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Biomedical subjects

A Feige

Publications and source records attributed to A Feige.

15 recordsLinked to original sources
PubMed1991

[Obstetric and ethical-legal problems in a twin pregnancy with anencephalus and polyhydramnios of the leading twin beyond the 28th week of pregnancy].

Malformations are found twice as often in twins than in singletons. In the following case, we report on a twin pregnancy with anencephaly and polyhydramnion of the leading twin I, which was first diagnosed after 28 weeks of pregnancy. The foetal disease of twin I led to an appreciable dyspnoea of the mother that exacerbated to an incipient respiratory failure by the thirty-second week of pregnancy. The projected termination of pregnancy by Caesarean section based on a maternal indication was not performed, but instead a selective foetocide of the diseased twin. The live twin was delivered spontaneously without complications after thirty-eight weeks of pregnancy. The obstetric and legal ethical problems are discussed.

Anencephaly↗
PubMed1990

[Prenatal diagnosis of a sacrococcygeal teratoma with hydrops fetalis and placental hypertrophy--consequences for the further course of pregnancy].

A fetal sacrococcygeal teratoma may cause hypertrophy of the placenta and fetal hydrops. This is dangerous for the fetus and also for the mother. The maternal risk results from preeclampsia and respiratory insufficiency, associated with elevated beta-HCG. In that case, pregnancy should be terminated by caesarean section due to maternal reasons.

Adult↗
PubMed1979

Plasma DBH, platelet MAO and proteins of red blood cell membranes in individuals with variants of the normal EEG.

Plasma DBH, platelet MAO and proteins of red blood cell membranes were examined in healthy male carriers of variants of the normal resting EEG. The variants included low-voltage EEG, badly synchronized alpha-EEG, diffuse beta-EEG and monotonous alpha-EEG. Mean DBH activity of the low-voltage EEG group was only half that of the monotonous alpha-EEG group. No difference between EEG types in platelet MAO activity and in polypeptide pattern of erythrocyte membranes after electrophoresis could be detected.

Adult↗
PubMed1977

Fetal and maternal blood glucose, insulin and acid base observations following maternal glucose infusion.

The aim of the present investigation was to examine the fetal and maternal blood glucose and insulin response following glucose infusion to the mother. The studies were performed on 11 primigravid patients with a gestational age of 38-40 weeks during the first stage of labor. Glucose was given intravenously by a bolus injection of 330 mg/kg body weight, followed by a glucose infusion of 27.5 mg/kg/min for 60 min. Glucose concentration, immuno-reactive insulin (IRI), pH and base excess of the maternal and fetal blood were measured before and during maternal glucose load. Maternal blood glucose rose within 10 min. up to 280.0 mg% (SD 25.9). This level could be fairly maintained throughout the experiment. The maternal glucose was after 60 min. infusion 326.5 mg% (SD 46.9). Fetal glucose concentration rose continuously from 65.8 mg% (SD 5.8) at control to 249.2 mg% (SD 23.3) after 60 min. The increase of maternal and fetal glucose was associated with an elevation of immuno-reactive insulin (IRI). The maternal insulin was 24.0 micronU/ml (SD 8.0). It was scattered over a wide range (55.4 micronU/ml-217.1 micronU/ml) after 60 min. glucose infusion. The fetal insulin was 17.0 micronU/ml (SD 5.2) at control and rose by 86.5% (SD 80.5) after 60 min. glucose load. One case of a mother with a subclinical diabetes mellitus deviated where the fetal insulin rose from 26.0 micronU/ml at control to 215.6 micronU/ml after 60 min. infusion. The increase of insulin per glucose rise was correlated to fetal body weight. During glucose infusion to the mother of both, fetal and maternal, acid base parameters remained unchanged. From these observations it may be concluded that in the human fetus insulin secretion following a single glucose load is generally low, however, it increases in cases where the maternal insulin response to glucose load is abnormal. This might be related to a chronic stimulation by glucose of the fetal pancreatic islet cells in poorly controlled diabetic and possibly prediabetic patients.

Acid-Base Equilibrium↗
PubMed1976

[The correlation of glucose-concentration and acid-base-balance of the maternal and fetal blood during labor (author's transl)].

The aim of the present paper was to investigate if the glucose concentration of the fetal blood is reduced already during parturition. It was further of interest if there is a relationship between the glucose concentration in the maternal blood and the acid-base-balance of the maternal and the fetal blood, respectively. The observations comprised 40 patients during labor. Blood was sampled from the hyperemized fetal scalp and the umbilical artery. The maternal blood was collected from the hyperemized earlobe and fingertip, respectively. The blood was analyzed for pH, PCO2, base excess and blood glucose. The dip area (DA) was taken from the cardiogram and measured by planimetry. During labor the blood glucose increased in the fetal blood from 67 mg% (SD 12) to 87 mg% (SD 23) (2 alpha less than 0,001) and in the maternal blood from 88 mg% (SD 14) to 113 mg% (SD 29) (2 alpha less than 0,02). There was a significant correlation between the fetal and maternal blood glucose concentrations. The increase of the fetal glucose concentration is, however, less with increasing maternal blood glucose. (b = 0,66). The base excess in the maternal and fetal blood fell significantly. The rise of the maternal and fetal base excess (= base deficit) was related to the increase of the glucose concentration (2 alpha less than 0,001). If the base excess was zero, the fetal and the maternal blood glucose was 46 mg% and 78 mg%, respectively. The difference between the maternal and fetal blood glucose was 28 mg%. With increasing DA the fetal blood glucose increased (2 alpha less than 0,001.). From the observations it is concluded that there developes no hypoglycemia during parturition. This is due to the correlation found between fetal and maternal blood glucose and due to the rise in fetal blood glucose during hypoxia. Obviously, the decrease in fetal glucose following delivery is caused by a lack of glycogen which is enduced during labor and strengthened by a deficit of enteral glucose supply.

Acid-Base Equilibrium↗