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Biomedical subjects

G Kleinberger

Publications and source records attributed to G Kleinberger.

At least 73 records · Page 4Linked to original sources
PubMed1982

Impaired secretion of TSH in critically ill patients with 'low T4-syndrome'.

Thyroid and pituitary function was studied in 10 male and 6 patients female during critical non-endocrine disease. Low concentrations of TT3 were observed in each case. Seven patients out of whom 3 survived, presented with low levels of TT4 due to deficiency in TBG in the presence of normal values of FTI and FT4, whereas a 'low T4-syndrome', characterized by low concentrations of both TT4 and FT4 was seen in 9 patients, 8 of whom died 1 to 16 days after evaluation of pituitary function. A diminished response of TSH to iv TRH (400 micrograms), as observed in 4 patients with normal FT4 and in all patients with 'low T4-syndrome', was not accompanied by a concomitant lack in stimulated release of LH, FSH and Pr1 in the majority of cases. However, the secretory maximum of LH and FSH following stimulation by LRH (100 micrograms iv) was delayed in 10 and in 9 patients, respectively, including patients both with normal and subnormal concentrations of FT4. From the above it appears that low stimulated concentrations of TSH in the presence of subnormal concentrations of FT4 indicate an extremely poor prognosis in critically ill patients. The abnormal behaviour of TSH in this group of patients cannot be explained by generalized pituitary insufficiency or by an increase in FT4.

Adult↗
PubMed1982

[Concomitant pancreatitis in hepatic coma].

Increased levels of serum amylase were found in 14 out of 34 patients (41%) with coma due to acute liver failure, in 8 out of 55 patients (14%) with hepatic encephalopathy, and in 5 out of 10 patients with a mixed pathogenesis. In 4 patients of the first group (11.7%) and 4 of the second group (7%) pancreatitis was diagnosed at post mortem. The pathogenesis of pancreatitis concomitant with liver failure is unclear. Virus infection and intoxication may do damage to both organs; hemodynamic factors, coagulation defects, and derangements of metabolism may play a role as well.

Acute Disease↗
PubMed1982

Pituitary-thyroid dysfunction in severe non-thyroidal disease: "low-T4 syndrome".

Thyroid function tests were obtained from 335 consecutive patients admitted to an intensive care unit. Twenty patients suffering from severe non-endocrine diseases (septicaemia, fulminant hepatic and renal failure, acute pancreatitis, polytrauma, cerebral haemorrhage) were found to have serum thyroxine levels in the hypothyroid range (less than 4 micrograms/dl). Serum concentrations of total thyroxine (2.3 +/- 0.2 micrograms/dl), triiodothyronine (0.23 +/- 0.03 ng/ml), and thyroxine binding globulin (15.1 +/- 1.3 micrograms/ml) were reduced, but were above normal for reverse triiodothyronine (0.43 +/- 0.06 ng/ml). Response of TSH secretion to iv TRH was found to be either normal, lowered or absent. Primary hypothyroidism was excluded, as no enhanced TSH response was observed in any case. Although decreased thyroxine levels may be due to increased thyroid hormone degradation it appears that associated impaired TSH responsiveness to TRH may result from illness-related inhibition of pituitary TSH release. Although the finding of decreased thyroid hormone levels is not rare in care patients, it represents an index of poor prognosis. Differentiation between this "low-T4 syndrome" and true hypothyroidism depends essentially on clinical symptoms and course of disease.

Acute Disease↗
PubMed1982

[Pulmonary complications in hepatic coma].

Incidence and extent of pulmonary complications were evaluated retrospectively in 101 patients with hepatic coma (34 patients with acute liver failure, 57 patients with hepatic encephalopathy and 10 patients with mixed forms). 76 patients (73.3%) had pulmonary complications (pulmonary edema 57 cases, pneumonia 20 cases, tracheobronchitis 30 cases). Lethality of the group with pulmonary complications was 97% as compared to 16% in the group without pulmonary complications. Pathogenesis of pulmonary complications is not completely clear; different mechanisms are being discussed like central mechanisms, vascular lesions caused by metabolic or toxic factors, cardiac failure, and increased susceptibility to infection. In 9 out of 59 cases (15.3%) with respiratory failure no morphological changes could be observed in the lungs; in these cases intrapulmonary shunts might have been the cause for the pulmonary complications. The incidence of pulmonary complications increased by a factor of 2.4 during intensive care unit treatment of the patients; this increase shows, that intensive care unit treatment still has to be improved.

