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Diabetic fetopathy


Diabetic fetopathy — the disease of the neonatal period which is developing at newborns whose mothers suffer from a diabetes mellitus, and characterized by polysystemic lesion, metabolic and endocrine dysfunctions.

Reasons of a diabetic fetopathy:

Women with a diabetes mellitus and their newborns enter into risk group of development of obstetric and neonatal complications. It concerns as cases of the diabetes mellitus diagnosed before pregnancy and gestational diabetes. The diabetes mellitus at pregnancy proceeds labilno, the probability of a decompensation increases, vascular complications progress. The forecast for mother and a fruit depends not so much on the disease duration how many from extent of its compensation to and during pregnancy, initial complications and their subsequent progressing.

According to official statistics,  incidence of a diabetes mellitus among pregnant women in the Russian Federation over the last 10 years grew by 20%.

Gestational diabetes, as a rule, develops after the 20th week of pregnancy when the placenta — the new closed gland developing chorionic lactosomatotropinum on biological properties close to somatotropic hormone begins to function actively. This hormone promotes development of insulin resistance of peripheral fabrics, activates a gluconeogenesis in a liver and by that increases the need for insulin. The greatest risk of development of this pathology is noted at the women of mature age (is more senior 25 years) with obesity and/or a big increase of body weight during pregnancy having the relatives sick with a diabetes mellitus. The risk increases also if the previous pregnancies were followed by gestational diabetes or the child's birth with body weight more than 4000 g, and during this pregnancy the macrosomia and a hydramnion are diagnosed.

The following complications of pregnancy and childbirth at women with a diabetes mellitus are possible:
diabetes mellitus decompensation with alternation of hypoglycemic states and ketoacidosis;
deterioration in a current of a nephropathy, retinopathy, etc. complications
diabetes mellitus;
misbirths, especially on early terms (at 30% of pregnant women that by 4 times more often than in the general population);
heavy gestoses which are noted almost at 50% of pregnant women with a diabetes mellitus (in the general population — 3-5%);
the arterial hypertension induced by pregnancy, and, therefore, increase in risk of a preeclampsia and eclampsia (by 4 times more often than in population);
fetoplacental insufficiency and chronic pre-natal hypoxia of a fruit;
renal infections and vulvovaginitis against the background of decrease in nonspecific resistance of an organism;
risk at the time of delivery in connection with a large fruit;
the increased risk of operative measures (Cesarean section), operational and postoperative complications;
high risk of premature births (are noted in 24% of observations in comparison with 6% in population);
malformations of a fruit and mortinatality (in 10 — 12%).

Диабет беременных приводит к диабетической фетопатии

Diabetes of pregnant women leads to a diabetic fetopathy

Symptoms of a diabetic fetopathy:

The most frequent malformation at children whose mothers are sick with a diabetes mellitus is the syndrome of caudal dyskinesia including absence or a hypoplasia of a sacrum, a tailbone, sometimes lumbar vertebrae, an underdevelopment of femurs. Describe also increased risk of development of defects of a brain (anencephalia), kidneys (aplasia), doubling of ureters, heart diseases, the return arrangement of bodies.

It is necessary to remember that the frequency of perinatal complications depends on weight and extent of compensation of a diabetes mellitus. In this regard it is necessary to try to obtain rigid compensation of a diabetes mellitus already when the woman plans pregnancy. The same requirement belongs also to the gestational period.

At pregnancy against the background of a diabetes mellitus in 90-100% of observations at a fruit the syndrome called by a diabetic fetopathy forms. Perinatal mortality at a diabetic fetopathy is 2-5 times higher, than in the general population.

Several factors are the cornerstone of a diabetic fetopathy: fetoplacental insufficiency, hormonal placental dysfunction, mother's hyperglycemia.

The hyperglycemia of mother leads to a hyperglycemia in the blood circulatory system of the child. Glucose easily gets through a placenta and continuously passes to a fruit from mother's blood. There is also active transport of amino acids and transfer of ketonic bodies to a fruit. Unlike it insulin, a glucagon and free fatty acids of mother do not get to blood of a fruit. In the first 9-12 weeks of pregnancy the fruit pancreas does not produce own insulin yet. This time corresponds to that phase of an organogenesis of a fruit when,  at a constant hyperglycemia of mother,  at it heart diseases, a backbone, a spinal cord and a GIT form preferential.

From 12th week of pre-natal development the pancreas of a fruit begins to synthesize insulin and in response to a hyperglycemia the reactive hypertrophy and a hyperplasia of β-cells of a fetalis pancreas develops. Owing to a giperinsulinemiya the fruit macrosomia, and also lecithin synthesis oppression develops that explains the high frequency of development respiratory a distress syndrome at newborns. Besides, in a pathogeny of a macrosomia excess intake of glucose and amino acids through a placenta, and also a hypercorticoidism matters. Lability of level of glucose stimulates activity of system in blood of mother a hypophysis — bark of adrenal glands of a fruit.

