Widness JA. Fetal risks and neonatal complications of diabetes mellitus. Endocrine Disorders in Pregnancy. Metabolic problems in infants of diabetic mothers IDM'S.
Congenital anomalies Because the incidence of congenital anomalies is increased in IDM's, a thorough physical examination is essential. Hypocalcemia The infant should be monitored for hypocalcemia frequently occuring in the first 24 hours see section on "Hypocalcemia". Diabetes mellitus complicating pregnancy. Gabbe's Obstetrics: Normal and Problem Pregnancies. Diabetes in pregnancy. The endocrine system. In: Kliegman RM, St. Nelson Textbook of Pediatrics. Updated by: Kimberly G.
Review provided by VeriMed Healthcare Network. Editorial team. Infant of diabetic mother. There are two forms of diabetes during pregnancy: Gestational diabetes -- high blood sugar diabetes that starts or is first detected during pregnancy Pre-existing or pre-gestational diabetes -- already having diabetes before becoming pregnant If diabetes is not well controlled during pregnancy, the baby is exposed to high blood sugar levels.
IDMs are more likely to have: Breathing difficulty due to less mature lungs High red blood cell count polycythemia High bilirubin level newborn jaundice Thickening of the heart muscle between the large chambers ventricles If diabetes is not well-controlled, chances of miscarriage or stillborn child are higher.
Other symptoms may include: Blue skin color, rapid heart rate, rapid breathing signs of immature lungs or heart failure Poor sucking, lethargy, weak cry Seizures sign of severe low blood sugar Poor feeding Puffy face Tremors or shaking shortly after birth Jaundice yellow skin color. Exams and Tests. Before the baby is born: Ultrasound is performed on the mother in the last few months of pregnancy to monitor the size of the baby relative to the opening to the birth canal.
Lung maturity testing may be done on the amniotic fluid. This is rarely done but may be helpful if the due date was not determined early in pregnancy. After the baby is born: The baby's blood sugar will be checked within the first hour or two after birth, and rechecked regularly until it is consistently normal.
To investigate the regulation of erythropoiesis in these infants, we measured cord blood erythropoietin EP levels by a sensitive radioimmune assay and examined the growth of erythroid progenitor colonies in a series of IDM and control infants.
Fifteen of 18 diabetic mothers were managed on a protocol emphasizing careful glycemic control throughout pregnancy; 10 had glycosolated hemoglobin values within the normal, nondiabetic range during the third trimester.
Plasma is separated and packed red cell volume is measured to give the hematocrit. An automatized analyzer gives lower values when compared to the centrifugation method [ 11 ]. In most of the studies conducted about polycythemia, centrifugation method has been used. Hyperviscosity and polycythemia are different definitions although they are often used interchangeably. Viscosity is, on the other hand, the property of the liquid which provides the resistance of that liquid against placing between the two layers of the fluid.
Viscosity equals to the ratio of powers effective on the unit square of the liquid or sliding tension to sliding velocity. Sliding resistance of the liquid or its response to changes in sliding velocity is somewhat different from other liquids as whole blood is not a homogenous liquid [ 9 ].
Hyperviscosity is the decrease of blood fluidity, and defined as a viscosity above the 2 standard deviation of the mean.
Hyperviscosity syndrome, on the other hand, is a syndrome of circulatory disorder developing secondary to increase in resistance against blood flow [ 9 , 11 ]. Except for the hematocrit level, there are a lot of factors affecting whole blood viscosity.
Leukocytes, platelets, plasma proteins, immunoglobulins and coagulation factors are the other cellular elements which affect the whole blood viscosity. It is not easy to measure viscosity, and Wells-Brookfield viscometer is used with this aim. However most of the neonatal intensive care units do not have this device, and high hematocrit level and the presence of polycythemia-associated symptoms are taken into account as the determinator of hyperviscosity [ 9 , 11 ].
Tissue hypoxia, acidosis and hypoglycemia develop secondarily to regional effects of hyperviscosity. Tissue blood supply and oxygenation are disrupted. Oxygen carrying capacity is determined by the hemoglobin level and blood flow, it is optimal at the normal hematocrit levels, and oxygen transport is decreased at low hematocrit levels as the oxygen binding capacity decreases [ 17 ].
