[Malrotation?].
Explore the source record for details and available documents.
Digestive System Abnormalities↗
Biomedical subjects
F Brus
Publications and source records attributed to F Brus.
Fatal ureaplasmal pneumonia and sepsis in a newborn infant.
Ureaplasma urealyticum was isolated in pure culture from blood tracheal aspirate and lung tissue in a newborn infant, who died of a severe pneumonia within 48 h after birth. The clinical course was characterized by persistent pulmonary hypertension of the newborn (PPHN). Post-mortem examination revealed extensive hyaline membrane formation combined with signs of inflammation in both lungs. The clinical and histopathological picture resembled that of early onset group B haemolytic streptococcal pneumonia/sepsis.
Humans↗
Streptokinase treatment for femoral artery thrombosis after arterial cardiac catheterisation in infants and children.
Data on 205 children who underwent retrograde arterial catheterisation were studied to assess the frequency of femoral artery thrombosis and the safety and efficacy of systemic streptokinase treatment for this complication. In 29 (14%) a transarterial balloon dilatation was performed. In 15 (7.3%) patients impaired arterial perfusion due to vascular spasm with or without thrombus formation was seen in the cannulated leg after catheterisation. Despite heparinisation, signs of impaired arterial circulation persisted in nine patients (4.4% of the total). In these patients femoral artery thrombosis was strongly suspected. Six (53%) of these had undergone a balloon dilatation. Therefore in this study the risk of femoral artery thrombosis developing was 12 times greater after transarterial balloon dilatation than after arterial catheterisation without dilatation (20.6% v 1.7%). Systemic infusion of streptokinase was started in all patients with femoral artery thrombosis. Arterial perfusion became normal in all patients, though in one this was delayed. Haematological monitoring showed lengthening of the thrombin time and a decrease of the fibrinogen concentration during streptokinase treatment. There were no serious complications. Systemic infusion of streptokinase is a safe and useful treatment in children with persistent femoral artery thrombosis after arterial cardiac catheterisation.
Cardiac Catheterization↗
[Obstructive disorders of the urinary tract in the unborn child].
The history of a patient with signs of urinary tract obstruction in utero is presented. After this presentation pathophysiologic, diagnostic and therapeutic aspects of prenatal detected obstructive malformations of the urinary tract are discussed. Obstructions of the fetal urinary tract may cause damage to the developing renal parenchyma, impairment of the normal lung development and fetal growth retardation. The seriousness of obstruction and the time of appearance during pregnancy determine the severity of the damage to the unborn child. Optimum management in case of prenatal detected obstructive uropathies needs good information about renal function of the fetus, the presence of other structural defects or chromosomal abnormalities and also the maturity and state of development of the lungs. Besides careful ultrasonography of the fetus invasive methods of investigation may be necessary. In case of fetal obstructive uropathy intrauterine decompression or extrauterine decompression after an induced premature delivery can be considered. However a good renal function and the absence of other severe structural or chromosomal malformations are necessary. When the gestational age has come to 32 to 34 weeks and the lungs are mature enough decompression of the urinary tract after an induced premature delivery can be done. When pregnancy is less than 32 weeks of gestational age and the lungs are immature intrauterine decompression is possible. The most used technique of intrauterine decompression so far is insertion of a percutaneous amniotic-bladder catheter. Antenatal detected obstructive abnormalities of the fetal urinary tract need optimum perinatal care besides good information and support of the parents.
Abnormalities, Multiple↗
[Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency in 2 patients with symptoms of Reye syndrome].
Two patients are described, who were submitted to our clinic with signs of the Reye syndrome. In both cases a medium-chain acylcoënzyme A dehydrogenase (MCAD) deficiency was diagnosed. This is an inborn error of the mitochondrial beta-oxidation of fatty acids. Stimulation of the fatty acid oxidation in case of this enzyme deficiency might result in a metabolic crisis presenting clinically as the Reye syndrome. The structure of a fatty acid molecule and the process of beta-oxidation of fatty acids are discussed shortly in this article. The most important clinical, diagnostic and therapeutic aspects of MCAD deficiency are presented next. A MCAD deficiency seems not to be rare in cases presenting as a Reye-like syndrome. Accurate distinction between MCAD deficiency and Reye syndrome can be made by gas chromatographic together with mass spectrometric analysis of urine. Investigation of so called crisis urine is of utmost importance. Confirmation of the diagnosis needs measuring of MCAD enzyme activity in cultured fibroblasts or in leucocytes of the patient.
Acyl-CoA Dehydrogenase↗
[Chlamydia pneumonia in infants].
Explore the source record for details and available documents.
Antigens, Bacterial↗