Perinatal Physiology

The transition from life in utero to life outside the womb brings many changes in the physiology and features are released. Also problems of perinatal period. Bilirubin metabolism old or damaged erythrocytes are removed by the reticuloendothelial system, the heme to bilirubin degrades (1 g hemoglobin yields 35 mg bilirubin), removed from the circulation. This bilirubin is then transported to the liver, where absorbed by the hepatocytes. Bilirubin there through the glucuronyl with Uridindiphosphoglukuronsäure (UDPGA) is converted (conjugated bilirubin) to Bilirubindiglukuronid and actively secreted into the bile ducts. From there, the Bilirubindiglukuronid enters the gastrointestinal tract into the meconium, but can not be eliminated because the fetus usually settles no chairs. The enzyme ?-glucuronidase, which is liberated from the brush border of the small intestine wall into the intestinal lumen, the deconjugated Bilirubinglukuronid. Free (unconjugated) bilirubin is then reabsorbed from the intestinal tract and absorbed into the fetal circulation. Fetal bilirubin is finally excreted in which it crosses the placenta along a concentration gradient and into maternal plasma and eventually conjugated from the maternal liver and is excreted. Immediately after birth, the connection is terminated with the placenta. Although the liver of the newborn can conjugate continue recording the accumulating bilirubin and eliminated in the bile and from there into the chair. But as the physiological intestinal bacterial colonization is not yet developed in the newborn, the bilirubin in the gut can not be oxidized to urobilinogen. The unchanged bilirubin remains in the chair, which gives this the typical light yellow color. As well as the fetus of the gastrointestinal tract of the neonatal ?-glucuronidase contains, so that a part of bilirubin is deconjugated. Feedings lead to gastrocolic reflex, so that bilirubin is excreted in the stool, before it can be deconjugated and reabsorbed. In contrast, the unconjugated bilirubin is reabsorbed from the intestinal lumen in many newborns and again the cycle fed (enterohepatic circulation of bilirubin), which then contributes to the physiological hyperbilirubinemia and jaundice (neonatal hyperbilirubinemia). Cardiovascular function in the fetal circulation, blood flows with right-left shunt through the patent ductus arteriosus (which connects the pulmonary artery and the aorta) and foramen ovale (the right and left atrium connects) from right to left, past the nichtoxygenierten lungs. This so-called. Right-left shunt is mainly due to the high pulmonary artery and the relatively low systemic (including the placenta is to count) resistance. Approximately 90-95% of the ejected from the right ventricle blood flow directly over into the systemic circulation and thus to the lungs. Due to the low fetal PaO2 (about 25 mmHg) and locally produced prostaglandins of the ductus arteriosus is kept open. The foramen ovale is held open by different pressure conditions in the courts: the left atrial pressure is relatively low due to the low blood reflux out of the lungs, the right atrial pressure, however, because of the large blood return flow from the placenta comparatively high. After the first breath occurs fundamental changes in the system, resulting oval to increased pulmonary blood flow and functional closure of the foramen. As a result of vasodilation by the expansion of the lung, to the increased PaO2 and PaCO2 of reduced pulmonary artery resistance decreases acutely. In addition, diminished by the elastic forces of the ribs and the thorax of interstitial pulmonary pressure, which leads to a further increase in blood flow through the pulmonary capillaries. Increased venous return from the lungs increases the left atrial pressure, thereby reducing the pressure difference between the left and right atrium; This effect contributes to the functional closure of the foramen ovale of. Once a normal blood flow has stopped in the lungs, the venous return increases from the lungs, then the left atrial pressure rises. By breathing PaO2 is increased, which leads to a constriction of the umbilical artery. The placental blood flow is reduced or interrupted, resulting in decreased blood flow to the right atrium. Thus, the right atrial pressure decreases, while the left atrial pressure increases; as a result, the two components of the fetal interatrial septum (septum primum and septum secundum) are pushed together, resulting oval for stopping flow through the foramen. For most people, the two septa eventually merge and the foramen ovale does not exist anymore. Shortly after birth exceeds the systemic pulmonary artery resistance; the fetal circulation conditions have been reversed. Accordingly, it (transition cycle called.) Results in a reversal of blood flow through the ductus arteriosus and thus to a left-right shunt. This state lasts from shortly after birth (when the pulmonary blood flow increases, and it comes to an oval functional closure of the foramen) up to 24-72 hours when the ductus arteriosus