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Biomedical subjects

M Hansmann

Publications and source records attributed to M Hansmann.

At least 127 records · Page 7Linked to original sources
PubMed1988

[Trisomy 22--prenatal findings in various developmental stages].

Four cases of trisomy 22 in different stages of pregnancy are reported, one of them showing a mosaicism. The diagnosis was made in three of the observations during the first trimenon, in one in the third trimenon. A typical pattern of malformations of developmental retardation could be demonstrated in the embryonic as well as in the extraembryonic tissues. Our findings confirm the different frequency of the single chromosome abnormality in the various stages of development in pregnancy.

Abnormalities, Multiple↗
PubMed1988

[2-dimensional color-coded fetal Doppler echocardiography--its value in prenatal diagnosis].

105 fetuses between 16 and 38 weeks of gestation were studied by fetal echocardiography using color-coded two-dimensional Doppler-echocardiography (2-DDE). Two-dimensional, M-mode, and spectral-Doppler analyses were also performed. In 11 fetuses, structural and/or functional abnormalities were detected. Abnormalities were correctly excluded in all other fetuses. The advantages of the 2-DDE are, in particular: rapid screening for flow abnormalities in the fetal heart and, thus, shortening of the Doppler-examination time; furthermore, a rapid diagnosis of valvular regurgitation, valvular stenosis and abnormal shunting of blood across the interatrial and interventricular septa; the diagnosis of complex congenital heart defects is facilitated by and, in certain case, only possible using 2-DDE.

Blood Flow Velocity↗
PubMed1988

[Fetal atrial flutter in complete atrioventricular canal and trisomy 18].

Fetal supraventricular tachyarrhythmias are very rarely associated with congenital heart diseases. Usually a circus movement (= reentry), often associated with a preexcitation, and occasionally an atrial ectopic focus are suggested as the pathophysiologic mechanisms of supraventricular tachyarrhythmias. In the reported case - atrial flutter, complete common atrioventricular canal with fetal trisomy 18 - the atrial flutter was probably provoked by the dilatation of the atria due to the regurgitation of both atrioventricular valves. This case indicates the need for a detailed echocardiographic examination (using two-dimensional, M-mode, and Doppler-echocardiography) in each case of fetal tachyarrhythmias in order to exclude associated cardiac defects, possibly in association with a chromosomal anomaly.

Adult↗
PubMed1988

Direct intrauterine fetal treatment of fetal tachyarrhythmia with severe hydrops fetalis by antiarrhythmic drugs.

In cases of non-immune hydrops fetalis caused by tachyarrhythmias, the transplacental passage of antiarrhythmic drugs may be hampered. When this is proven by fetal blood sampling in cases of tachyarrhythmia refractory to transplacental treatment, additional administration of antiarrhythmic drugs into the fetus is necessary and seems to improve the results. Although injections of antiarrhythmic agents in fetal ascites are also highly effective, intravascular administration by sonographic guidance is to be preferred. Then, simultaneous measurements of fetal and maternal drug levels are possible for the evaluation of pharmacokinetics and for monitoring the antiarrhythmic therapy.

Anti-Arrhythmia Agents↗
PubMed1988

Intrauterine therapy of fetal tachyarrhythmias: intraperitoneal administration of antiarrhythmic drugs to the fetus in fetal tachyarrhythmias with severe hydrops fetalis.

In cases of fetal tachyarrhythmia with congestive heart failure accompanied by signs of non-immune hydrops fetalis, the transplacental treatment of the fetus with antiarrhythmic agents by administration of drugs to the mother is only rarely successful. In the two cases reported, the cardioversion of a supraventricular tachycardia to a sinus rhythm or a constant 2:1 AV conduction block to a 1:1 AV conduction with atrial flutter could only be achieved after additional antiarrhythmic treatment directly administered to the fetus using ultrasound guidance. Drugs used include: beta-methyldigoxin, verapamil, propafenon, and they were administered according to the dosing amounts for intravascular injections. This was carried out 12 times in case 1 by the intraperitoneal route into the fetal ascites and twice in case 2. This led in both cases to varying durations of a sustained sinus rhythm after 5-15 minutes. This technically relatively simple procedure affords the option of rapidly achieving high concentrations, even when antiarrhythmic agents are administered which do not adequately cross the placenta. This direct treatment is indicated in cases of tachyarrhythmia with advanced signs of non-immune hydrops fetalis as a supplement to the high-dose transplacental therapy using antiarrhythmic agents.

Adult↗
PubMed1987

Listeriosis: a cause of non-immune hydrops fetalis.

A case of prenatally diagnosed non-immune hydrops fetalis, that was later shown to be caused by listeriosis, is presented, and the clinical course, as well as the appropriate diagnostic and therapeutic procedures are described. We conclude, that listeriosis should be excluded, whenever a non-immune hydrops fetalis is associated with septicemia, influenza-like illness and fever of unknown origin.

Adult↗
PubMed1987

[Decreased alpha fetoprotein in maternal serum in relation to increased alpha fetoprotein in amniotic fluid in a case of fetal trisomy 21 associated with esophageal atresia].

