Search results
Results From The WOW.Com Content Network
From November 1995 to November 1996 in France, a national survey of pediatric departments for children under 15 years of age with unexplained encephalopathy and a threefold (or greater) increase in serum aminotransferase and/or ammonia led to the identification of nine definite cases of Reye syndrome (0.79 cases per million children). Eight of ...
The serum-ascites albumin gradient (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites. [12] A high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension. A low gradient (< 1.1 g/dL) indicates ascites of non-portal hypertensive as a cause. [13]
ascites, and; liver enlargement. It is usually seen in younger adults, with the median age at diagnosis between 35 and 40 years, and it has a similar incidence in males and females. [2] The syndrome can be fulminant, acute, chronic, or asymptomatic. Subacute presentation is the most common form.
The diagnosis of hepatic encephalopathy is a clinical one, once other causes for confusion or coma have been excluded; no test fully diagnoses or excludes it. Serum ammonia levels are elevated in 90% of people, but not all hyperammonaemia (high ammonia levels in the blood) is associated with encephalopathy.
The serum-ascites albumin gradient (SAAG) is the most useful index for evaluating peritoneal fluid and can help distinguish ascites caused by portal hypertension (cirrhosis, portal vein thrombosis, Budd-Chiari syndrome, etc.) from other causes of ascites. SAAG is calculated by subtracting the albumin measure of ascitic fluid from the serum value.
This causes many of the sequelae of chronic liver disease including esophageal varices (with associated variceal bleeding), ascites and splenomegaly. The chronic inflammation seen in alcoholic hepatitis also leads to impaired hepatocyte differentiation, impairments in hepatocyte regeneration and hepatocyte de-differentiation into cholangiocyte ...
In general, people are more sensitive to pleural effusions then ascites; much smaller effusions can cause symptoms. [6] Most people have progressive difficulty breathing and reduced exercise tolerance. Rarely, there may be acute cases that accumulate fluid rapidly and result in circulatory collapse. [7]
Portal hypertension is defined as increased portal venous pressure, with a hepatic venous pressure gradient greater than 5 mmHg. [3] [4] Normal portal pressure is 1–4 mmHg; clinically insignificant portal hypertension is present at portal pressures 5–9 mmHg; clinically significant portal hypertension is present at portal pressures greater than 10 mmHg. [5]