Adult↗
PubMed1982

Duration of the hypotensive effect of guanfacine.

Guanfacine given intravenously causes a brief rise in blood pressure. This is followed by a sustained decrease of blood pressure, accompanied in one case by a marked orthostatic effect. In addition to its lowering effect on blood pressure, guanfacine also reduces heart rate. The duration of action for up to 72 h is due to the long half-life of the drug. The main side effects observed are fatigue and sedation.

Adult↗
PubMed1982

[Effect of parenteral administration of fat on the glucose and fat metabolism in acute pancreatitis].

Glucose intolerance is well known in acute pancreatitis. The question of this study was to clarify, if fat used partly instead of glucose in the parenteral nutrition of these patients allows to reduce the insulin necessary to control the blood glucose. A second question was if hypertriglyceridemia is caused by long term infusion of fat in such patients. 10 patients with acute necrotising pancreatitis were divided in two groups: group I (5 patients) were infused with a parenteral nutrition with fat, group II (5 patients) with a parenteral nutrition without fat. As parameters the amount of insulin needed to maintain the blood glucose at levels less than 200 mg% and the serum triglycerides were used. The blood glucose was controlled three times a day. For statistical evaluation the Student-t-test was used. The patients in group I (parenteral nutrition with fat) were infused 44 days and received insulin on 40 days. 69 units insulin/day were needed with a glucose dose of 243 g/day. The insulin dose per 100 g glucose was 29.9 U. The fat dose was 74 g/day. Group II (parenteral nutrition without fat) was infused 45 days and received insulin on 38 days. 103 units insulin/day were needed metabolized 295 g of glucose. The insulin per 100 g glucose was 28.7 units. The dose of insulin per 100 g glucose was not different between the two groups. In 1 patient a hypertriglyceridemia occurred after infusion of fat and disappeared immediately after withdrawal of the fat infusion. In the other patients no hypertriglyceridemia occurred during fat infusion. The parenteral infusion of fat has no influence on the glucose intolerance of patients with acute necrotising pancreatitis.

Acute Disease↗
PubMed1982

[Antagonism of the ammonia effect on serotonin receptors by L-valine].

Ammonia and valine influence the activity of serotonin receptors in membranes of frontal cortex taken from brain removed at postmortem: Ammonia reduces maximal binding capacity of serotonin receptors, and this effect can be antagonized by valine. This modulatory effect of valine seems to be efficient at a lower level in tissues of patients with hepatic coma. Branched chain amino acids may have efficient therapeutic effects in hepatic coma due firstly to effects on the blood brain barrier by a well known mechanism of action and secondly to molecular interaction at the synaptic membrane.

Aged↗
PubMed1982

[Neuropsychiatric symptoms of hepatic encephalopathy].

The words "hepatic encephalopathy" and "hepatic coma" are used synonymously to describe the course of a disease state which is characterized by at least transient, gradual or complete loss of consciousness. Own results regarding the incidence of various neurological and psychiatric symptoms are described. Evaluation of these symptoms in a longitudinal study allows to differentiate between an acute and a subacute form of this disease state. The prominent neuropsychiatric symptoms are characterized by a disintegration of complex neuronal functions. A rating scale comprising four different symptoms is proposed, allowing grading of the disease state. Such a scale cannot replace a careful neurological work up; such work ups have to be done in regular intervals in these patients, so that neurological symptoms can be recognized at an early state.

Consciousness Disorders↗
PubMed1982

[Pharmacotherapy in severe liver failure].

