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At least 199 records · Page 11Linked to original sources
PubMed1975

Silent acute pancreatitis with encephalomalacia mimicking hepatic coma.

A very rare case of acute pancreatitis with concurrent encephalomalacia and ascites mimicking hepatic coma is described. The possibliity that the pancreatitis was caused by the administration of chlorothiazide in a diabetic patient is suggested as possible etiology. It is emphasized that when a cirrhotic patient develops coma, the possibility of painless,silent pancreatitis with encephalomalacia as well as hepatic coma should be considered in the differential diagnosis.

Acute Disease↗
PubMed1989

Reduction of highly elevated plasma levels of gamma-aminobutyric acid does not reverse hepatic coma.

The pathogenesis of coma in patients with fulminant hepatic failure is still unknown, but there is some evidence that decreased hepatic metabolism of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) may be involved. If this hypothesis is true, reduction of increased GABA levels in patients with hepatic encephalopathy should reduce the depth of hepatic coma. In the case described here, highly elevated plasma GABA levels were reduced by cross-circulation with baboon liver. No amelioration of the coma was observed, thus suggesting that decreased hepatic metabolism of GABA is not critically involved in hepatic encephalopathy.

Adult↗
PubMed1988

Serum apoproteins A and B and the lecithin: cholesterol acyl transferase activities in liver cirrhosis and hepatic coma patients.

Serum apoproteins A and B and LCAT activities were estimated in 80 patients, 46 with posthepatic cirrhosis and 34 with alcoholic cirrhosis. The cirrhosis patients were also divided into compensated, decompensated, and hepatic coma subgroups. Apo-A and LCAT activities were significantly decreased in both cirrhotic groups without any significant difference between posthepatitic and alcoholic cirrhotic groups, while Apo-B was decreased in hepatic coma patients only. The decompensated cirrhosis patients showed lower Apo-A levels than the compensated cirrhosis patients and hepatic coma patients showed still lower levels compared to decompensated subgroup, while no significant decrease was observed in LCAT activities between compensated and decompensated cirrhosis patients. Apo-A level was correlated more significantly with serum albumin level than the LCAT activity. The study confirms that Apo-A level is highly related to the degree of liver injury and also suggests that this decrease may be mainly due to impaired liver synthesis and that the serum levels of Apo-A and Apo-B can be utilized in the differential diagnosis of chronic liver diseases.

Adult↗
PubMed1981

[On the neuro-psychiatric symptomatology of the so-called "hepatic coma" (author's transl)].

The definition of hepatic coma has been used for the most severe course of hepatic insufficiency, independent from the pathogenesis. This means, that from the psychiatric point of view the hole survey of the exogen reaction type was subdivided. The neurologic symptomatology was rather neglected. In this study an attempt is made to show--using the reports of 77 patients with severe hepatic insufficiency of different etiology--that with very exact and repeated examinations a typical course of neuro-psychiatric symptoms can be observed. A distinct hierarchy of symptoms is existing, which is similar to the well known princip of dissolution (Jackson). As a main factor one has to differentiate between an acute and a subacute course. The acute course is characterized by a rapid decrease of vigilance and increase of neurologic symptoms, which end in most of the cases with an acute midbrain- and bulbarbrain-syndrome, while the subacute course shows primary a disturbance of thymo- and noopsychic function in different relations. In addition to the organic "Achsensyndrom" amnestic or amentiell symptoms can be found, which might be covered by a decrease of the vigilance--if the primary noxis continoues--end up with unconsciousness. The parallel developing neurologic symptomatology shows a distraction of the general motoric, including so-called basic movements. later stereotypies and automatismes, and the delicate distal movements change into rough general-rotation-and pointing movements of the hole body. There is also a temporary bending of all extremities and at this time also a rigidospasticity. In the following course preponderate transient bending or stretching, finally there exists a lack condition, which does not respond to external provocations. The symptomatology is not always symmetric. Transient or longstanding hemiparetic symptoms and also crossed brainstem symptoms can be seen frequently. Sometimes there are general or focal epileptic seizures. If a brain edema occurs it leads to a tentorial herniation with the symptoms of an acute midbrain- or bulbarbrain syndrome, which exists in nearly every second patient. If the course turns, the clinical symptomatology is passed in reverse direction. A good relation exists to the known biochemical changes. The disturbed monoaminmetabolism influences the structures, which are important for the vigilance. The serotonin and 5-hydroxyindolaminoacid level in the tegmentum and the hippocampus are increased. Worth to mention, that this is not a specific hepatic disturbance. Additional one can find false transmitters, for example octopamin, which are concerning the excitation, less potent than dopamin or noradrenalin and also a decrease of the latter in the extrapyramidal structures, which corresponds very well with the motoric deficiency and defectsymptoms. Not all of the symptoms can be explained by disturbances of the catecholaminmetabolism. It seems, that electrolyt and acid-base disturbances are also of some value...