narrowed. The blood that has the ductus arteriosus and the flows through the vasa vasorum of the aorta from a high Po2, which, together with changes in the prostaglandin metabolism to a constriction and closure of the ductus arteriosus. Once it is closed, there are circulatory condition as in adults. The two ventricles now pumps in series and there are no significant shunts more between the pulmonary and systemic circulatory system. During the first days after birth may lead to a return to fetal circulation situation in a stressed newborns. By asphyxia with hypoxia and hypercapnia there is a vasoconstriction of the pulmonary vessels and dilatation of the ductus arteriosus, which means a reversal of physiological adaptation processes previously described and a new right-left shunt through the further or again patent ductus arteriosus or reopened foramen ovale, or both leads. This leads to a pronounced hypoxia; This circulatory situation is called persistent pulmonary hypertension (Persistent pulmonary hypertension of the newborn) of the newborn (PPHN) or persistent fetal circulation (but without the involvement of the umbilical cord vessels). The aim of treatment must be to eliminate the factors that have led to the pulmonary vasoconstriction. Endocrine function The fetus is completely dependent on the transplacental glucose supply through the mother and does not contribute to glucose production. Early in pregnancy, the fetus to invest hepatic glycogen begins, with the largest share in the second half of the third half of the 3rd Glucose care of the newborn ends with the cutting of the umbilical cord at the same time increase the level of circulating epinephrine, norepinephrine and while decrease glucagon insulin levels. These changes gluconeogenesis and mobilization of glycogen stores are stimulated in the liver. In healthy newborns, the lowest glucose levels is achieved about 30-90 minutes after birth; after a glucose homeostasis is usually ensured. A very high risk of neonatal hypoglycemia have children with reduced glycogen stores (SGA and preterm children), critically ill newborns with increased glucose catabolism and children of diabetic mothers (secondary fetal hyperinsulinism). Hematopoietic function, the production of red blood cells is regulated exclusively by in utero fetal erythropoietin, erythropoietin maternal can not cross the placenta. Approximately 55-90% of the red blood cells contain fetal hemoglobin, which has a high O2 affinity. This achieves a high O2 concentration gradient in the placenta is maintained, thus ensuring an ample O2 transfer from mother to infant circulation. After the birth of this high O2 affinity is not as useful as the O2 is less easily released into the tissue. This has a particularly damaging for serious pulmonary or cardiac diseases with hypoxia. The switch from fetal to adult hemoglobin begins before birth; the site of erythropoietin production by a so far unspecified mechanism changes from the liver to the more sensitive peritubular cells of the kidney. By the abrupt increase in PaO 2 of 25-30 mmHg to 90-95 shortly after birth leads to a fall in the Serumerythropoetinspiegels, which in turn has the consequence that the formation of red blood cells between birth and the age of 6-8 weeks suspended , It comes to the physiological anemia in term infants or for anemia of prematurity (Perinatal Anemia: Physiological anemia). For immunological function due date most immune mechanisms are not yet fully functional even in full-term infants; all the more so, of course, is true for premature babies. is therefore a function of the immune system is designed weaker in newborns and young infants than in adults, so that an increased risk of serious infections. This risk is further increased by prematurity, maternal diseases, neonatal stress and medications (immunosuppressive and anti-epileptic drugs). The reduced immune responses in the newborn also explains the absence of fever or local clinical signs of disease (eg. As meningism) infection. The first already present in the yolk sac stage phagocytic cells are largely responsible during the fetal period for the anti-inflammatory response in the defense against bacterial and fungal infections. Granulocytes can be identified in the second month of pregnancy and monocytes in the 4th Pregnant month. Their ability to function improves with increasing gestational age is at term but still limited. The ultrastructure of neutrophils is indeed normal at birth, but the chemotaxis of neutrophils and monocytes in most newborn is reduced due to intrinsic malfunction of cell motility and adhesion. In immature children, this impairment of the function is more pronounced. The thymus is working approximately from the 14th week of pregnancy and the fine blood cells produced lymphocytes accumulate in the development in the thymus to. Also with the 14 week T-cells are present in the fetal liver and spleen, suggesting that at this age mature T cells are present in the secondary peripheral lymphoid organs first. The thymus shows its greatest activity during fetal