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Biomedical subjects

G Kleinberger

Publications and source records attributed to G Kleinberger.

At least 109 records · Page 6Linked to original sources
PubMed1978

[Pancreatitis after renal transplantation (author's transl)].

A renal transplant patient in whom acute pancreatitis developed 2 1/2 years after surgery is presented. Pancreatisis was accompanied by hyperlipaemia, diabetes mellitus and acute renal failure possibly due to acute tubular necrosis. Pancreatic abscesses necessitated subtotal pancreatectomy 2 months later. Because of generalized tuberculosis finally the patient succumbed 6 weeks thereafter. As aetiological factors cytomegalovirus disease, disorders in lipid metabolism and immunosuppressive therapy must be discussed. It is concluded that prophylactic measures as well as early diagnosis, intensive care and therapy are necessary for reducing the high risks of pancreatis in renal transplant recipients.

Acute Kidney Injury↗
PubMed1978

[Hypophosphatemia during parenteral nutrition of patients with renal insufficiency (author's transl)].

Hypophosphatemia is a much commoner condition than generally recognized from investigations on this subject so far. Hypophosphatemia may cause ill-defined disturbances in the course of illness in patients with renal insufficiency. On the basis of our results we recommend the addition of 5--10 mmol phosphate (155--310 mg phosphorus) per 1000 kcal. of the nutrient solution right from the start of parenteral nutrition in patients with chronic renal insufficiency. The phosphate dosage must be further increased, at least temporarily, in hypophosphatemic patients with acute renal insufficiency. Serum phosphate determination should be obligatory in patients with renal insufficiency at the time when the patient is first seen. It should also be performed at least every second day during the first week of parenteral nutrition. Thereafter, the determination of serum phosphate twice weekly should suffice to control the dosage of phosphate required by the patient.

Acute Kidney Injury↗
PubMed1978

Human cerebral free amino acids in hepatic coma.

Free amino acids and some related compounds in autopsy specimens of different human brain areas have been determined by column chromatography. Only in patients with hepatic coma could a significant difference in the contents of tyrosine and lysine between caudate nucleus and N. amygdalae be found. In comparison with control subjects the brains of patients with hepatic coma contained significantly higher concentrations of glutamine, isoleucine, histidine and ammonia. In patients with hepatic coma after complete parenteral nutrition plus L-valine administration, dying from other causes, the brain levels of alanine and valine were decreased, while the content of taurine was significantly increased. However, most of the amino acid levels in brain tended toward lower levels. A very significant reduction after treatment with L-valine could be observed in glutamine and ammonia concentration. It is suggested that L-valine has some beneficial action on ammonia detoxification and has also a competing action on amino acid uptake mechanism (specially with the large neutral amino acids).

Adult↗
PubMed1978

[Differences in plasma aminograms in hepatic and diabetic coma].

In hepatic coma as well as diabetic coma severe disturbances occur in the amino acid metabolism. The defect lies in completely different levels which result two different plasma aminograms (PAG). In 24 patients with hepatic encephalopathy stage III-IV (7 patients with acute and 17 with chronic liver failure) the PAG were evaluated. The determination of the plasma amino acids (PAA) was carried out on Multichrom B (Beckmann, Munich). In hepatic coma high concentrations of Met, Tyr, Ala, Lys and Arg are found. The deviations of PAA from normal controls show between acute and chronic hepatic failure no qualitative but only quantitative differences. In diabetic coma the three branches chain AA (Val, Leu and Ile) were elevated upon 3--5 times of normal. Near normal concentrations are found for the AA Thr, Ser, Gly, Ala, Met and the aromatic AA (Phe and Tyr). The quotient between the branched chain and aromatic AA lies for hepatic coma at a mean of 1.18 and by diabetic coma at 7.18 (p less than 0.001). In hepatic coma a correlation exists between the level of the AA-quotient improvement and the decrease with a deterioriation of the metabolic encephalopathy. The high level of the AA-quotient in the patients of diabetic "coma" gives therefore a good explanation for the rare unconscious state of these patients.

Adult↗
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↗
PubMed1977

[The disseminated intravascular coagulation. Diagnosis and therapy on a medical intensive care unit (author's transl)].

Disseminated intravascular coagulation (DIC) is a frequent acquired disorder of haemostasis in the patients at the medical intensive care unit. The pathogenesis, the different possible clinical manifestations and the obligatory laboratory tests are reviewed. In addition to the treatment of the underlying disease, the importance of adequate restoration of fluid volume and early administration of heparin is stressed.

Adolescent↗
PubMed1976

[Haemodynamic changes in acute myocardial infarction following high doses of furosemide (author's transl)].

Haemodynamic measurements were carried out after administration of furosemide to 10 patients suffering from acute myocardial infarction and congestive heart failure. It was observed that a transient deterioration in cardiac function (decreased cardiac output, increased enddiastolic pulmonary arterial pressure and increased pulmonary and systemic resistance) occured in the pre-diuretic stage in these failing hearts. After the onset of diuresis the haemodynamic parameters showed a reversal of the previous trends (increased cardiac output, decreased enddiastolic pulmonary arterial pressure and pulmonary resistance). The consistently lower enddiastolic pulmonary arterial pressure in the diuretic phase as compared with the pre-diuretic value ensured an improvement in cardiac haemodynamics. An attempt was made to interpret the haemodynamic results in the light of the Frank-Starling's curve.

Acute Disease↗
PubMed1976

[The effect of "standardized forced diuresis" (SFD) on serum and urinary electrolytes(author's transl)].

The effect of standardized forced diuresis (SFD) on the serum and urinary electrolyte levels was investigated in 10 cases of severe self-poisoning with hypnotic drugs. Diuresis was initiated by furosemide and maintained at an hourly urinary ouput of 2 litres. Fluid and electrolyte substitution was carried out with a standardized electrolyte solution. Initiation and termination of the SFD was performed abruptly. The mean values of sodium, potassium, chloride and phosphorus in the urine varied widely at the beginning of the SFD, while the calcium and magnesium values varied only slightly. During SFD, urinary stabilization occured at a particular ionogram, in correlation to the electrolyte concentrations in the infusion fluid and with only minimal individual variation. Owing to this satisfactory correlation, none of the patients developed signs of electrolyte disturbances, so that no correction of the infusion constitution was necessary. The abrupt termination of the SFD prevented electrolyte disturbances in the recovery phase.

Adult↗
PubMed1976

[Angiotensin - a possible cause of acute renal failure (author's transl)].

The hypertensive action of angiotensin is purely brought about by peripheral vasoconstriction and may, thus, lead to reduced perfusion of vital organs, especially the kidneys. The dangers of angiotensin in triggering off acute renal failure are illustrated by a case report in which this drug was administered to a comatose patient with hypovolaemic hypotension following barbiturate self-poisoning.

Acute Kidney Injury↗
PubMed1976

[Severe intoxication with leponex (author's transl)].

The clinical picture and the therapeutic management of a severe case of self-poisoning with Leponex (clozapin) are presented. In particular, the grave complications, their possible aetiology and the value of the administration of cortisone are discussed. Forced diuresis or haemodialysis are ineffective measures on account of the low serum concentrations of Leponex.

Adult↗
PubMed1976

[Clinical results with dopamine in acute renal failure (author's transl)].

Dopamine possesses specific pharmacological actions which distinguish it from the other catecholamines. Apart from its positive inotropic effect, dopamine exerts a favourable influence on renal function with an increase in renal blood flow and alterations in intrarenal haemodynamics. The use of dopamine in the early stages of acute oliguric failure is recommended on the basis of the good therapeutic response achieved in a series of cases.

Acute Kidney Injury↗