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At least 91 records · Page 5Linked to original sources
PubMed1978

Tryptophan and hepatic coma.

To clarify the involvement of tryptophan in the pathogenesis of hepatic coma, plasma and cerebrospinal fluid (CSF) tryptophan was studied in three patient groups (hepatic coma, stable cirrhosis, and control). An assessment of free fatty acids, some of the amino acids reported to compete with tryptophan for brain uptake, and albumin was also made. The data demonstrated that, whereas the elevated CSF tryptophan levels in cirrhotic patients compared to controls may have been attributable to decreased plasma branched chain amino acids, the elevated CSF tryptophan levels in hepatic coma compared to stable cirrhotic patients were probably attributable to increased plasma free tryptophan concentrations. Associated with the elevated plasma free tryptophan in coma patients was an increase in plasma free fatty acids and a marked decrease in serum albumin levels. Of all the amino acids investigated in the CSF, only tryptophan was significantly increased in patients in hepatic coma compared to cirrhotic patients not in coma.

Amino Acids↗
PubMed1979

[Eliciting factors and clinical picture of hepatic coma in 152 patients with cirrhosis of the liver (author's transl)].

Exogenous hepatic coma was found 102 times (group A) and a combination of exogenous and endogenous hepatic coma 50 times (group B) in 152 patients with hepatic coma. The most frequent eliciting factors in group A were too high a protein supply and gastrointestinal hemorrhage and diuretics, in group B necrotic exacerbations and infections, 2/3 of them having severe portal hypertension with ascites and esophageal varices at the same time. A typical fetor hepaticus was found in only 25% of group A and 50% in group B. 10% had a primary liver cell carcinoma. The prognosis depends largely on the stage of the coma and the treatment of the eliciting factors. Altogether 50 of the 152 hepatic coma patients died. The most frequent complication was a terminal renal failure which no longer responded to therapy.

Acute Kidney Injury↗
PubMedDate not supplied

Intensive therapy for hepatic coma.

Of 45 patients observed in the ICU with severe acute hepatic insufficiency, 15 patients were in hepatic coma. All patients received combined treatment consisting of standard conservative methods (drug therapy) and surgical methods for temporary support of liver function (hemodialysis, exchange blood transfusion, pig liver perfusion). Intensive therapy which began during the early phase of hepatic coma enabled us to bring six patients out of the coma, four of whom completely recovered. These studies showed that of the diseases causing hepatic coma, the worst results were obtained with viral hepatitis. This may be explained both by the extensive liver damage and marked metabolic disturbances, which led to failure of other vital organs and systems. At present, the combined therapy contributes to a greater percentage of recovery of patients with hepatic failure and coma.

Adrenal Cortex Hormones↗
PubMed1977

[Pathology of liver failure and hepatic coma (author's transl)].

Liver failure and hepatic coma present with various clinical and morphological counterparts. While fulminant viral hepatitis is the most common cause of acute liver failure, liver cirrhosis with vascular bypass most often is responsible for the hepatic coma in chronic diseases. Prognosis is mainly determined by the extent of liver cell necrosis and regeneration, provided extrahepatic complications do not cause death. Prognosis can best be judged by stereology of liver biopsies and determination of the alpha-fetoprotein.

Alcoholism↗
PubMed1977

Clinical course and prognosis of one hundred and two patients with hepatic coma 1958 through 1975.

The clinical course and prognosis of hepatic coma were examined in 102 patients treated in the period from 1958 to 1975. The diagnoses included 9 fulminant hepatitis, 7 subacute hepatitis, 53 liver cirrhosis without liver carcinoma (40 cases of the acute type, 10 cases of the chronic type and 3 cases of another type, according to Sherlock's classification of hepatic coma) and 33 liver cirrhosis with primary liver carcinoma. Four of 9 fulminant hepatitis patients gained consciousness within 1 week and recovered completely. Seven subacute hepatitis patients died within 2 weeks after onset of hepatic coma. In the period from 1958 to 1969, 20% of liver cirrhosis patients with the acute type of coma recovered from coma, and in the period from 1970 to 1975, 45% of patients recovered. Seven of 10 patients with the chronic type of coma died between 4 months and 9 years after the onset of coma. Three other patients are presently still alive. The median survival time was 2.5 years. Nine primary liver carcinoma patients with coma were hospitalized from 1958 to 1969 and 24 from 1970 to 1975. Hepatorenal syndrome was present in 31 of 71 examined patients. Twenty-three patients with hepatorenal syndrome were in the period from 1970 to 1975.

