[The calculation of the physical-chemical transfer processes in human and artificial lungs (author's transl)].
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Biomedical subjects
Publications and source records attributed to K G Schmidt.
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We examined two groups of fetuses in which echocardiography had been performed and in which ventricular volume overload eventually led to fetal hydrops. The first group (18 fetuses) had atrioventricular valve regurgitation and almost all of the fetuses had structural heart disease. No fetus in this group survived the neonatal period; only two of the pregnancies in this first group were terminated. A second group of three fetuses had ventricular volume overload from sacrococcygeal teratomas at 21 to 24 weeks' gestation. These fetuses also had nonimmune hydrops (or it developed), but they did not have structural heart disease or atrioventricular valve regurgitation. Combined ventricular output in this group was calculated by Doppler ultrasound to be greater than twice the normal output for fetuses of the expected gestational weight. The proportion of the combined output to the lower body and the placenta was increased with the increase to the teratoma, exceeding the increase to the placenta. In one fetus, serial study demonstrated increasing output and the development of hydrops. Intrauterine surgery was undertaken to control the high output failure. The abnormal variables tended to revert to normal after replacement of blood loss, and the hydrops disappeared. The pregnancy continued until the spontaneous rupture of membranes at 26 weeks' gestation forced delivery by cesarean section. The infant died from severe hyaline membrane disease. These findings suggest that, in some circumstances, fetal hydrops is a late sign of cardiac failure and heralds incipient death.(ABSTRACT TRUNCATED AT 250 WORDS)
With color Doppler flow mapping (CFM), we studied 16 children with total anomalous pulmonary venous connection (TAPVC), which was confirmed at cardiac catheterization, surgery, or autopsy in all but one case. The drainage was supracardiac in nine children, cardiac in four, and infracardiac in three. Obstruction to pulmonary venous return was present in seven children. Increased variance, reflecting disturbed blood flow, as well as increased velocities and aliasing were present in all patients. In patients without obstruction turbulence was present in the right atrium and throughout the common pulmonary venous structures. In patients with obstruction a discrete site of increased turbulence and velocity was identified at the site of obstruction. CFM allows rapid differentiation between normal and abnormal venous and arterial structures in TAPVC. In patients suspected of having TAPVC with obstruction, CFM complemented by pulsed Doppler facilitates the determination of the site of obstruction. CFM allows a more rapid appreciation of the anatomy in TAPVC than can be achieved by two-dimensional imaging alone.
During indoor building renovation a nosocomial epidemic of pulmonary aspergillosis occurred in a haematological ward, involving 10 patients with acute leukaemia undergoing intensive chemotherapy. Antifungal treatment included the combination of amphotericin B and 5-fluorocytosine during periods of granulocytopenia, followed by itraconazole after bone-marrow recovery. In five patients, lung aspergillomas disappeared completely, while significant improvement was observed in a further two patients. Itraconazole appeared to contribute significantly to the result, but the drug did not work during granulocytopenic episodes. Air analyses showed increased counts of fungal spores in ward locations with heavy traffic of patients and staff, suggesting the need to identify and avoid risk areas when placing patients undergoing intensive chemotherapy.