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Biomedical subjects

G Kleinberger

Publications and source records attributed to G Kleinberger.

126 records · Page 7Linked to original sources
PubMed1976

[Parenteral nutrition in hepatic coma (author's transl)].

A special program of parenteral nutrition was established in 16 patients with genuine hepatic coma and in 24 patients with portal encephalopathy; this program involves stepwise addition of various nutritional components. On the day of admission water and electrolyte balance is normalized, on the following morning infusions with 40% glucose solutions are started, and the patient is adapted to glucose as the source of calories within the next 48 hours. After this period total parenteral nutrition is instituted comprising all essential ingredients of nutrition. Application of amino acids was especially adjusted to the situation of hepatic coma taking into account not only the typical derangements of metabolism in hepatic coma, but the essential complications of this disease as well. Serial determinations of plasma amino acids were done in order to assess the program of nutrition. Before the beginning of parenteral nutrition plasma levels of amino acids were altered in a manner typical for liver failure; these alterations could be normalized almost completely by total parenteral nutrition.

Adult↗
PubMed1975

[Partial parenteral nutrition in acute myocardial infarction (author's transl)].

The influence of partial parenteral nutrition (PPN) was compared with the effect of a calorie-free solution in 2 groups of patients (n = 10) with acute myocardial infarction. Both groups received the same daily diet of 800 to 1000 Cal. The control group was given, in addition, a calorie-free electrolyte solution and the PPN group was given a nutritious solution consisting of 1000 Cal carbohydrate and 26.5 g 1-amino acids daily by means of a subclavian catheter. The exact monitoring of the water balance indicated that patients with acute myocardial infarction can safely be given parenteral nutrition. Neither haemodynamic nor metabolic complications occurred in the group with PPN due to the small infusion volume and the continuous administration of the infusion volume and the continuous administration of the infusion. The control group was in negative nitrogen, potassium and phosphorus balance in comparison with the PPN group. This demonstrates that a hypocaloric diet is insufficient in the acute phase of myocardial infarction and causes catabolism, which can be prevented by PPN. Stimulation of healing of the myocardial infarct can be expected through the improvement of protein metabolism by PPN.

Diet↗
PubMed1975

[Fatal self-poisoning with the tetracyclic antidepressive drug, ludiomil (author's transl)].

The clinical and analytical data are presented of a case of severe Ludiomil self-poisoning (assumed total ingested dose: 3000 mg). Ludiomil resembles the tricyclic antidepressive drugs in regard to its toxic effects. Two essential observations made in Ludiomil poisoning are: 1) the limited therapeutic possibilities due to delayed elimination and 2) the severe degree of respiratory distress.

Adult↗
PubMed1975

[Hypoglycaemic coma in Boeck's sarcoidosis (author's transl)].

The diversity of clinical manifestations of Boeck's sarcoidosis may also include endocrine disorders. One year after diagnosis of sarcoidosis in a 29 year-old female patient, endocrinological complications became manifest with amenorrhoea. The course of the disease was additionally complicated by hypoglycaemic episodes. Thorough clinical investigation of the patient revealed sarcoid involvement of the skin, lungs, liver and lymph nodes and an extensive retroperitoneal surgically-verified lymph tumour. After tolbutamide and in reaction to an intravenous glucose tolerance test the blood glucose was found to be very low, whilst the immunoreactive insulin was normal. Further investigation of the endocrine functions of the patient revealed normal functioning of the thyroid gland, subnormal values for the follicle stimulating hormone and extremely low serum ACTH and serum cortisol values, without any diurnal changes in these parameters. The clinical symptoms of the patient and the biochemical findings were regarded as manifestations of secondary adrenal failure due to sarcoid involvement of the hypothalamus and pituitary. Hence, treatment with corticosteroids was started. Hypoglycaemia has not since been observed in this patient and the other clinical features of (secondary) adrenal failure have disappeared slowly.

Adrenocorticotropic Hormone↗
PubMed1975

[Acute pancreatitis with shock and acute renal failure (author's transl)].

Acute pancreatitis is discussed from the viewpoint of a medical intensive care unit, with particular reference to the early and late complications. The measures which must be promptly implemented in order to successfully combat the grave early complications of shock and acute renal failure are stressed. Continuous monitoring ensures that prompt surgical management is undertaken in cases of late complications-abscess formation, sequestration and sepsis. A review of the characteristic clinical and laboratory data of patients with acute pancreatitis treated in our unit is presented in table I.

Acid-Base Equilibrium↗
PubMedDate not supplied

Neuroleptanalgesia in acute myocardial infarction: effects of hemodynamic parameters and plasma catecholamines.

The use of neuroleptanalgesia in acute myocardial infarction offers the possibility of reducing pain and emotional stress. The influence of such treatment on hemodynamic parameters (heart rate, cardiac output, stroke volume, peripheral resistance, systemic blood pressure, and pulmonary pressure) and on the plasma level of adrenaline and noradrenaline has been studied in 6 patients with acute myocardial infarction. This results demonstrate that during neuroleptanalgesia the already elevated levels of noradrenaline and adrenaline further increase. This increase was most pronounced in the patients with the highest initial levels of catecholamines. Since the peripheral resistance and systolic and diastolic blood pressures decrease concomitantly, it is concluded that the increase in levels of noradrenaline and adrenaline further increase. This increase was most pronounced in the plasma catecholamines is due to a reaction of the sympathetic nervous system to the alpha-adrenergic receptor blocking activity of droperidol causing vasodilation. The data indicate that pain, emotional stress, and anxiety in the acute phase of myocardial infarction do not play the expected essential role for the activation of the sympathetic nervous system generally observed in acute myocardial infarction. Additionally, the data demonstrate that drugs producing a vasodilation can have a deteriorating effect on the hemodynamic situation and that a reduction of the afterload by vasodilating drugs can result in a further increase in the release of catecholamines.

Aged↗
PubMedDate not supplied

Function of the autonomic nervous system in patients with hepatic encephalopathy.

To obtain further pathophysiological details concerning the development of cardiovascular disturbances in severe liver disease, the state of the autonomic nervous system, the function of the baroreceptor reflex pathway and the responsiveness of the cardiovascular system to noradrenaline, angiotensin II and isoprenaline were investigated in 11 patients with hepatic encephalopathy and in 10 healthy control subjects. Increased plasma levels of noradrenaline and adrenaline and an attenuated increase in heart rate in response to atropine were found in patients with hepatic encephalopathy. These changes and the hemodynamic disturbances tended to be more pronounced in patients with hepatic encephalopathy Grades III-IV as compared to hepatic encephalopathy Grades I-II. The increase in systolic blood pressure induced by infusion of noradrenaline (400 ng per kg per min) and angiotensin II (20 ng per kg per min) was higher in the patients than in healthy control subjects (hepatic encephalopathy Grades I-II: p less than 0.001; hepatic encephalopathy Grades III-IV: p less than 0.02). The changes in mean and diastolic blood pressure in response to angiotensin II were more pronounced in hepatic encephalopathy grades I-II than in hepatic encephalopathy Grades III-IV (p less than 0.02). The decrease of heart rate in response to blood pressure increase in patients with hepatic encephalopathy was not different from control subjects except a smaller decrease during angiotensin II infusion in hepatic encephalopathy grades III-IV (p less than 0.05). The responsiveness to isoprenaline was diminished (p less than 0.001). The present results indicate that the increased activity of the sympathetic nervous system in hepatic encephalopathy is associated with decreased parasympathetic tone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