Acetoin↗
PubMed1994

[Hepatic coma].

The term "hepatic encephalopathy" describes the neuropsychiatric signs and symptoms of patients with acute or chronic liver disease, irrespective of the presence or absence of liver cirrhosis. Cerebral edema, the pathophysiology and treatment of which being quite different from hepatic encephalopathy, is the leading cause of death in patients with acute liver failure. Lactulose (orally or as enema) is one of the cornerstones of the treatment of hepatic encephalopathy; most important for the management of patients with cerebral edema is close monitoring (including intracranial pressure monitoring) of the patients and rapid reduction of intracranial pressure (e.g. with mannitol). The pathophysiologic and therapeutic concepts in the care of patients with hepatic encephalopathy and cerebral edema are described.

Blood-Brain Barrier↗
PubMed2006

Effects of L-acetylcarnitine on cirrhotic patients with hepatic coma: randomized double-blind, placebo-controlled trial.

Multiple therapeutic modalities have been used to treat hepatic encephalopathy. L: -Acetylcarnitine (LAC) is a physiologically active substance that improves both the energetic and the neurotransmission profiles. LAC is able to cross the hematoencephalic barrier and reach the cerebral regions, where the acetylic group may be utilized. The aim of this work was to evaluate the efficacy of LAC in the treatment of hepatic coma in cirrhotic patients. Twenty-four suitably selected patients were enrolled in the study and, following randomization, received either LAC (n=13) or placebo (n=11). Statistically significant differences in neurological findings, as evaluated by the Glasgow Scale, as well as in ammonia serum levels and BUN were found following LAC treatment. In the placebo group we observed two cases of improved neurological findings as well as one case of improved EEG grading. In the other group we observed an improvement of neurological findings and of EEG grade in 10 and 8 subjects, respectively. Noteworthily, seven (54%) patients went from grade 4 down to grade 3, and one from grade 4 down to grade 1. The improvement in the neurological picture was evident at between 1 and 4 hr after the end of treatment, remaining until 24 hr after. No side effects were observed in our study series. Our study demonstrates that LAC administration improved neurological and biohumoral symptoms in selective cirrhotic patients with hepatic coma.

Acetylcarnitine↗
PubMedDate not supplied

[Plasmapheresis in the treatment of hepatic coma].

Fourteen patients, including 6 with viral hepatitis B and 8 with liver cirrhosis were treated with plasmapheresis for hepatic coma. Altogether 29 plasmaphereses were carried out. Complete recovery was achieved in one patient with viral hepatitis B and in 3 patients with liver cirrhosis. Plasmapheresis should be performed in patients with severe lesions to the liver. Classification of patients to the treatment should include clinical examination, biochemical and enzymatic tests, and evaluation of liver reserve with isotope hepatography. In case of the acute poisoning with hepatotoxic agents indications to plasmapheresis should be evaluated from the toxicologic point of view.

Adolescent↗
PubMed1977

[Effect of exchange transfusion on the plasma amino acid concentration in hepatic coma].

Exchange transfusion (ET) were made twice on a 22 year old patient with fulminant hepatitis and hepatic coma. The influence of the ET on the plasma amino acids (PAA) was examined. The 1. ET reduced the concentration of the total PAA from 10,023 to 7,152 mugmol/l (about 28.6%) and the 2. ET from 11,770 to 9,706 mugmol/l (about 17.5%). Three hours after the 1. ET the concentration of the total PAA has passed over the prevalue and after the 2. ET has nearly reached it. The influence of both ET on the concentration of the individual PAA was very different (- 47.9% to + 71.2% after the 1. ET and - 32.9% to + 41.8% after the 2. ET respectively). Therefor the ET seems to be not a suitable method to reduce the pathologic concentration of the PAA in the hepatic coma.

Adult↗
PubMed1994

Flumazenil in cirrhotic patients in hepatic coma: a randomized double-blind placebo-controlled crossover trial.

