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Biomedical subjects

D Müting

Publications and source records attributed to D Müting.

At least 37 records · Page 2Linked to original sources
PubMed1983

Polypectomy in the presence of portal hypertension--an increased risk of bleeding?

A report is presented on 58 polypectomies performed in the stomach and colorectum in 46 patients. Twenty-five patients had portal hypertension consequent on liver cirrhosis, while 21 patients had healthy livers. The question as to whether haemorrhage occurred immediately after polypectomy or within the next 24 hours, was investigated. Furthermore, either the stalk (of pedunculated polyps), or the polyp itself (when sessile) was investigated pathologically-anatomically, with respect to its vascularity pattern. The submucosal and intramucosal vascularity patterns were classified in 4 categories, I to IV. A tentative interpretation of the results obtained indicates, on the basis of their mucosal and submucosal vascularity patterns, that patients with portal hypertension developing from a cirrhosis of the liver, are not at any higher risk of haemorrhage than patients with no portal hypertension.

Adult↗
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↗
PubMed1982

[Chronic destructive non-suppurating cholangitis].

Initially liver morphology of chronic destructive non-suppurative cholangitis (CDNC) is rather atypical. Therefore, early morphological diagnosis is difficult. First symptoms are severe pruritus and an increase of IgM, AP and gamma-GT. Own investigation of 101 CDNC patients showed that antimitochondrial antibodies (AMA) are generally later present than the increase of the a/m enzymes. Also remarkable is the fact that among 101 patients are 13 men generally observed during the last 3 years. The most difficult problem is the treatment of CDNC. Here we have to differentiate between symptomatic basic treatment and so-called specific treatment. As basic treatment, ammonia-reducing amino acids, phenobarbital and finally cholestyramine are administered in order to diminish the severe pruritus. The diet must be rich on pectine. Lactulose and bifidum milk improve the diminished detoxication function of the liver. As specific treatment prednisolone and/or azathioprin have disappointed. D-penicillamine can influence CDNC at least temporarily. Because of the frequent side-effects D-penicillamine should be administered only in low doses (100-200 mg daily together with 300 mg vitaminee B6). Until not it is uncertain if the extremely bad prognosis of CDNC can be improved by medical treatment of its early stages.

Aged↗
PubMed1980

[Oral gallbladder contrast agents in liver damage].

Jopron acid a new peroral cholangiographic agent and did not increase serum enzymes, bilirubin and some other parameters in 21 patients with active chronic liver diseases identified by laparoscopy and biopsy. For the patient the peroral radiographic examination of the biliary system in the ambulance seems to be quite safe.

Administration, Oral↗
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↗
PubMed1977

[Therapy of hepatic insufficiency].

Hepatic insufficiency is generally caused by active liver cirrhosis with portal hypertension. The final stage is the exogenous hepatic coma. Much rarer is the endogenous hepatic coma caused by fulminant acute hepatitis or severe intoxications. In the treatment of hepatic insufficiency it is first necessary to eliminate all exacerbating factors such as too high protein-intake, gastrointestinal bleedings, abuse of alcohol and diuretics. Because hepatic encephalopathy is mainly produced by toxic intestinal protein metabolites no protein should be adminstered at the beginining of the disease. The production of toxic protein metabolites in the gut can be diminished as well by enemas with sodium acetate buffer (pH 4, 5) as by neomycin (6-8 gm daily). Because long-term treatment with neomycin reduces also the physiological intestinal bacteria combination with lactulose (70-100 gm daily) is better. Treatment with lactulose reduces not only significantly hyperammoniemia but also increases serum phenols. The same effect have so-called ammonia reducing amino acids such as arginine, ornithine and glutamic acid. In endogenous hepatic coma blood exchange transfusions, liver perfusions and charcoal perfusions are necessary. Nevertheless, the prognosis of hepatic insufficiency caused by fulminant hepatitis is very poor in the final stage of the disease. Therefore early diagnosis and treatment in special departments with intensive care is necessary.

Alcoholism↗