Management and delivery of pregnant women with diabetes


The most universal definition of diabetes is found in a report by the WHO Expert Committee (1981): “A condition of chronic hyperglycemia that can develop as a result of exposure to many exogenous and genetic factors that often complement each other.” Thus, the cardinal sign of diabetes is hyperglycemia.

There are two main types of diabetes mellitus (DM):
1. Insulin-dependent (IDDM).
and. Insulin secretion is significantly reduced.
b. Insulin sensitivity is high.
with. Clinical symptoms are usually well defined.
2. Non-insulin independent (NIDDM).
and. Insulin secretion is reduced moderately.
b. A decrease in insulin sensitivity to insulin-dependent tissues is characteristic.
with. Slow development without vivid symptoms.

CLASSIFICATION (WHO Scientific Group, 1985).
1. Clinical classes.
and. Diabetes mellitus (diabetes).
– Insulin-dependent diabetes.
– Insulin-independent diabetes.
b. Impaired glucose tolerance (NTG).
with. Pregnant diabetes (gestational diabetes).
2. Statistically significant risk classes.
(individuals with normal glucose tolerance, but with a significantly increased risk of developing diabetes).

1. A clear form of diabetes occurs in approximately 1 out of 325 pregnancies, but this is only 10% of all cases of diabetes during pregnancy.
2. The remaining 90% of cases of diabetes during pregnancy (or 4% in relation to all pregnant women) are attributable to gestational diabetes.

1. Changes in the metabolism of a pregnant woman are due to:
a. The consumption of glucose by the fetus as the main source of nutrition.
b. Accelerating the breakdown of fats with a tendency to ketoacidosis.
with. Insulin resistance associated with an increase in the blood of potentially diabetogenic (counterinsular) hormones (placental lactogen, cortisol). Progesterone and estrogens cause pancreatic B-cell hyperplasia and increase glucose secretion, which leads to increased glucose utilization, glycogen deposition in peripheral tissues and a decrease in liver glucose production. The consequence of this may be periods of hypoglycemia observed in early pregnancy.
2. Under normal conditions, the overall metabolic effect will be manifested by the following shifts:
a. Fasting hypoglycemia (3.37 plus or minus 0.49 mmol / L).
b. Hyperglycemia after ingestion and a later decrease in blood glucose after exercise (9.2 mmol / l instead of 7.7 mmol / l. After 2 hours in non-pregnant women).
with. The tendency to ketoacidosis, especially during fasting.


In 80% of women with uncompensated diabetes, pregnancy occurs with complications, the severity of which depends on the degree of compensation of the disease.

1. Greater susceptibility to infections.
2. High risk of developing late gestosis (30%).
3. An increase in the number of spontaneous abortions (30%).
4. An increase in insulin demand (by 30%).
5. Increased predisposition to acidosis and diabetic coma.
6. High frequency of fetal death after 36 weeks of gestation.
7. The high frequency of injuries in the mother due to the birth of large fruits (more than 4 kg).
8. Polyhydramnios (30-60%) associated with fetal polyuria and the reaction of the amniotic membrane to a high sugar content in water.

Children born to mothers with diabetes differ from the offspring of healthy mothers, which made it possible to introduce the concepts of “diabetic embryopathy” and “diabetic fetopathy.”
1. Antenatal fetal death is the most severe consequence of diabetic fetopathy.
2. Macrosomia – characterized by the birth of large children (more than 4000 g).
and. Some of these children have organomegaly, characterized by an increase in the kidneys and pancreas.
b. Fetal hyperinsulinism due to “overfeeding” with glucose contributes to:
– Lipogenesis,
– Fluid retention,
– Edema (fetal insulin edema),
– Body mass increase.
– The development of obesity, and subsequently type II diabetes (NIDDM).
3. Multiple malformations (7-8 times more often).
4. Dysfunction of many organs due to enzymatic immaturity.
5. The syndrome of respiratory disorders in the newborn. Hyperinsulinemia in the fetus blocks the activating effect of cortisol on enzymes involved in the synthesis of phospholipids in the cells of the alveolar epithelium, which leads to a decrease in the production of surfactant.
6. Fetal growth retardation in the presence of diabetes with vascular lesions.