Previous reports have suggested that "endogenous" benzodiazepines could contribute to neural inhibition in hepatic encephalopathy. RO 15-1788 (flumazenil), a specific antagonist of brain benzodiazepine receptors, could thus reverse the neurological symptoms of hepatic encephalopathy. To test this possibility, we conducted a double-blind, placebo-controlled crossover trial of the efficacy of flumazenil in cirrhotic patients in hepatic coma. Seventy-seven cirrhotic patients in hepatic coma were evaluated. Fifty-six were excluded from the trial because of multiorgan failure or because coma was precipitated by prior use of benzodiazepines, and 21 patients were randomly assigned to the flumazenil group (11 patients) or the placebo group (10 patients). Treatment was administered intravenously as a 20-ml solution (placebo or 2 mg flumazenil); seven patients were crossed over. Clinical status was assessed blindly by two observers, using a modified Glasgow scale, every 15 min for 6 hr. Electroencephalogram tracings obtained before and after drug administration were evaluated blindly by two independent observers. Serum concentrations of benzodiazepines before treatment were measured by means of a fluorescence polarization immunoassay. Improvement in neurological symptoms was observed in six patients treated with flumazenil, whereas none in the placebo group showed improvement (p < 0.05; Fisher's exact test). Improvements in electroencephalogram tracings were demonstrated in four patients treated with flumazenil, compared with two patients in the placebo group (p = NS). Benzodiazepines were found in the serum of four patients treated with flumazenil (two responders and two nonresponders); all of these patients had received pharmaceutical benzodiazepines 4 to 6 days before the trial.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1981

[Infection in patients with hepatic coma (author's transl)].

66 patients with hepatic coma were treated from 1972 to 1979 in the intensive care unit. Incidence and etiology of bacterial infections in these patients were evaluated retrospectively. Bacterial cultures were positive in a high proportion of the cases investigated as compared to the situation on a normal ward. Bacterial cultures were performed in 51 patients (77.3%); cultures from 35 patients were positive. Gramnegative bacteria accounted for 56.4%, grampositive bacteria for 34.8% and candida albicans for 8.8% of all the cases. It is pointed out, that invasive diagnostic and therapeutic manoeuvers in intensive care patients carry a high risk of infection.

Adolescent↗
PubMed1980

[Experience in treating hepatic coma by extracorporal liver perfusion (author's transl)].

19 extracorporeal liver perfusions have been performed for treating hepatic coma in 11 patients. No improvement was found in 3 patients, improvement in 8.5 of these 8 patients recovered full consciousness. All 7 patients with pre-existent liver disease died. Of 4 patients without pre-existent liver disease, 2 were discharged and are still alive. At present, extracorporeal liver perfusion seems to be the most promising treatment for hepatic coma. It should be undertaken at Stage IV and at Stage III with increasing prothrombin time. Pre-existent liver disease should be excluded before by laparoscopy.

Adult↗
PubMed1976

[Treatment of hepatic coma using extracorporeal perfusion with baboon and human liver as well as with activated charcoal].

In the 6 patients with hepatic coma hemoperfusions with 8 baboon and 2 human livers were carried out. Four awoke from the coma, one women could be discharged, but the others died of various complications and liver insufficiency. In the 4 patients with hepatic coma, 11 hemoperfusions with activated charcoal columns were performed. Two awoke from the coma, but they died of liver insufficiency. We were able to detect the elevation of preforming antibodies in a discharged patient.

Acute Disease↗
PubMed1991

Fractional excretion of beta-2-microglobulin in the urine of patients with normal or reduced renal function and hepatic coma.

The purpose of this prospective study was to evaluate beta-2-microglobulin (beta 2m) as a differential diagnostic indicator between hepatic nephropathy (HN) and acute tubulointerstitial nephropathy (ATIN) in patients with reduced renal function and hepatic coma, and to determine whether beta 2m excretion could be used as a marker of renal impairment before increased serum creatinine (S-Cr) concentration or decreased creatinine clearance (Cr-Cl). Finally, the use of beta 2m as a prognostic indicator was investigated. Eighteen patients in hepatic coma grade III-IV were entered in the study and were divided into two groups in accordance with their renal function (serum creatinine above/below 180 mumol/l). The fractional excretion of beta 2m (FE-beta 2m) was used to monitor beta 2m elimination. The study failed to show any distinction in FE-beta 2m between HN and ATIN patients, presumably owing to the small number of patients. FE-beta 2m could not predict the development of renal failure earlier than the increase in S-Cr or decrease in Cr-Cl. However, a few patients who survived paracetamol intoxication had increased FE-beta 2M in the beginning of the coma and normal S-Cr and Cr-Cl. Patients who died as a result of paracetamol intoxication had both abnormal FE-beta 2m and abnormal S-Cr and Cr-Cl, suggesting that if therapy had been initiated earlier, when only FE-beta 2m was affected, these patients might have survived. All patients who survived, except three paracetamol- and one aminoglycoside-intoxicated patient, had normal FE-beta 2m in the beginning of the coma.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaminophen↗
PubMed1979

Hypothermia, a grave prognostic sign in hepatic coma.

