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At least 55 records · Page 3Linked to original sources
PubMed1976

[Acute hepatic coma. Experimental study on the predictive value of clinical-chemical findings for the prognosis of acute hepatic coma].

In order to determine the validity of clinical-chemical parameters for the prognosis of hepatic failure, 28 pigs were subjected to liver ischemia for 40--160 minutes duration. The following parameters were studied: GOT, GPT, gamma-GT, LAP, LDH, GlDH, AP and isoenzymes, total bilirubin, potassium, sodium and chloride. In a statistical comparison in the surviving animals, an unexplainable increase in GlDH activity was observed. In the other clinical-chemical parameters none was seen to be of use for the prognosis for either life or death in acute hepatic failure.

Acute Disease↗
PubMed1984

Cerebral abnormalities in hepatectomized rats with acute hepatic coma.

When hepatectomized rats develop hepatic coma, they are found to have cerebral edema, together with a failure of the blood-brain barrier to contain materials usually limited to the circulation. The present studies were carried out to characterize the associated ultrastructural changes in the barrier. Rats were allowed to develop hepatic coma after a two-stage hepatectomy. Electrocortical and behavior monitoring during this period indicated deterioration similar to that seen in man with acute liver injury; the water contents of the brains of the animals in hepatic coma were increased. Electron microscopic examination of the brains from control rats and animals with hepatic coma were carried out after perfusion fixation. The examination of the brains from the comatose animals showed the appearance of greatly increased numbers of vesicles in the capillary endothelium and a marked watery swelling of adjacent astrocytes, which seemed to begin in foot processes and then to spread through the cell. Intravenous peroxidase was given to most rats in the late stages of coma, and the tracer was found to be included within the capillary endothelial vesicles. Occasional accumulations of peroxidase in the underlying capillary basement membrane were found. No interendothelial cell distruption was found. Low molecular weight microperoxidase was used as well as horseradish peroxidase; the results were the same with both compounds. The findings indicate as association between capillary endothelial vesicle formation and the cerebral edema found in animals with hepatic coma following hepatectomy.

Animals↗
PubMed1983

[Causes and diagnostic criteria of hepatic coma--an analysis of 560 cases].

560 patients with hepatic coma were treated during the years 1958 to 1982 in Homburg and Bad Kissingen . 82 patients had an endogeneous and 478 an exogeneous hepatic coma. Endogeneous hepatic coma was caused most frequently by fulminant virus hepatitis, intoxication, and hepatorenal syndrome accompanying serum hepatitis. Exogeneous hepatic coma in patients with cirrhosis of the liver was caused in most cases by gastrointestinal bleeding, by a diet too high in protein, or by excessive diuresis. Early clinical symptoms are changes in writing tests and ability to concentrate, whereas hepatic foetor occurs in coma stage III and IV. Clinical chemistry findings pointing to imminent hepatic coma are increase of arterial ammonia in exogeneous hepatic coma, and increase of free phenols in endogeneous hepatic coma. The increase of prothrombin time is prognostic for imminent hepatic coma in both types. Prognosis of endogeneous hepatic coma is still rather bad; 87% of the patients suffering from it died; in exogeneous hepatic coma prognosis has improved for stage I and II in the last 23 years, whereas however the total prognosis for all 4 stages is still unchanged, letality being 55%.

Adult↗
PubMed1983

A study of disseminated intravascular coagulopathy in hepatic coma complicating acute viral hepatitis.

Thirty cases of viral hepatitis with and without coma and 15 normal healthy age and sex matched controls were studied for disseminated intravascular coagulopathy (DIC). Cases of viral hepatitis with coma showed strong evidence of DIC in the form of increased plasma FDP (240 +/- 190.64 dilution), diminished fibrinogen half life (48.1 +/- 15.3 hours) and increased fractional catabolic rate (46.13 +/- 14.7% per day) with normal Euglobulin clot lysis time and reduced fibrinogen (147.33 +/- 43.5%) and platelet count (1.27 +/- 0.324 lakhs/cm.). The possible role of heparin in the reversal of coagulation abnormalities have been discussed.

Adult↗
PubMed1984

[Hepatic coma in fulminating viral hepatitis--treatment results in 1981 in a district hospital].

n the basis of clinical case reports on liver disintegration comata in foudroyant virus hepatitis the coma therapy was explained which was performed in the clinic for infectious and tropic diseases of the County Hospital St. Georg Leipzig in 1981 and this therapy was compared with the possibilities mentioned in literature. The aim of the article was to determine the present position of a county hospital in the great number of forms of therapy proposed. The basic therapy aimed at the reduction of neurotoxic protein metabolites and the application of intensive-medical therapeutic methods in interdisciplinary cooperation of internal specialist, specialist in dialysis and haemostaseologist are valuated as successful. The combined haemoperfusion/haemodialysis--two out of three patients treated survived--as a constituent of the present concept of therapy is assessed positively.

