Alex

Dear colleagues! Allow me to share a brief observation that may explain some physiological and pathophysiological aspects of placental and umbilical cord circulation. Like everyone else, I was convinced of the arterial origin of umbilical cord pulsation. This is partially true, but not entirely true. With careful and relatively prolonged observation of umbilical cord pulsation, you can detect two stages of pulsation cessation. The first is associated with the cessation of arterial blood flow and the cessation of umbilical cord arterial pulsation. The second is manifested by the cessation of slow, weak pulse waves, resulting from the maternal blood flow pulse wave and the pulsation of the placental lacunae, and, as a result, umbilical vein pulsation. This type of placental circulation ceases with placental separation. Little attention has been paid to the second type of pulse waves in the umbilical vein. So how does venous placental blood flow to the fetus? The following factors contribute: the pumping function of the heart, the kinetic energy transferred from the pulsating umbilical arteries to the walls of the umbilical vein, and the pulsating energy of the uterine arteries and placental lacunae, which generates a pulse wave in the umbilical vein. The final waves of umbilical pulsation are like the mother's final letter, after which mother and child will be finally physically separated. Thus, these two types of pulsation are equivalent to the negative intrathoracic pressure created by inspiratory efforts. Based on this observation, it seems to me that the mechanism for the development of distress is more obvious in the presence of a single umbilical artery or thrombosis of one of the two umbilical arteries, as one artery cannot generate sufficient kinetic energy for umbilical venous return. This is especially true in the presence of excessive umbilical vessel tortuosity, endothelial damage (for example, during meconium passage), or slowed umbilical cord blood flow (for example, when the umbilical cord is wrapped around the fetus's neck, torso, and limbs). Previously, I was convinced that the physiologically justified time for delayed cord clamping and effective placental transfusion is the cessation of pulsation in the umbilical arteries. Cessation of arterial pulsation reflects recruitment and the establishment of sufficient blood flow in the pulmonary vessels. Now, I believe, given the right conditions, the physiologically justified time for umbilical cord clamping is separation of the placenta. The process of evolution is very rational. An example of this is the Hyrtla anastomosis, which is characteristic of New World primates and human fetuses. The blood volume in the placenta is likely identical to the volume of pulmonary vessels, and physiologically justified, personalized, delayed cord clamping will prevent circulatory disturbances and associated complications (such as significant ductus arteriosus, intraventricular hemorrhage, and necrotizing enterocolitis) in a significant proportion of premature infants. Thank you for your attention. Sincerely, Alex Nouzdin

Dear colleagues! May I ask you about your experience using helium in respiratory therapy? This experience appears interesting and promising for treating children at 22-24 weeks of gestation. Thank you in advance. Sincerely, Alex Nouzdin

Dear colleagues, good day to all! Allow me to share with you some thoughts on non-nutritive feeding. We all know the important role of non-nutritive sucking, its significance in the formation of a healthy infant gut microbiota and psychological comfort for mother and child. But we rarely consider the differences in the structure of the nipple skin from the rest of the skin. The nipple skin is extremely resistant to mechanical and chemical stress, and the breastfeeding period is a case in point. Any other area of skin becomes malignant as a result of chronic mechanical and chemical trauma associated with breastfeeding. Any area, but not the nipple skin. And I thought about the epidermis that the infant receives during feeding, which enters the bloodstream and serves as an important factor in training the immune system to recognize cells susceptible to mutagenic activity. The initial learning period occurred in utero, and the baby's immune system, already well-acquainted with the cell membrane proteins of various maternal cells (primarily blood cells), continues this training after birth through numerous nutritional and non-nutritive factors in feeding. What is so special about the nipple skin that it is responsible for training the infant's immune system, even if my description is rather primitive? What are the significant differences between the skin of the mother's nipple? Quite recently, a very simple idea occurred to me while examining the baby while the mother was breastfeeding. Unlike the rest of the skin, the nipple skin is pigmented. Why this particular area of skin, and what is its evolutionary significance? Could melanin not be the cause not only of these external differences, but also be the main factor in the nipple skin's increased stress resistance to external influences and a factor in the fine-tuning of the infant's immune system, ensuring effective antimutagenic activity throughout childhood, despite rapid growth and high proliferative cellular activity? Sincerely, Alex Nouzdin

Hi! We use CUROSURF in ELBW, VLW groups, and Survanta in 1500g+.