As a result of a hyperplasia of β-cells and a giperinsulinemiya tendency to heavy and long gipoglikemiya at newborns appears. At department of a placenta intake of glucose to a fruit sharply stops, and the giperinsulinemiya at the same time does not decrease owing to what within the first hours after the birth the hypoglycemia develops.

Clinic and diagnostic criteria:
the big mass and length of a body at the birth (macrosomia);
pastosity, hypertrichosis, crimson and cyanotic coloring of integuments;
bloated plethoric face (as at treatment by glucocorticoids);
disturbance of post-natal adaptation;
morfo-functional immaturity;
clinical symptoms of a hypoglycemia;
syndrome of respiratory frustration because of surfactant synthesis disturbance;
cardiomegaly in 30% of cases, inborn heart diseases;
other inborn defects;
gepato-, splenomegaly;
the pre-natal hypotrophy is possible, but even at the same time lines of a cushingoid syndrome soyokhranyatsya;
hypocalcemia and hypomagnesiemia.

Speak about a hypoglycemia of newborns if in the first 72 hours of life sugar level in blood at the full-term newborns makes less than 1,7 mmol/l, at premature and newborn with an arrest of development — less than 1,4 mmol/l. In practice, however, recognize that if sugar level in blood at the newborn is lower than 2,2 mmol/l, then therapy is already necessary.

Criterion of a hypoglycemia after 72 hours of life is sugar level less than 2,2 mmol/l.

It is necessary to emphasize that the hypoglycemia can develop not only at a diabetic fetopathy. Can lead to this state, for example, gestoses and a Rhesus factor sensitization owing to deep disturbance of fetoplacental metabolism and preferential use by a fruit of endogenous glucose. The hypoglycemia can be expected at prematurity, a pre-natal hypotrophy, at twins, at asphyxia and overcooling in labor, an intracranial birth trauma, SDR, GBN, a kernicterus. If at a diabetic fetopathy the hypoglycemia is defined in the first 2-6 hours of life (an early neonatal hypoglycemia), then in other situations a bit later — in the range of 12-36 hours after the birth, is more often by the end of the first days (a classical tranzitorny hypoglycemia).

Clinical symptoms of a hypoglycemia at newborns are various also nepatognomonichna. On occurrence they are distributed as follows: a hyperexcitability, revival of reflexes, a tremor, cyanosis, spasms, apnoea attacks, the angry shout, is more rare — block, weakening of suction, a nystagmus. Complexity of diagnosis consists that at newborns of risk group similar symptoms arise also at a normoglikemiya. A decisive diagnostic character, in addition to definition of sugar in blood, disappearance of symptoms after administration of glucose is.

For timely diagnosis of a hypoglycemia at newborns with a diabetic fetopathy sugar level in capillary blood needs to be determined at once after the birth and repeatedly in 1-2 hours. In the subsequent the level of sugar is determined by each 3-4 hours within 2 days, and then — each 6-8 hours within 2 more days. Approximately normalization of sugar occurs for 6-7 days.

Treatment of a diabetic fetopathy:

The principles of nursing of newborns at mothers with a diabetes mellitus:
strict maintenance of optimal conditions of the environment;
rational feeding;
adequate oxygenotherapy;
prevention and correction of a hypoglycemia and other disturbances of a homeostasis;
use of antioxidants;
symptomatic therapy of the revealed disturbances.

Prevention and correction of a hypoglycemia and electrolytic disturbances is carried out as follows. To all children in 15-20 minutes after the birth suction of contents of a stomach and in need of its washing is carried out by normal saline solution. Then oral introduction of 5% of solution of glucose at the rate of 30-40 ml/kg a day is appointed. In 2 hours after the birth it is possible to begin feeding with a breast or the decanted breast milk. Within the first days feeding is carried out by each 2 hours.

If in 1-2 hours after the birth the size of a glycemia makes 1,65-2,2 mmol/l, it is necessary to continue administration of glucose in the oral way. At development of a hypoglycemia enter 10% glucose solution intravenously struyno in a dose of 2 ml/kg (at spasms — to 10 ml/kg or 20-25% solution of glucose of 4-5 ml/kg). Further pass to drop introduction 10% of solution of glucose at the rate of 0,1 ml/kg a minute (daily volume no more than 80 ml/kg). More strong solutions of glucose are not recommended to be entered as it causes further increase in level of insulin and provokes development of a secondary hypoglycemia. Sugar in blood each 1-2 hours before increase define it to 2,2 mmol/l. At achievement of this level intravenous administration of glucose is reduced on intensity, combining it with peroral purpose of glucose. Sugar in blood is controlled by each 4-6 hours.

At inefficiency of administration of glucose use a hydrocortisone in a dose of 2,5 mg/kg each 12 hours or Prednisolonum of 1 mg/kg a day, a glucagon of 0,3-0,5 mg intramusculary.

The hypocalcemia korregirutsya by intravenous administration of 10% of solution of a gluconate of calcium (1-2 ml on each 50 ml of glucose or 0,3 ml/kg a day), a hypomagnesiemia — intravenous administration of 15% of solution of magnesium sulfate in a dose of 0,3 ml/kg (perhaps intramuscular introduction of 25% of solution of 0,2-0,4 ml/kg a day).

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