table 14. Causes of ascites.

Ascites causes abdominal distension with fullness in the flanks, shifting dullness on percussion, and a fluid thrill when the ascites is marked.

Fig. 6. Abdominal swelling in ascites.

These signs do not appear until the ascites volume exceeds a litre even in thin patients. Associated features of ascites include distortion or eversion of the umbilicus, herniae, abdominal striae, divarication of the recti. Pleural effusions can be found in about 10% of patients, usually on the right side.

Table 15. Appearance and causes of ascites.

 

Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver disease. It occurs most often in patients with cirrhosis but also occurs in acute hepatic failure.

Liver failure and portosystemic shunting of blood are two important factors underlying hepatic encephalopathy.

Clinical features

These include changes of intellect, personality, emotions and consciousness, with or without neurological signs. When an episode develops acutely a precipitating factor may be found.

Table 16. Factors precipitating hepatic encephalopathy.

 

The earliest features are very mild but, as the condition becomes more severe, apathy, inability to concentrate, confusion, disorientation, drowsiness, slurring of speech and eventually coma develop. Convulsions sometimes occur. Examination usually shows a flapping tremor, inability to perform simple mental arithmetic tasks or draw objects such as a star.

 

Combination of changes of enzyme activity gives important diagnostic information:

1.      Cytolisis syndrome – increased activity of ALT, AST, LDG and hyperbilirubinemia with predominance of bound fraction indicates mainly necrotic damage of the liver.

2.      Cholestatic syndrome - increased activity of alkaline phosphotase in combination with hyperbilirubinemia, hypercholesterolemia and β-lipoproteinemia is typical to cholestatic hepatitis, long-standing and grave obstructive jaundice.

3.      Hepatic-cellular failure syndrome – decreased albumins, cholesterol, protrombin contents in combination with hyperbilirubinemia.

4.      Immunoinflammatory syndrome – increased γ-globulins level, hyperproteinemia, elevated thymol test and immunoglobulins G and M contents are typical to immunoreactive damage of the liver.

 

 

 

 

 

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