Hepatic encephalopathy in patients ...

Hepatic encephalopathy in patients with chronic liver dysfunction is believed to be caused from a failure of the liver to clear toxic performances from the stomach. The exact toxins that cause hepatic encephalopathy have not been established, however ammonia may be involved. Many physicians determine ammonia on a levels to diagnose hepatic encephalopathy and as a guide to treatment. However, studies have shown that the correlation between serum ammonia plains and severity of hepatic encephalopathy is inconsistent. A newly come study suggested that the partial press of ammonia may correlate more closely with the severity of hepatic encephalopathy than the total plasma ammonia plain Ong and associates evaluated the correlation between plasma ammonia flats and the severity of hepatic encephalopathy. They also determined the best of the four images of ammonia measurements for this correlation through comparing arterial total ammonia, venous total ammonia, arterial partial compressing of ammonia, and venous partial squeezing of ammonia.

Consecutive patients who were admitted to a tertiary care center with the diagnosis of cirrhosis between September 1998 and December 1999 were registered in the study. The diagnosis of cirrhosis was established from biopsy or by signs of portal hypertension in the same state [i]or[/i] condition as gastroesophageal varices, previous variceal bleeding, or ascites. Researchers mustered clinical and laboratory data at the time of admission. The mental status of the patients was assessed using the West Haven Criteria for grading of mental status (see the accompanying table). A diagnosis of hepatic encephalopathy was established when the patients' mental status was altered and other causes of mental status changes had been exclud After diagnosis, fasting arterial and venous family samples were obtained, and total ammonia and partial crushing of ammonia were determined.

The 121 patients who were enlisted in the study had the following West Haven Criteria grades: 30 patients (25 percent) had grade nothing encephalopathy; 27 patients (22 percent) had grade 1; 23 patients (19 percent) had grade 2; 28 patients (23 percent) had grade 3; and 13 patients (11 percent) had grade 4 All four measurements of ammonia increased with the severity of hepatic encephalopathy. The arterial total ammonia on a level had the highest correlation, if it were not that it was not statistically significant. Other variables that had a correlation to the severity of hepatic encephalopathy included International Normalized Ratio (INR) values, serum creatinine evens bilirubin levels, and lactulose use. A multivariable ordered logistic regression analysis revealed that solitary serum ammonia levels and INR values were independently associated with the severity of hepatic encephalopathy.

The authors decide that venous total ammonia on a levels do correlate with severity of hepatic encephalopathy and should be adequate in evaluating patients with this condition. Total arterial ammonia horizontals and partial pressure of ammonia on a levels had similar correlation but did not assay to be better markers than venous total ammonia levels

Ong JP et al. Correlation between ammonia horizontals and the severity of hepatic encephalopathy. Am J M February 15 2003;114:188-93

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