Hepatic congestion

Claims for acute hydrogen sulfide exposure that occurred over a 5-year period (1969-1973) in Alberta, Canada, primarily among petrochemical workers, were reviewed by Burnett et al. (1977). Acute effects noted included coma, disequilibrium, and respiratory insufficiency with pulmonary edema. Of 221 cases, there were 14 deaths. A follow-up study of 250 workers claims for hydrogen sulfide exposure from 1979 to 1983 in Alberta, Canada, found 7 fatalities that usually involved the central nervous and respiratory systems hepatic congestion and cardiac petechiae were also noted (Arnold et al. 1985). The difference in fatality rate (6% down to 2.8%) was attributed to improved first aid training and an increased awareness of the dangers of hydrogen sulfide. 

When drugs are administered orally, they typically are absorbed in the small bowel, enter the portal circulation, and pass through the liver. Both CYP enzymes in the bowel wall and in the hepatocytes can metabolize a fraction of the drug before it reaches the systematic circulation (i.e., first-pass metabolism or first-pass effect). The extent of this effect can be broadly altered by diseases (e.g., cirrhosis, portacaval shunting, persistent hepatitis, congestive heart failure), and by some drugs (e.g., alcohol, ketaconazole, fluoxetine) influencing the peak concentrations achieved and the ratio of the parent compound to metabolites ( 11, 19, 20). 

Diseases that directly affect hepatic integrity include cirrhosis, viral infections, and collagen vascular diseases. Diseases that indirectly affect function include metabolic disorders (e.g., azotemia secondary to renal insufficiency) and cardiac disease. Although decreased left ventricular output can result in a decrease in hepatic arterial flow, right ventricular failure causes hepatic congestion, reducing the first-pass effect and delaying biotransformation. 

It was noted that she had gram-negative rods on her blood smear her blood culture grew penicillin-sensitive Streptococcus pneumoniae, in 6 hours. At autopsy, she was noted to have Streptococcus pneumoniae endocarditis of the right ventricle, focal ischemia of the left ventricle, bilateral pleural effusions, hepatic congestion with thrombosis, renal congestion, bilateral adrenal hemorrhage, and necrosis. Death was due to septic shock from Streptococcus pneumoniae. 

Primary pulmonary diseases (e.g. primary pulmonary hypertension, pulmonary fibrosis, chronic obstructive respiratory diseases) cause chronic hepatic congestion due to chronic pulmonary heart disease, possibly leading to insufficiency. Hypoxaemia as a result of acute or chronic respiratory insufficiency can impair metabolic liver functions considerably. In 40—70% of patients with cirrhosis, hypoxaemia can be found in about 50% of cases with advanced cirrhosis, a reduced diffusion capacity for CO is detectable. Furthermore, pulmonary tissue contains a high level of glutamine synthetase, so that ammonia detoxification is possible (ultimately by perivenous hepatocytes) before the blood reaches the systemic circulation. In existing pulmonary diseases, localized ammonia detoxification is impaired. 

Liver damage was reported in 22 (0.35%) of 6294 patients given disopyramide, with jaundice in 6 (0.09%) (17). Liver damage due to disopyramide can be associated with direct hepatocellular damage (18) and intrahepatic cholestasis (19,20). However, it can also occur indirectly, because of heart failure and hepatic congestion (21). Thus, the incidence of direct liver damage quoted above may be an overestimate. 

Maintenance dosages should be reduced in the presence of renal or hepatic impairment, including hepatic congestion due to cardiac failure (58). 

Animals are susceptible to toxicity following Convallaria majalis exposure. In one case report, a dog that ingested an unknown quantity of lily of the valley leaves suffered seizures and death. Autopsy findings revealed severe hepatic congestion and caudal vena cava distention. Gross and microscopic lesions consistent with cardiac shock were also evident. Leaves of the plant were found in the middle section of the jejunum. Animals exposed to... 

Other additional studies or pertinent information which lend support to this MRL Studies of w orkers exposed to 1,1-dimethylhydrazine have reported changes indicative of a hepatic effect (elevated serum alanine aminotransferase activity, positive cephalin flocculation test) (Petersen et al. 1970 Shook and Cowart 1957). Angiectasis was observed in the livers of all exposed mice. Hepatic congestion was noted in mice exposed to 0.5 or 5 ppm 1,1-dimethylhydrazine (Haun et al. 1984). No NOAEL was identified. 

Primary peritonitis in adults occurs most commonly in association with alcoholic cirrhosis, especially in its end stage, or with ascites caused by postnecrotic cirrhosis, chronic active hepatitis, acute viral hepatitis, congestive heart failure, malignancy, systemic lupus erythematosus, or nephritic syndrome. It also may result from the use of a peritoneal catheter for dialysis or central nervous system ventriculoperitoneal shunting for hydrocephalus. Rarely, primary peritonitis occurs without apparent underlying disease. 

Pyruvic and a-ketoglutaric acids are increased in the blood of patients with decompensated cardiac failure it is likely that these changes are related to the hepatic congestion, as they are not found in patients with mitral stenosis without decompensation (D14). 

In diseases where there is interference with the hepatic circulation —hepatic congestion, compression of the i>ortal vein by biliary calculi, cirrhosis, atrophy, fatty degeneration, etc. 

The oral bioavailability and pharmacokinetics of hydralazine are not altered significantly by heart failure unless there is severe hepatic congestion or hypoperfusion. Intravenous hydralazine provides little practical advantage over oral formulations except for urgent use during pregnancy, a state in which relative or absolute contraindications exist for most other vasodilators. 

Acetaminophen-induced hepatotoxicity has been reported to occur with hepatic congestion in humans (Rose 1969 Thompson et al. 1972) and rodents (Dixon et al. 1971 Walker et al. 1980,1985). In mice, it occurs early and before the appearance... 

L superpuiga-tion, colic, fSeira on, ret and hepatic congestion... 

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