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At least 109 records · Page 6Linked to original sources
PubMed1977

[Hepatic coma--causes, recognition, treatment].

The name of the disease coma hepaticum is a collective notion for etiologically, pathologo-anatomically and biochemically different kinds of a failure of the function of the liver. A demarcation of different forms of the liver coma is necessary above all for prognostic and therapeutic reasons: hepatic disintegration coma, coma in hepatic failure, mixed coma, false hepatic coma, ferment block coma. Despite certain progress the therapeutic possibilities in hepatic coma cannot satisfy in recent years. Also the use of different, partly very expensive methods of the so-called liver substitute (exchange function and plasmapheresis, heterologous and homologous extracorporal liver perfusion, parasymbiotic crossed circulation, haemoperfusion with encapsulated activated charcoal, liver transplantation) up to now did not lead to a decisive improvement of the nearly infaust prognosis of the hepatic disintegration coma. Therefore preventing measures and careful control of endangered patients deserve particular attention.

Anti-Bacterial Agents↗
PubMed1981

[Acute experimental (endogenous) hepatic coma and the clinical syndrome of acute hepatocellular injury].

In search of the adequate experimental model for creating endogenous coma, the characteristics of which would be identical to the clinical picture of acute hepatic coma in men, the ischaemic method of experimentally originated acute endogenous hepatic coma was applied. The experiment was carried out on 12 dogs in which the terminolateral portocaval shunt with ligation of all the collateral of the arterial irrigation leading to the liver was performed, while the double ligation was performed on the hepatic artery. After the animals had emerged from the postoperative state of shock, the hepatic artery was ligated in local anesthesia and the created state was controlled by clinical observations and laboratory tests. Experimentally created acute endogenous hepatic coma achieved by applying ischaemic method proved to be a good model. Its true value manifested itself in the clinical picture as well as in the laboratory findings which resembled considerably the state of acute hepatic coma in men.

Acute Disease↗
PubMed1975

[Cerebral manifestations in the hepatic coma syndrome (author's transl)].

The pathogenesis of hepatic encephalopathy has been investigated in a two-stage devascularization model in the rat with portavacal shunt and hepatic artery ligation. There is a significant increase in brain octopamine and phenylethanolamine and a decrease in brain norepinephrine (NE) 6 to 9 hours after hepatic artery ligation. The depletion of NE seems the sequel of diminished synthesis in the presence of an unaltered turnover rate, due to a blockade of tyrosine hydroxylase either by accumulation of false neurochemical transmitters or by phenylalanine. It is most marked in the cortex and midbrain. The high-energy phosphate compounds, ATP, phosphocreatine and glucose-6-phosphate are not diminished in hepatic coma, nor is glucose, indicating that other mechanism are involved in the pathogenesis of metabolic state by the increased ammonia level. "intestinal sterilization" and total colectomy have no significant effect on the ammonia level, but cause a decrease in the level or aromatic precursor amino acids in the plasma and brain, with normalization of the level of cerebral transmitters. These results permit the formulation of a unified concept of the hepatic coma syndrome and its clinical manifestations such as flapping tremor, the hyperdynamic cardiovascular state and the hepatorenal syndrome. Moreover, they form the basis for the introduction of a new therapeutic principle in the management of hepatic encephalopathy by L-dopa or modified amino acid solutions, which act by altering the central and peripheral neurotransmitters.

Animals↗
PubMed1982

[Disorders of kidney function in hepatic coma].

Renal function was evaluated in 80 patients with hepatic coma stage III-IV (24 patients had acute fulminant hepatic failure, 48 patients chronic hepatic failure, 8 patients had a mixed form). Urea, creatinine and electrolytes were measured in plasma and urine as well as creatinine clearance and sodium/potassium ratio in urine. Renal failure was defined as an increase of serum creatinine above 3 mg/dl. In 15 of the 24 patients with fulminant hepatic failure creatinine clearance was reduced; hyperaldosteronism was present in 13 cases; in 2 patients there was necrosis of the tubulus, in 9 patients overt renal failure. In patients with chronic hepatic failure creatinine clearance was pathological in 36 cases, hyperaldosteronism was diagnosed in 23 cases and necrosis of renal tubules in 3 cases; 8 patients had overt renal failure. In the group with the mixed form of hepatic coma creatinine clearance was pathological in 3 cases, in 6 cases hyperaldosteronism was diagnosed; necrosis of the tubules could not be found in this group; 4 patients had overt renal failure. It is suggested that for treatment of this condition dopamine should be given prophylactically as well as intravenous sodium and water substitution.

Acute Kidney Injury↗
PubMed1977

[Extracorporeal perfusion with baboon liver in the treatment of hepatic coma (author's transl)].

In 11 patients with hepatic coma (stage IV and V according to Abouna) extracorporeal haemoperfusion using the Scribner shunt (radial or profunda femoris artery) was performed over 12 to 27 hours with 22 baboon and one human livers. Eight patients emerged from coma, six of them showed sufficient regeneration of the diseased liver. Four patients were discharged as cured, one patient died of acute pancreatic necrosis, a further one due to bleeding from an old gastric ulcer. In the 2 remaining patients the coma recurred within 48 hours. Tree patients never came round from coma. After perfusion no antibodies against baboon proteins were demonstrable in the patients. Thus there is very little danger of an anaphylactic reaction when perfusion is repeated. The titre of preformed cytotoxic antibodies against baboon cells in patients' serum rises only after 1-2 weeks and decreases again after 4 weeks. In our experience extracorporeal liver perfusion with baboon or human livers is the most promising method for treatment of hepatic coma.

Adult↗
PubMed1955

[Hepatic coma].

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Coma↗
PubMed1984

Prostacyclin-synthesis-stimulating plasma factor in patients with different stages of hepatic coma.

In patients with acute hepatic coma the prostacyclin synthesis stimulating plasma factor is significantly enhanced. This increased activity has been verified by using various test systems. However, there is no correlation between the actual plasma factor activity and the coma stage, respectively. The increase of plasma factor activity in these patients might account at least in part for the increased bleeding tendency seen in these patients.

Adolescent↗
PubMedDate not supplied

Exchange transfusion with plasmapheresis in the management of hepatic coma.

In two cases of hepatic coma following advanced liver cirrhosis exchange transfusions were applied with plasmapheresis. In both cases the general condition of patients improved and consciousness returned. After exchange transfusions with plasmapheresis the serum levels of bilirubin, urea and ammonia decreased. Using appropriately selected fluids for erythrocyte suspension it is possible to affect selectively protein depletion and depletion of plasma blood clotting factors.

Adolescent↗
PubMed1972

Acute hepatic coma successfully treated by extracorporeal baboon liver perfusions.

Two patients in deep hepatic coma due to fulminant viral hepatitis were treated by extracorporeal baboon liver perfusion after failing to respond to medical treatment and three consecutive exchange transfusions. Both patients recovered full consciousness after one liver perfusion, made a complete recovery, and were leading normal lives seven and eight months after treatment. Perfusions were maintained for 13(1/2) and 16(1/2) hours without complication, and neither clinical immunological reactions nor antibaboon serum antibodies developed as a result of treatment.Whereas normal consciousness could be restored only by liver perfusion, both exchange transfusion and liver perfusion were effective in clearing bilirubin and in raising the level of clotting factors. Extracorporeal baboon liver perfusion provides a safe and effective method for the treatment of acute hepatic coma.

Adolescent↗