In the presence of diabetes in the mother, the following points should be borne in mind:
1. The risk of developing diabetic fetopathy is great regardless of the depth of the malfunction of carbohydrate metabolism in the mother and it can be observed even with slight hyperglycemia.
2. Infants born to mothers with diabetes that developed during pregnancy have the same fate as babies born to women with clinically apparent forms of diabetes.
It should be remembered: there is no evidence of a negative effect of the mother’s disease on the long-term consequences of the physical or intellectual development of offspring. The risk of juvenile diabetes in children from mothers with diabetes does not exceed 2%.


Gestational diabetes is defined as “intolerance to carbohydrates of various severity, which began or was first detected during a real pregnancy. The definition is true regardless of whether or not insulin was used for the purpose of treatment, or if the disease continues after pregnancy. The definition does not exclude that glucose intolerance could precede pregnancy. ”

1. About 4% of all pregnant women, due to pronounced hormonal changes, experience a state of moderate insulin deficiency, increase glucose production by the liver, mobilize glycogen stores, and normal glucose tolerance is impaired, which leads to the development of diabetes mellitus in pregnant women (gestational diabetes).
2. The latter accounts for 90% of all cases of diabetes in pregnant women.


1. Complaints.
and. RDS is usually asymptomatic or the symptoms are mild and do not cause anxiety in a pregnant woman.
b. Sometimes there may be complaints of polyuria, thirst, increased appetite, but this is more often the case with untreated clinically apparent diabetes prior to pregnancy.

2. Risk factors for developing RDS.
RDS during previous pregnancy.
Childbirth is a large fruit (more than 4000 g) in the past.
History of stillbirth.
An unexplained death of a newborn in history.
Indication of a history of congenital malformations.
History of prematurity.
Miscarriage (more than 3 spontaneous abortions in I or II trimesters).
Chronic hypertension
Re-infection of the urinary tract.
Obesity (over 90 kg) A
family history of diabetes.
Pregnant women with glucosuria under conditions of normal or near normal fasting blood sugar levels.

3. Objective data.
and. The physical examination data for compensated SDB do not differ from the norm. Possible exceptions are:
– Patients with obesity
– Patients with hypertension
b. In the urine, glucosuria> 2+ is detected in more than two definitions.
with. Ketone bodies with uncompensated SDB.
d. The presence of bacteriuria.
e. VDSM is 2 cm higher than expected in the 2nd and 3rd trimesters (suspected macrosomia or polyhydramnios).
f. With the help of ultrasound with uncompensated SDB, fetal macrosomia, polyhydramnios and “thick placenta” (placenta thickness more than 4 cm) can be detected.
g. With compensated SDB, fasting blood glucose should
be less than 5.8 mmol / L, the maximum level after eating is no more than 7.7 mmol / L, and 2 hours after eating <6.6 mmol / L.

Screening for gestational diabetes.

a. Per os 50 g of glucose is given and after 1 hour the blood sugar is determined. The test is proposed to be carried out for all pregnant women at 24-28 weeks of gestation, at risk at 14-20 weeks.
b. If the test is performed in the morning on an empty stomach, the normal limit is 7.7 mmol / L, if after breakfast – 7.2 mmol / L.
Upon receipt of glycemic numbers less than the specified values ​​of RDS is excluded.
– Pregnant women without risk factors are not examined further.
– For pregnant women at risk, the test is repeated at 24-28 weeks.