We discussed many time about hypoglycemia. And because both babies were with normal weight, normal nutrition, the energy store isn’t so important in hypoglycemia origin. Probably transient hyperinsulinemia is the main reason of. If we extrapolate the case on term infant, we know that in 2 weeks age the nutrition is 200 ml/kg per day and more, but in post term group the volume of nutrition is 70-90 ml/kg per day, and energy intake is restricted too. But, probably, the pancreas stimulation accordingly postconceptual age can be transient excessive, but appropriate the term infant of 2 weeks. It may the key point of hypoglycemia in post term group infant. Sorry my poor English. The both infants were clinically before and after hypoglycemic episodes absolutely normally. They haven’t breastfeeding difficulties, the frequencies of feeding were 10-12 times per day, without the night pause. We can’t image so low level of glucose only with low energy store. May be we are wrong.

Many thanks, Stefan, for your answer and links! Unfortunately we haven’t the opportunity of insulin level measurement. We many discussed our cases about, and hypothesized the next: babies were with normal trophic and haven’t problem with breastfeeding, haven’t serious weight loss, on hypoglycemia day they were 42+2, 42+3 postconceptual weeks, that poor glycogen store and transient hyperinsulinism are the reason. It’s only our hypothesis, unfortunately.

Good time for all! Dear colleagues, we are talking about preterm, late preterm, early term babies, and it’s very important for everybody. But the babies with gestational age about 42+ weeks are without our attention. We observed two babies with serious hypoglycemia (0,1 mmol/l) with seizures at 3 days of life, which we explained by transient hyperinsulinism associated with post term age. Seizures rapidly stopped by intravenous glucose infusion without any complications. Intravenous glucose 10% 12-8- 6 mg/kg/min infusion was 3 h, oral 20% 2 ml/kg hourly 6 h, and didn’t use after 9 hours of start with normal glucose blood tests. Both babies were on breastfeeding, 3500&3880 g weighted, and haven’t complications in pregnancy and mother’s diabetes before or during pregnancy. I couldn’t find any studies dedicated hypoglycemia and other metabolism problems in post term group of neonates, and with to ask your thoughts and your help. We haven’t any hormonal and genetics tests now. Many thanks for attention.

Many thanks, for answer! 5 days ago we repeated out experience with good result, with low flow O2. Only one think disturbed baby. He was hungry.

Good time for you, dear colleagues! I wish to ask about your Bevacizumab and Ranibizumab experience in ROP. Some earlier we star Ranibizumab injections in babies with ROP. We used it with local anesthetic expose in our third case. It was very easy for us and baby, especially for his respiratory statues (severe BPD, with PH in anamnesis). Innovation for us was no general anesthesia for Lucentis injections use. All our colleagues use fentanyl, ketamin and other intravenous anesthetics in same cases. If you Avastin or Lucentis use in ROP treatment, what type of anesthesia you prefer? Many thanks for your attention. Sorry. With good result for both eyes.

Dear colleagues, do you have experience with surfactant treatment in innate and nosocomial pneumonia? Many thanks for attention.

Baby is stable. Abdomen is not distention. After 5 days of TPN we began nutrition with small volume of breast milk. Stool is regularly. Some photo from mobile. Many thanks for advice

Dear netters Have a question? Baby 31 WG with IUGR (1030g). Clinically good, without respiratory, cardio support. Ultrasound N. Stool regular (2 times per day). In R graph peritoneal air on 2 day of life. Feeding is about 4 ml breast milk with good tolerance. Do you continue small feeding or TPN only?

Hi all! Baby 24 week gestation (820 g) in 21 day after birth without previous infection, anemia, O2 therapy, IV infusion, in good condition, develop osteomielitis of left hip. Blood culture- negative, stool – Staph. epidermidis. In R the slot of left hip joint is more than right on 2 mm. Do you use a local therapy, and what? Do you use immobilization, and how? Many thanks, Alex.

Dear colleagues! I meet a cases with different hemorrhage locations (4 intracranial, 1 in adrenal hematomas in both glands). All stories communicated with low-molecular- weight heparin use in pregnancy. Some later I sow in literature a case about subdural intrauterine hematoma of fetus associated with low-molecular- weight heparin use. Do you have information about complications in newborns after heparin administration in pregnancy? Thanks to you. Alex.

Dear member! Hi! Some later we observed a case with sever feto-maternal transfusion. Baby had mass 2900g, term of gestation. The RBC 0.59, Hb 23 g/l was in delivery room. pH 6.79, BE -20. No pulse of peripheral artery or umbilical artery was. The algorithm of therapy was like youth. O negative ErM 30 ml was done immediately after birth (total volume 95 ml). Totally NS before NICU was about 100 ml. We could correct shock, but miltiorgan disfunction was in progress for a 2 days. The leading syndrome of miltiorgan disfunction was respiratory distress. We do not have NO. A trying surfactant use was unsuccessful. The baby died in 2,6 days. It was a third case of severe intrauterine hemorrhage. We had get two babies before. The bleeding was acute with Hb about 37 and 42 g/l. A babies survive without problems. The therapy was same.