Increase of blood volume, while the hematocrit is the same, increases blood flow and oxygen transport by decreasing peripheral vascular resistance with vasodilatation. This mechanism constitutes the basis of treatment of polycythemia [ 7 ]. Decreased microcirculation has been deemed responsible for the morbidity associated with polycythemia. Thrombi ocurring in microcirculation may cause symptoms in central nervous system, kidneys, surrenal glands, cardiopulmonary and gastrointestinal systems [ 19 ].
Drew, et al. As a conclusion perfusion and tissue oxygenation are disturbed, plasma glucose concentration decreases, cerebral glucose uptake is disturbed and risk of cerebral morbidity is increased with microthrombi formation as the viscosity increases [ 7 , 17 , 21 ]. In neonatal polycythemia increased destruction of increased erythrocyte mass with a relatively shorter erythrocyte life span primarily contributes to hyperbilirubinemia. Hypervolemia may lead to congestive heart failure, pulmonary edema and cardiopulmonary failure, and hypovolemia may cause hypoxic-ischemic organ injury [ 12 ].
Although the etiology of polycythemia is multifactorial, there are two primary mechanisms: passive erythrocyte transfusion and active increased intrauterine erythropoiesis Table 1 [ 22 ]. Polycythemia secondary to excess erythrocyte transfusion to the fetus Passive polycythemia may occur due to delayed clamping of the cord, acute fetal distress and intrapartum hypoxia, twin-to-twin transfusion syndrome, materno-fetal transfusion and holding the baby below the level of introitus [ 9 , 11 ].
Table 1: Etiology of neonatal polycythemia [ 22 ]. View Table 1. In acute fetal distress and peripartum hypoxia transcapillary leakage of plasma occurs and blood flow from placenta to fetus increases, and all these result in increased plasma volume and erythrocyte mass in the fetus [ 9 ]. Clamping of the umbilical cord later than 3 minutes after delivery of the baby is defined as "delayed cord clamping" [ 11 ]. Carpasso, et al. Therefore, early cord clamping and holding the baby at the level of introitus at the time of delivery could play a role in prevention from polycythemia by minimizing materno-fetal transfusion.
On the other hand, however, no statistically significant differences were reported in the hematocrit values of newborns whose umbilical cord was clamped early or late [ 24 ]. Polycythemia secondary to increased intrauterine erythropoiesis active polycythemia is usually observed in cases of placental insufficiency, intrauterine hypoxia and situations associated with the fetus.
Maternal hypertension [ 26 ], preeclampsia, maternal diabetes mellitus type 1 diabetes mellitus and gestational diabetes [ 27 ], maternal cyanotic heart disease, intrauterine growth retardation, postmaturity, living at high altitude and maternal smoking are all associated with this mechanism.
Situations associated with fetus may develop secondarily to problems either in fetus or maternal diseases Table 1.
There is an increased risk of polycythemia in diseases with a genetic inheritance such as trisomy 18 and trisomy 13 [ 28 ], trisomy 21 [ 29 ], and Beckwith-Wiedemann syndrome. Congenital hypothyroidsm, neonatal thyrotoxicosis and congenital adrenal hyperplasia are the other causes of polycythemia associated with the fetus [ 9 , 11 ].
Another etiologic classification of polycythemia is the one based on the volume status of plasma: normovolemic, hypervolemic and hypovolemic [ 12 ].
There is an increase in erythrocyte mass while intravascular volume is normal. There is an increase in plasma volume in association with an increased erythrocyte mass. It is usually seen in cases of acute transfusion such as maternofetal transfusion and twin-to-twin transfusion. It is due to the relative increase of erythrocyte mass in comparison to plasma volume. This situation usually develops due to intravascular dehydration [ 12 ]. In symptomatic newborns polycythemia may affect many organs and systems.
Hyperviscosity, decrease of tissue perfusion, and metabolic complications such as hypoglycemia and hypocalcemia are responsible for clinical signs [ 10 , 32 ].
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