Keep in mind: – a decrease in glucose tolerance is simply a marker for other concomitant conditions (obesity, large fetus, fetal malformations, previous stillbirths) that adversely affect the perinatal outcome
– the benefits of screening for blood glucose during pregnancy have not been established, therefore testing for glucose tolerance in all pregnant women seems unnecessary (possibly at risk).

a. The test is carried out after a period of nightly fasting for at least 8 hours.
b. Before testing, urine should be checked for glucose.
If the result is positive, it is necessary to check the fasting blood glucose level so that the test does not lead to ketoacidosis in women with undiagnosed diabetes (fasting blood glucose> 7.2 mmol / L).
If the result is negative, a test is performed.
with. The pregnant woman takes 100 g of glucose orally, then within 3 hours they determine the glucose content in the plasma of venous blood.
Normal blood glucose values:
– on an empty stomach – 5.8 mmol / l.
– after 1 hour – 10.6 mmol / l.
– after 2 hours – 9.2 mmol / l.
– after 3 hours – 8.1 mmol / l.
(indicators are shown using the Somogy-Nelson method)
If any 2 measurements are above normal, a diagnosis of
gestational diabetes is made.
If only one value is on the border of the norm or exceeds it, the diagnosis of SDB is not made.

1. During pregnancy, glucose is detected in the urine of approximately 10% of women, which is associated with a decrease in the glucose excretion threshold.
2. To solve the question of whether glucosuria reflects any pathological processes (with normal fasting blood sugar) or is physiological only when determining blood sugar after a load of carbohydrates.
3. TSH is performed immediately after the detection of glucosuria with a repeat of 30 weeks, when the likelihood of diabetes is highest.
4. Urine culture is necessary to detect asymptomatic bacteriuria (sometimes glucosuria is a symptom of renal tubule damage caused by chronic pyelonephritis).
5. Small meals are recommended to avoid the high glycemia observed with a rare but plentiful diet.

1. Diet.
and. Most women with SDB can maintain normal blood glucose with a single diet.
b. The most rational and physiological is the 6-tyrazovy diet.

It should be remembered: Regulation of the diet for diabetes of pregnant women does not significantly affect the outcome of pregnancy and the frequency of fetal macrosomia.

2. Necessary:
a. weekly or every 2 weeks to determine the level of fasting blood sugar (5.8) and three times after meals (7.7): 11 hours, 16 hours and 21 hours.
b. If the blood glucose determined on an empty stomach and after eating is constantly above normal, the possibility of treatment with insulin preparations should be discussed.

Keep in mind: – There is no evidence that treating women with a pathological result of glucose tolerance analysis reduces perinatal morbidity and mortality.
– no clear reduction in perinatal mortality has been obtained with the treatment of diabetes in pregnant women with insulin.
– Injection therapy without clear evidence of benefit, as in other areas of medical practice, should be considered unethical.

3. Mode.
and. It is necessary to recommend a pregnant woman a 10-20 minute walk before and after a meal, which helps to lower blood glucose levels.
b. Daily gymnastics.
with. A safe level of intensity of physical exercise is approximately 70% of the maximum possible: Pulse = (220 – age) x 0.7
4. Assessment of the fetus.
and. Daily self-registration of the number of movements of the pregnant fetus, starting from 28 weeks.
– The fetal movements should be considered for 1 hour in the position on the left side in the morning and evening hours (9 hours and 18 hours).
– Only large movements of the fetus due to its movements in the uterine cavity are taken into account.
– In all cases when less than 5 movements per 1 hour of self-registration are noted, the use of more objective examination methods is shown to prove the true hypoactivity of the fetus.
b. Ultrasound is necessary to exclude abnormalities in the development of the fetus (at 20 weeks) and to identify signs of fetal macrosomia, polyhydramnios (according to indications).
with. Non-stress test: from 36 weeks weekly until delivery.


If there are clinical manifestations of diabetes mellitus, then additional confirmation of the diagnosis is not required. In other cases, see also section C.

SEVERITY (out of pregnancy).
1. EASY – diabetes compensation is achieved by diet, there are no complications.
2. MEDIUM SEVERITY – compensation can be achieved by insulin in a dose of not more than 60 PIECES / day, there are no severe vascular complications.
3. HEAVY – involves complications (ketoacidosis, lability, retinopathy, nephroangiopathy, etc.) or the need for a dose of insulin more than 60 units / day.