Adolescent↗
PubMed1976

L-dopa in hepatic coma.

The use of L-Dopa in hepatic coma has been the subject of numerous reports since 1970. The following represents our experience with a rather heterogenous group of patients treated at the Massachusetts General Hospital over the past 4 years. Thirty-five patients with severe liver disease, a mean age of 53 +/- 3.5 years, including nutritional cirrhosis with acute coma and acute hepatitis were treated. Four patients were judged grade III, 31 patients grade IV. All patients had previously been treated with protein restriction, orally administered non-absorbable antibiotics, fluid and electrolytes, and in some cases, steroids. L-Dopa was given orally in 21 patients, and as a retention enema in 14. Thirteen of the 35 patients did not respond to therapy. Seventeen responded, but did not survive, and 5 patients responded and survived. There was no difference between any of the groups as far as dosage of L-Dopa and clinical features. The one striking finding as the differences between groups was the time of initiation of L-Dopa therapy. In Group I, the survivors, therapy was started within 1.4 +/- 0.8 days after the onset of coma. In Group II, there was an initiation of therapy at 6.7 +/- 1.6 days, and in the non-responders 9.5 +/- 1.6 days. These differences are highly significant. The results suggest that coma may pass from a reversible to an irreversible stage, and that L-Dopa therapy initiated early in the course of hepatic coma, may be of some benefit.

Alcoholism↗
PubMed1983

[Hepatic coma. Principles of pathogenesis and treatment. 2: Treatment, prognosis].

According to the multifactorial pathogenesis of hepatic coma, generally caused by the increased formation of toxic protein metabolites in the gut, the most important therapeutical measure is the cleaning and acidifying of the gut. This is possible very simply and cheaply by high enemas of sodium acetate buffers of pH 4,5 and lactulose. If necessary, neomycin or paromomycin must be administered in high doses of 6--8 gm/daily to reduce the pathogenic intestinal bacteria. The detoxification capacity of liver and brain can be improved by intravenous and later oral administration of ammonia reducing amino acids such as arginine, ornithine, and aspartic acid (10--20 gm/daily). They diminish also the elevated serum phenols. Very helpful are also branched chain amino acids which improve apparently the detoxification capacity of the muscle. Very important is the normalization of disturbances of the water and electrolyte balance, especially the normalization of hypokalemia. Very difficult is a successful treatment of cerebral edema and the disturbances of blood coagulation. In special cases of endogenous hepatic coma liver perfusions, hemodialysis, charcoal perfusions a.s.o. can eliminate successfully toxic protein metabolites, whilst this treatment is generally insufficient in the more frequent exogenous hepatic coma. In summary the prognosis of hepatic coma is also nowadays very serious and can only be improved by the early recognition and elimination of exacerbating factors.

Combined Modality Therapy↗
PubMed1995

[Effect of lactitol (NS-4) on the increase in blood and brain ammonia concentration and on coma in newly developed rat models of hepatic coma].

Encephalopathy caused by hepatic cirrhosis is often associated with portasystemic shunt and hepatic parenchymal injury. Together, these are known as a combined-type symptom. Two experimental hepatic comatose models with combined-type symptom were developed in rats. Both of these models involve the administration of ammonium acetate (500 mg/kg) into the cecum in portacaval shunted (PCS) rats. In addition, hepatic injury was induced in one model by carbontetrachloride (CCl4) and in the other by dimethylnitrosamine (DMNA). These model rats showed a higher increase in the concentration of ammonia in the blood and a higher incidence of coma as determined by the loss of the righting reflex than did rats subjected to a shunt only (PCS operation + ammonia loading) or hepatic parenchymal injury only (CCl4 treatment + ammonia loading). The effect of lactitol, administered orally for 7.5 days, on the experimental hepatic coma was compared with that of lactulose. Lactitol significantly inhibited the increase in blood and brain ammonia concentration at doses of 3 and 6 g/kg/day and also reduced the incidence of coma. The effects of lactitol were similar to those of lactulose, a therapeutic agent for hepatic encephalopathy. Therefore, lactitol should be useful in the clinical treatment of hyperammonemia or hepatic encephalopathy.

Ammonia↗