Hypothermia is a grave prognostic finding in hepatic coma. Occasionally, it is found in patients whose conditions are stabilized clinically or are improving. When hypothermia occurs, the patients usually die within 24 to 48 hours. All of the patients described herein who eventually improved sufficiently to be discharged from the hospital achieved normal temperatures.

Aged↗
PubMed1988

Lactulose detoxifies in vitro short-chain fatty acid production in colonic contents induced by blood: implications for hepatic coma.

Short-chain (C2-C6) fatty acids constitute the major anions of colonic contents. Acetate is nontoxic in contrast to C(3)4-C6 fatty acids, which induce coma in animals and have been reported to be of importance in the development of hepatic coma in humans. An in vitro fecal incubation system was used to demonstrate how blood, hemoglobin, albumin, lactulose, galactose, fructose, and glucose influence short-chain fatty acid production in the colon. Blood, hemoglobin, and albumin caused increased production of all C2-C6 fatty acids, with the most pronounced increase (fourfold) in C4-C6 fatty acids. Lactulose was converted to acetate only, as were its monosaccharide components, D-galactose and D-fructose. In assays incubated with blood, the production of C4-C6 fatty acids was completely inhibited by lactulose, D-galactose, D-fructose, and D-glucose, respectively, whereas the production of acetate was increased. Lactulose thus "detoxified" the profile of short-chain fatty acids produced in the presence of blood and proteins, indicating that colonic fermentative bacteria prefer lactulose to blood when both substrates are available. The effect of lactulose in the treatment of hepatic coma caused by episodes of gastrointestinal bleeding may therefore be due to a shift in bacterial metabolism from blood or proteins, or both, to lactulose in the colon, resulting in a simultaneous reduction in toxic nitrogenous and organic acid products.

Bacteria↗
PubMed1991

Serum levels of short-chain fatty acids in cirrhosis and hepatic coma.

Short-chain fatty acids cause reversible coma in animals and may contribute to the pathogenesis of the hepatic coma in humans. The concentrations of short-chain fatty acids in peripheral venous blood were significantly elevated in 15 patients with hepatic encephalopathy caused by cirrhosis (362 +/- 83 mumol/L; mean +/- S.E.M.) compared with 17 cirrhotic patients without encephalopathy (178 +/- 57 mumol/L) and 11 normal individuals (60 +/- 8 mumol/L). However, no correlation between the depth of coma and the level of short-chain fatty acids was found after repetitive measurements in the coma group. Compared with normal individuals, all short-chain fatty acids, except valerate, were elevated in patients with hepatic encephalopathy, whereas only the concentrations of isobutyrate and isovalerate were significantly elevated in cirrhotic patients without encephalopathy. The concentrations of short-chain fatty acids in 21 nonencephalopathic cirrhotic patients who underwent catheterization were equally distributed in the aorta (187 +/- 56 mumol/L), the hepatic vein (212 +/- 75 mumol/L), the azygos vein (140 +/- 37 mumol/L) and the renal vein (135 +/- 43 mumol/L) compared with peripheral venous blood (178 +/- 57 mumol/L). This study does not support the idea that short-chain fatty acids are of major importance in the pathogenesis of hepatic coma in patients with cirrhosis.

Adult↗
PubMed1976

In vitro polarographic studies of rat brain oxygen uptake in simulated uraemia and hepatic coma.

A polarographic technique has been used to study the oxygen uptake of rat brain homogenates incubated with metabolites known to accumulate in uraemia and hepatic coma. In general, results with individual metabolites were in agreement with those previously obtained with brain slices using the Warburg technique. Inhibition was induced at higher concentrations with urea, creatine, indoxysulphate, guanidine, dimethylamine hydrochloride, ammonium chloride, taurocholate, glycodeoxycholate, sodium deoxycholate, skalote and indole. Serum and ultrafiltrate from drowsy uraemic patients also caused inhibition, and this was reversed by renal dialysis. Similarly serum and ultrafiltrate from patients in hepatic coma inhibited oxygen uptake but in this instance reversal of the inhibition was not demonstrated following exchange blood transfusion to the patients.

Adenosine Diphosphate↗