Adult↗
PubMedDate not supplied

[Hepatic coma. The nursing care].

The hepatic coma is an entity tending to occur as a complication of severe hepatic diseases and in which the recognition of symptoms and signs by the personnel caring for those patients is essential for the early detection of this condition. A review of the literature is made making emphasis on the pathogenesis, clinical picture and the trigger factors of the hepatic coma. The nursing care for patients with hepatic coma are described; stressing that the nursing diagnosis of the first signs Ia essential for the prognosis and the clinical course of these patients. It is pointed out how health education in these patients is oriented to maintain and improve their health condition, to have a better response to the treatment and to avoid a relapse in prone patients.

Combined Modality Therapy↗
PubMed2003

Increased concentrations of histamine and its metabolite, tele-methylhistamine and down-regulation of histamine H3 receptor sites in autopsied brain tissue from cirrhotic patients who died in hepatic coma.

BACKGROUND/AIMS: Hepatic encephalopathy (HE) is a serious neuropsychiatric complication of chronic liver disease. To determine whether changes in the central histaminergic system are a feature of human HE, we studied histamine, tele-methylhistamine, and presynaptic autoregulatory H(3) receptors in cerebral cortex and caudate-putamen obtained at autopsy from six cirrhotic patients and six appropriately matched controls. METHODS: Histamine was assayed by HPLC; tele-methylhistamine by GC-MS. H(3) receptors were studied by in vitro receptor binding using [3H]R-alpha-methylhistamine as ligand. RESULTS: In HE patients, there was a significant fourfold increase of histamine in caudate-putamen and a significant increase in all cortical regions studied. tele-Methyhistamine was also increased and the densities of histamine H(3) receptor sites were significantly decreased in patient material. CONCLUSIONS: These findings are consistent with activation of the histaminergic system in HE. Given that histamine participates in the regulation of arousal and circadian rhythmicity, they indicate that induction of central histamine mechanisms may contribute to the development of neuropsychiatric symptoms, such as sleep disturbances and altered circadian rhythms in chronic HE and suggest that pharmacological manipulation of the histaminergic system could be beneficial in the treatment of HE in chronic liver failure.

Adult↗
PubMedDate not supplied

[Endogenic hepatic coma in the course of acute hepatitis treated with arterialization of portal blood].

Symptoms of endogenic hepatic coma were observed in the course of acute hepatitis in 17 patients admitted to the I Clinic of Infectious Diseases of Silesian Medical School between 1987 and 1992. Five of them were treated with the arterialization of portal blood. At least one exchange transfusion preceded the arterialization in four cases. Recovery was obtained in 3 patients. Two patients died because of complications which occurred during the twenty-four hours after the intervention. In the first case the reason of the death was the extensive myocardial infarction, in the second one-DIC and ARDS. As it has been observed, the prothrombin rate should not be lower than 30% in these patients who are to undergo the arterialization of portal blood. This value of the prothrombin rate is provided by at least one exchange transfusion.

Adult↗
PubMed1982

Successful treatment of hepatic coma probably caused by acute infectious hepatitis with balanced solution of amino acids.

Therapy with balanced amino acid solution enriched in branched amino acids has been reported to favourably influence hepatic encephalopathy due to liver cirrhosis. We here report the same favourable effect in 3 patients aged 29, 30 and 41 yr with hepatic coma at least in part induced by acute viral hepatitis. The patients regained consciousness within 8, 12 and 12 h, respectively. The treatment was continued for 9, 6 and 5 days, respectively.

Adult↗
PubMed1986

Brain cholecystokinin and vasoactive intestinal polypeptide: immunoreactivity in rabbits with hepatic coma.

Recent studies have suggested that decreased excitatory neurotransmission in the brain may contribute to the overall neural inhibition which characterizes the syndrome of hepatic encephalopathy (HE), and that vasoactive intestinal polypeptide (VIP) and cholecystokinin (CCK) may promote neural excitation in the brain. To determine if brain levels of these neuropeptides are altered in HE, measurements were made of the concentrations of immunoreactive VIP (iVIP) and immunoreactive CCK (iCCK) in cerebral cortex, cerebellum and hypothalamus isolated from normal rabbits and rabbits with galactosamin-induced hepatic coma. Hepatic coma was associated with reduced concentrations of iVIP, small molecular weight iCCK and large molecular weight iCCK in the cerebral cortex but not in the cerebellum or hypothalamus. These findings are compatible with decreased VIP- and CCK-mediated neural excitation occurring in the syndrome of HE.

Animals↗