In severe liver failure pharmacokinetics and pharmacodynamics of different drugs are changed as compared to normals. The disturbances observed may be due to hepatic or extrahepatic mechanism, which allows a rough classification of the different drugs. The hepatic clearance of a drug is dependent upon blood perfusion of the liver (flow limited elimination) or upon the metabolic capacity of the liver (capacity limited elimination). Extrahepatic factors are protein binding and changes of the distribution volumes. Adjustment of the initial and chronic doses of any drug should depend primarily upon the pharmacokinetic profile of the drug and secondarily upon the clinical effects. Repeated measurements of drug levels can only be done in special hospitals and in patients severely in danger. Classification of drugs into groups with high, medium or low therapeutic risk may help, when a treatment plan is drawn up and may economize control of the patient.

Biotransformation↗
PubMed1982

[Hepatic coagulopathy--principles and therapeutic statements].

In liver parenchymatous disease there is a significant correlation between plasma concentrations of coagulation factors of the prothrombin complex and antithrombin III on the one hand and the severity of the disease on the other hand. These coagulation factors are suitable for following the course of the disease because of their short biological half time. In liver failure hepatic clearance of activated coagulation factors may be delayed which will have influences upon the hemostatic mechanisms. An increased disposition for disseminated intravasal coagulation thus exists in infections, hemorrhagic shock and during monotherapy with concentrated prothrombin complex. Therapy with blood or plasma and its derivatives should always be directed at keeping an equilibrium between activating and inhibiting coagulation factors. Fresh plasma, fractionated blood exchange, or a combined application of equivalent units of antithrombin III and prothrombin complex concentrate with minimal heparin doses are suited for such therapy.

Antithrombin III↗
PubMed1982

[Shock liver].

UNLABELLED: Hypoxic, central lobular necrosis of the liver has been observed in patients with severe shock of different origin. In many cases diagnosis is not established, since clinical symptoms are unrevealing, and since SGPT levels rise rather late in the course of the disease. 3,788 patients have been treated in the intensive care unit of the Department of Medicine of the Vienna Medical School, within 10 years; liver damage caused by shock has been found during this period only in 32 cases. Diagnosis was established in 31 cases because of highly elevated SGPT levels, and substantiated in 5 cases by liver biopsy; diagnosis was established in one case by biopsy only. The median value of SGPT activity was 1,160 U/l and of lactate concentration 7.5 mmol/l. In 18 patients shock was caused by acute myocardial infarction, in 4 patients by pulmonary infarction and in 3 patients by cardiac as well as pulmonary events. In 4 cases there were heart valve lesions, one case had myocarditis, one case acute pancreatitis and one case hemorrhagic shock. Lethality was 78.1%. There was no correlation between central venous pressure and the maximal SGPT levels. There was however a correlation between prothrombin time and creatinine clearance. IN CONCLUSION: In severe shock typical lesions of the liver may originate as a complication of shock, this complication being due to reduced blood flow leading to central lobulare necrosis of liver cells.

Adult↗
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↗
PubMed1981

[Hypernatraemic hyperosmolar syndrome (author's transl)].

Between 1972 and 1979 34 patients with severe hypernatraemia (serum sodium larger than or equal to 160 mmol/l) were admitted to the intensive care unit. Among these there were 45% of neuropsychiatric patients with reduced consciousness. Maximal serum sodium concentration was 168 (160--204) mmol/l, maximum serum osmolality 391 (340--520) mosm/kg H2O. Treatment consisted of infusion of hypotonic solutions and potassium substitution. Fluid balance was positive (5,9 during 43 hours) until normal serum sodium concentrations had been reached. The mortality of 77% was exclusively due to the underlying diseases.

Adolescent↗
PubMed1981

[Acute leukemia associated with lactic acidosis].

The clinical course and metabolic disturbances in three patients with acute leukemia and severe lactic acidosis (lactic acid concentrations 11.2, 17.0 and 21.0 mmol/l) are described. Circulatory failure could be ruled out as a possible cause of elevated lactic acid. Clinical findings included somnolence, hyperventilation and diffuse abdominal pain. In patients with malignant disease, a number of factors may contribute to elevated lactic acid levels. However, in our cases the excessive lactic acidosis was due to increased production of lactic acid by the leukemic cells, together with impaired hepatic metabolization. The diminished hepatic gluconeogenesis is also documented by a severe hypoglycemia in our patients. The essential step in treatment is early diagnosis of this syndrome and prompt initiation of cytotoxic medication.

Acidosis↗