Gestational diabetes: risks to mother and fetus

Gestational diabetes mellitus (see also gestational diabetes by the same author ed. ), if not properly treated, carries a risk to the mother than to the fetus; increases the risk of spontaneous abortion, even late (after the third trimester), and congenital malformations.

Risks for the mother

Complications that occur during pregnancy are of concern poliamnios (or polyhydramnios – excess amniotic fluid) and hypertension, factors that can influence age and type childbirth.

Risks to the newborn

For a newborn, at birth, it may pose a higher risk of neonatal hypoglycemia, hyperbilirubinemia, hypocalcemia and exposure to abnormal sugar levels, macrosomia (overdevelopment of the fetus compared to gestational age) with a newborn weight equal to or greater than 4.5 kg ( diabetes pending).


Macrosomia: the incidence is about 25% of pregnancies d The diabetic mother is mainly associated with impaired growth in the second and third trimester, but this is also evident from events that occurred during the first trimester.

This may be the reason why babies of diabetic mothers set them slightly more than women who develop gestational diabetes, which causes less hyperglycemia and usually only in the second half of pregnancy. Fetal growth depends on the release of nutrients (glucose, amino acids and free fatty acids) and oxygen, which is regulated by placental blood flow and corresponding gradients at the placenta level.

In women with diabetes, the concentration in the blood of the three classes of nutrients increases, and their release into the fetus increases. Moderately high levels of glucose and amino acids stimulate fetal B cells, followed by insulin hypersecretion and cellular hypertrophy.

This combination appears to promote fetal growth.

The most important consequence of macrosomia is dystonia; vaginal delivery may not be possible in babies with high macro counts. (john c.pickup, 1994). Therefore, weight gain at birth is associated with birth trauma, both for the mother (trauma to the vagina, perineum and rectum) and for the fetus (damage to the brachial plexus nerve and collarbone fractures). ).

Dystochia of the shoulder and nerve lesions of the brachial plexus are serious consequences of macrosomia, caused by an increase in the diameters of the upper chest. Delivery is recommended before the 40th week, and if the estimated fetal weight exceeds 4500 g, a caesarean section is often recommended to reduce the risk of injury (O’Sullivan j. 1991). Morphological characteristics are mainly represented by the classic face of a cherub for subcutaneous fat, with a plump face, abundant hair along a spiral, bent and abducted limbs, a relatively small head circumference (as it is appropriate for gestational age, but not in harmony with the centiles of weight and length) (Barnes-Powell, 2007)


Determination of hypoglycemia in the first 24 hours of life requires detection of whole blood glucose levels below 40 mg / dL, both in term and in preterm labor.

The incidence of hypoglycemia in a child in a mother with well-controlled diabetes is 25%. and 40% of cases; hypoglycemia in newborns is a consequence of fetal hyperglycemia associated with maternal hyperglycemia.

Fetal hyperglycemia, in turn, is responsible for hyperinsulinism due to constant overstimulation of the islet cells of the baby’s pancreas.

If maternal hyperglycemia persists during labor, the fetal pancreas is constantly overstimulated and particularly severe neonatal hypoglycemia occurs.

Average values ​​- high blood sugar (at birth (and / or after the first hour of life) should be considered as a signal of subsequent hypoglycemic “risk”, since fetal glucose is approximately 70-80% of maternal glucose. p>

The recommended protocol for glycemic monitoring is to retest 30 minutes after birth, then 1.3 and possibly depending on levels found, even at 6, 12, 24, 36 and 48 hours of age.

In addition, being a lucosio is an important energetic substrate for the brain of a newborn; physiological adaptation of the newborn involves the rapid mobilization of endogenous glucose immediately after birth by catecholamines, which rapidly interact with positive effects on glucagon and inhibit in comparison with insulin.

Among the serious complications of unrecognized and untreated hypoglycemia, we note, in particular, neurological damage and seizures.

Hypocalcemia and hypomagnesemia

They pose an additional risk of seizures and, like hypoglycemia, correlate with poor glycemic control. maternal.

Calcium and magnesium levels tend to decline after 24 to 48 hours of life in 50% of babies born to diabetic mothers, so protocols recommend a first check 24 hours after birth.

The etiological basis can be found in maternal-fetal exchanges during pregnancy. In fact, during pregnancy, calcium, phosphorus and magnesium are actively transported across the placenta: fetal calcium exceeds on average 1 mg% of maternal calcium.

The supply of these minerals increases with the age of the gestational period and from the 28th week of gestational age, the increase reaches a peak.

At birth, when the umbilical cord is cut, nutrition is abruptly interrupted, causing a rapid decrease in the level of extracellular calcium and, therefore, the body’s need to activate hemostatic equilibria.

hypomagnesemia is defined as magnesium levels below 1.5 mg / dl.

The severity of hypocalcemia is directly related to the severity of maternal diabetes, which can affect homeostatic control mechanisms. It has been shown that a severe diabetic condition corresponds to an increase in the loss of magnesium in the urine. Maternal hypomagnesemia is followed by fetal hypomagnesemia, which in turn is responsible for the inability to secrete PTH and therefore hypocalcemia.

Polycythemia / hyperbilirubinemia

Polycythemia is defined as a hematocrit of venous levels of 65% or more.

This conclusion, physiologically obvious in 5% of children born at high altitudes, occurs with a frequency of 20% to 40% of cases in a child from a diabetic mother. The situation is likely to depend on the decrease in arterial oxygen and the increase in oxygen consumption that occurs in the presence of hyperglycemia, hyperketonemia, and hyperinsulinemia.

This fetal hypoxemia corresponds to a powerful stimulus for the production of erythropoietin in secondary erythropoiesis.

In the umbilical cord blood of a diabetic mother’s child, plasma erythropoietin concentrations are actually increased, which correlate with glucose and insulin levels in the amniotic fluid.

Therefore, abnormal maternal glycemic control may be associated with chronic intrauterine hypoxia, a factor responsible for the definition of polycythemia. Do not underestimate the fact that untreated polycythemia can lead a child to central neurological problems of varying severity from hyperviscosity syndrome. Polycythemia is hyperbilirubinemia caused in part by poor maternal glycemic control, as evidenced by the directly proportional correlation between bilirubin levels and glycosylated hemoglobin levels.

Risk of respiratory distress syndrome

Respiratory distress in newborns secondary to surfactant defect is a pathology typical of prematurity and the risk gradually decreases until 34 weeks of gestational age.

In the case of a newborn diabetic mother, the risk of this pathology is 5-6 times higher than in children of the same age, gestational children of a non-diabetic mother and continues until the end of pregnancy.

In fact, in these newborns, lung maturation and lung maturation, as well as surfactant production, are delayed during pregnancy, as shown by studies that assessed lecithin / sphingomyelin ratios and amniotic phosphatitylglycerol levels, probably because high insulin levels inhibit the stimulatory effect synthesis of surfactant with steroids.

Hypertrophic or congestive myocardiopathy

Since glycogen synthesis is increased due to increased consumption of glucose in the liver, possible accumulation in the interventricular septum causes hypertrophic myocardiopathy, which can develop in 30% of those born to diabetic mothers.

It is characterized by hypertrophy of the septum and ventricular walls, hypercontractivity, decreased ventricular filling and ventricular outflow obstruction, as well as the risk of developing RDS.

Congestive myocardiopathy may also occur. due to hypoxia, hypoglycemia, hypocalcemia and polycythemia. (Gasparoni, 2010) Finally, in terms of long-term effects, they are mainly represented by an increased risk of metabolic syndrome (obesity, insulin resistance, glucose intolerance, hypertension and dyslipidemia in adults).