1. The survey.
and. Determine the gestational age (ultrasound in the first trimester).
b. Sowing urine on the bacterial flora (every 4-6 weeks).
c. Ophthalmological examination (the first with dilated pupils to detect diabetic retinopathy).
– In some women, worsening retinopathy may result from pregnancy.
– Therefore, at least one complete ophthalmological examination is required in each trimester of pregnancy, and then 3 months after birth in pregnant women with retinopathy.
d. Renal function by serum creatinine level (every 4 weeks).
– If the level of creatinine in the blood serum is higher than 0.078 mmol / L. it is necessary to check the creatinine clearance.
– Normally, the clearance of endogenous creatinine in pregnant women is 110-120 ml / min, reaching 130 ml / min at the beginning of the second trimester.
e. Standard urine tests.
f. Determination of sugar in urine is not a reliable test (see also section Sh).
g. Control of blood sugar (the best control is daily, up to 7 times a day, the determination of glycemia using a glucometer).
h. Standard laboratory tests in the antenatal

2. Assessment of the condition and development of the fetus.
and. Daily self-registration of the number of movements of the pregnant fetus, starting from 28 weeks (see also section III).
b. Ultrasound:
– In the first trimester of pregnancy to determine the exact gestational age.
– At 20 – 22 weeks to exclude developmental abnormalities (necessarily fetal echocardiography).
– Then after 3-4 weeks to detect signs of macrosomia, polyhydramnios, and in the presence of vascular lesions in the pregnant woman to diagnose fetal growth retardation (with diabetes compensation, the number of studies can be reduced).
with. Non-stress test, starting from 34 weeks weekly (with labile form of diabetes – from 28 weeks).
d. A decrease in insulin demand may be a sign of developing placental insufficiency when insulin is more active due to a decrease in the production of placental lactogen.

3. Insulin therapy.
and. General principles.
– You need tight control of blood sugar throughout the day. This is the only way to minimize perinatal mortality.
– Fasting sugar should not exceed 5.6 mmol / L, 2 hours after a meal should be below 6.7 mmol / L.
– To control blood sugar levels, only insulin preparations are used.
Sugar-lowering oral preparations should not be used, since they alone can cause hyperinsulinemia in the fetus and hypoglycemia in the newborn.
It is better to use human insulin preparations to reduce the likelihood of developing antibodies to it. The degree of difference in the structure of insulin preparations from human increases in the following sequence: human <pork <bovine.
It should be borne in mind that large doses of insulin last longer, small ones are shorter: so 4 PIECES of simple insulin after s / c administration lasts about 4 hours, 9 PIECES – about 6 hours, and 40 PIECES over 8 hours.
b. Determination of insulin requirements.
– There are no universal treatment regimens for diabetes; in each case, the dose is selected individually.
– In a patient without residual secretion of his own hormone, insulin during subcutaneous injections is administered at a rate of 0.7-0.8 U / kg body weight, with about 60% to maintain the basal level (prolonged) and about 40% to cover post-caloric hyperglycemia (short) . Absolute insufficiency of endogenous insulin occurs, as a rule, 5 years after the first manifestations of childhood and youthful diabetes.
– In the first half of pregnancy, the need for insulin can be 1/3 lower than before pregnancy, from 20-24 weeks the need for insulin increases.
– The need for insulin is established on the basis of the glycemic profile, which includes the following multiplicity of determination of glucose in the blood (9 studies):
* Before each meal.
* 2 hours after each meal (breakfast, lunch, lunch, dinner).
* At 2 a.m.
– The glucosuric profile in pregnant women is unacceptable for these purposes.
– If the preliminary, obviously safe, dose of insulin is insufficient, it should be increased by about 20% and re-analyze the situation after 2-3 days.
– If the pregnant woman who received insulin has an increased fasting sugar or after eating, the dose should also be increased by 20%.
– In accordance with the obtained glycemic profile, the dose is selected as follows:
* Morning short insulin – based on sugar level after breakfast (11 hours) and before lunch (13 hours).
* Morning prolonged insulin – in accordance with the blood sugar after lunch (15 hours) and before dinner (17-18 hours).
* Short evening insulin – depending on blood sugar after dinner (19-20 hours) and before bedtime (22 hours).
* Evening prolonged insulin – taking into account blood sugar at 2 a.m. and on the morning of the next day on an empty stomach (8-9 hours).
with. Regimen of administration.
– In the morning before breakfast, 2/3 of the daily dose: 33% short insulin and 66% prolonged (short: prolonged ratio – 1: 2).
– In the evening before dinner, 1/3 of the daily dose: 50% short insulin and 50% prolonged (short: prolonged ratio – 1: 1).