development. Intrauterine he has a strong growth and is easy to recognize the healthy newborn on the X-ray image of the thorax. The maximum size is reached by the age of 10, from then on, the thymus is many years back slowly. The number of T-lymphocytes in the fetal circulation increases during the second trimester continuously and reached in the 30th-32. Week of pregnancy normal. Immediately after birth, infants have a relative lymphocytosis when compared to adults. The functionality of neonatal T lymphocytes is less than that of adult T-lymphocytes. This can lead to an insufficient immune response to antigens and inadequate production of cytokines. B-lymphocytes can be detected in the fetal bone marrow, blood, liver and spleen in the 12th week of pregnancy. Traces of IgM and IgG can be discovered in the 30th week of pregnancy in the 20th and IgA; because the fetus is typically located in an antigen free environment, immunoglobulins are formed (mostly IgM) in utero only small amounts. Increased IgM levels in umbilical cord indicate an intrauterine examination of antigens, usually by a congenital infection. Almost all IgG is purchased placenta from the mother. The placental transfer of IgG increases from the 22nd week of gestation, reached at birth or exceeds the IgG concentration maternal values. In preterm infants, the IgG concentration is low according to the degree of immaturity. The passive transfer of maternal immunity by transplazentares IgG and secretory IgA and antimicrobial factors in human milk (eg., IgG, secretory IgA, white blood cells, complement, lysozyme and lactoferrin) compensates for the immature immune system of the newborn and confers immunity against many bacteria and viruses. Protective immune factors from the milk dress the gut and the upper airways in association with the mucosa-associated lymphoid tissue and thereby reduce the likelihood of contamination of mucous membranes with respiratory and intestinal pathogens. Over time, the passive immunity decreases and reaches the age of three to six months minimum. In particular, premature infants may have a pronounced hypogammaglobulinemia in the first 6 months of life. In the first year of life of the IgG level is about 60% of the adult value. The concentration of IgA, IgM, IgD and IgE, which does not cross the placenta and are therefore present at birth only in traces, take slowly during childhood. IgA, IgM and IgA levels correspond to the age of 10years those of an adult. Lung function The fetal lung development precedes by phases of organogenesis and differentiation. Fairly well-developed alveoli and type II pneumocytes surfactant producing are around the 25th week and continue to mature throughout gestation. The liquid is continuously produced by the lung is composed of a transudate from the pulmonary capillaries, and the surfactant-factor which is secreted by the type II pneumocytes, together. In order for a normal gas exchange can take place at birth, the pulmonary alveolar and interstitial fluid must be removed immediately. On the one hand, this is achieved by the compression of the fetal thorax at birth and the other by absorption of liquid through sodium channel activation in epithelial cells in the lungs. The transient tachypnea of ??the newborn (transient tachypnea of ??the newborn) is probably caused by a delay of these mechanisms. At birth, the elastic restoring forces of the ribs and the first strong respiratory movements that air is drawn into the bronchial tree and creating an air-water interface in the alveoli provide. First breath surfactant is released in this interface. Surfactant, a mixture of phospholipids (phosphatidylcholine, phosphatidylglycerol, phosphatidylinositol), neutral lipids and four surface-active proteins that are all stored in lamellar inclusion bodies of type II pneumocytes, reduces the surface tension, which would atelectasis and increased work of breathing result otherwise. Surfactant acts effectively in small alveoli than in large alveoli, that is against the normal tendency of the small alveoli in large alveoli collapse (gemäßg the Laplace’s law, which states that in a resilient cavity of the pressure decreases while the volume increases). Some neonatal surfactant may not be produced in sufficient quantities to prevent diffuse atelectasis effective, so that then a respiratory distress syndrome (RDS, respiratory distress syndrome) developed (Idiopathic respiratory distress syndrome in newborns). Neonatal surfactant production in preterm infants may be increased by given to the mother before delivery corticosteroids. The production and function of surfactant can be reduced by maternal diabetes, neonatal meconium and neonatal sepsis. Renal At birth, renal function v. a. in preterm infants reduced generally. Glomerular filtration rate (GFR) increases with increasing gestational steadily, v. a. during the third trimester. Glomerular filtration rate (GFR) increases in the first months of life quick, but do not reach GFR, urea clearance and maximum tubular clearance by the age of 1-2 years, the values ??of adults.