A subnormal maternal serum alpha-fetoprotein level associated with elevated alpha-fetoprotein level in amniotic fluid was found in a case of trisomy 21 combined with esophageal atresia in a fetus at 36 + 5 weeks of gestation. The significance of this observation is discussed in view of the possible biologic mechanisms resulting in maternal serum alpha-fetoprotein reduction in cases of fetal autosomal trisomies. The most likely hypotheses seem to be a reduced fetal alpha-fetoprotein production and/or an alteration of the placental regulation of the alpha-fetoprotein transfer from fetal to maternal blood via the placenta.

Adult↗
PubMed1987

[Concanavalin A reactivity of alpha-fetoprotein in the amniotic fluid in autosomal trisomies of the fetus].

Fetal trisomies 21 and 18 have been found to be associated with low maternal serum alpha-fetoprotein values in the second trimester of pregnancy. The concanavalin A reactivity of amniotic fluid alpha-fetoprotein of 35 fetuses with trisomy 21 and 7 fetuses with trisomy 18 between the 16th and 24th week's gestation has a normal pattern of distribution. In 7 cases of autosomal trisomies in association with other malformations (neural tube defect, omphalocele, non-immune hydrops fetalis), the percentage of the fraction without affinity for concanavalin A was significantly lowered. These results do not support the hypothesis of a qualitatively altered fetal production of alpha-fetoprotein as a cause of lowered maternal serum alpha-fetoprotein levels in cases of fetal autosomal trisomy.

Chromatography, Affinity↗
PubMed1987

[Supraventricular tachycardia of the fetus in the 3d trimester of pregnancy following persistent supraventricular extrasystole].

Persistent supraventricular extrasystoles are antepartally, intrapartally and postpartally the most frequent form of arrhythmias, and do not cause fetal congestive heart failure (hydrops fetalis). The premature beats often disappear spontaneously prenatally, but in most cases within the first two weeks of life. The extremely rare observation of the occurrence of a supraventricular tachycardia in the 37th week of gestation in a fetus with persistent supraventricular extrasystoles from the 20th week of gestation onward and with a postnatally diagnosed Wolff-Parkinson-White syndrome is described. Because of the importance of this complication of supraventricular extrasystoles (a supraventricular tachycardia of the fetus can cause a cardiac failure with hydrops fetalis and eventually intrauterine death), it is important that all fetuses with supraventricular extrasystoles be closely monitored by frequent observation of the fetal heart rate using ultrasound (M-mode-echocardiography), cardiotocography and auscultation. Postpartally a cardiologic examination of these newborn infants is necessary, particularly in order to exclude the presence of a preexcitation.

Cardiac Complexes, Premature↗
PubMed1987

[Cystic hygroma of the neck and non-immunologic hydrops fetalis].

Fetal cystic hygromas are a manifestation of early lymphatic obstruction. They are mostly associated with nonimmune hydrops fetalis. They often occur in a number of chromosome abnormalities (Turner syndrome and Down syndrome). We report on a prenatally detected case with nuchal cystic hygroma and nonimmune hydrops fetalis without chromosome aberration and without further major malformations. Postnatally hygroma and hydrops regressed.

Ascites↗
PubMed1986

Hydrothorax, ascites, and right diaphragmatic hernia.

Hydrothorax and/or ascites may be the most striking finding in children with right diaphragmatic hernia. The clinical, radiographic, and pathologic findings of five children with right diaphragmatic defects through which the liver had herniated are described. Three presented with a right hydrothorax, one with a right hydrothorax and ascites, and another with ascites. All four children with large right hydrothoraxes were found to have an incarcerated peritoneal sac filled with fluid in the right side of the chest at surgery or autopsy. Lymphatic congestion and obstruction was the probable cause for the fluid collection, which tended to enlarge with time. This condition may be life threatening, and two of the four patients died soon after birth because of hypoplasia of the lungs. Fetal ultrasonography in both had disclosed right intrathoracic cystic masses, and in one, intrauterine aspiration to decompress the lungs had been attempted. The other two patients are alive and well following surgical repair at 1 week and 7 months of age. Ascites was present in two patients and was believed to be due to hepatic venous obstruction, a mechanism similar to that responsible for the Budd-Chiari syndrome.

Ascites↗
PubMed1985

Prenatal diagnosis of genetically determined early manifestation of autosomal dominant polycystic kidney disease?

A case of an unusually early manifestation of autosomal dominant polycystic kidney disease (ADPKD) is reported that was prenatally diagnosed by ultrasound. The ultrasonographic picture showed greatly enlarged kidneys and increased echogenicity that was indistinguishable from cases of autosomal recessive polycystic kidney disease or Meckel syndrome without further information. Because of two further cases of early manifestation of ADPKD within the family reported (brother and cousin), as well as several other "familial" cases reported in the literature, we postulate that genetic factors are involved (modifying alleles). When reported observations of "familial" cases of early manifestations of ADPKD are made, genetic counseling should be considered.

Female↗