3 INJECTION MODE (if morning hyperglycemia is observed when using the 2-injection regimen):
– In the morning before breakfast, 2/3 daily dose (ratio of short insulin: prolonged insulin = 1: 2)
– Before dinner, short insulin (50% of the total evening doses of insulin).
– Before going to bed (22 hours), prolonged insulin (50% of the total evening dose of insulin).
4 INJECTION MODE (if after using the previous schemes, afternoon hyperglycemia is observed):
– In the morning before breakfast, 2/3 daily dose (ratio of short insulin: prolonged insulin – 1: 2)
– Before lunch, insulin is short.
– Before dinner, insulin is short.
– Before bedtime, 1/3 of the daily dose of prolonged insulin.
d. Hypoglycemia. (see also section VIII)
1) The result of tight glycemic control is a tendency to develop hypoglycemia, especially at night, which is manifested by the following symptoms:
– Nightmares.
– Sweating during sleep.
– Cramps.
– Feeling overwhelmed, excessive weakness after sleep.
2) The hypoglycemic state usually develops with a decrease in blood sugar to or less than 2.7 mmol / L. In the occurrence of a hypoglycemic state, not only the absolute value of glycemia is important, but also the rate of its decrease.
3) The hypoglycemic state occurs acutely with the appearance of:
– General weakness,
– Hunger,
– Sweating,
– Hand shake,
– Heartbeat,
– Dizziness.
4) In the future, excitement increases, signs of disorientation appear, sweating becomes profuse.

4. Terms of hospitalization.
and. For pregnant women with diabetes, there should be a tactic of free hospitalization (according to indications) at any time.
b. The first hospitalization is necessary immediately upon pregnancy for metabolic correction and a complete examination.
with. Subsequent hospitalizations are carried out:
– At 20-24 weeks, when the need for insulin most often changes.
– At 32-36 weeks (depending on the severity of disorders of carbohydrate metabolism and the degree of its correction) to prepare for childbirth.

5. Management of pregnant women with diabetes with vascular lesions.
and. Diabetic retinopathy:
– Nonproliferative (background) retinopathy.
The mild form does not affect the management plan, with the exception of the more frequent full ophthalmological examination. In cases of moderate or severe non-proliferative retinopathy, immediate ophthalmic care is needed.
– Proliferative retinopathy of any form requires urgent ophthalmic care. Pregnancy, if any, is contraindicated.

It should be remembered: During pregnancy in women with diabetes mellitus, the frequency of retinopathy doubles. The course of retinopathy can significantly deteriorate even with good glycemic control.

b. Diabetic nephropathy. Management as pregnant with kidney damage of a different etiology depends on:
– The presence or absence of hypertension.
– Severity of impaired renal function
– Degrees of proteinuria.
An unfavorable prognosis of pregnancy outcome is most likely if in its first half:
– proteinuria exceeds 2.0 in daily urine
– serum creatinine exceeds 1.5 mg / dl (0.14 μmol / l)
– anemia is accompanied by hematocrit less than 25%
– hypertension constant symptom (GARDEN> 107 mm Hg)

It should be remembered: nephropathy without a significant increase in blood pressure, with a normal level of creatinine in the blood does not lead to adverse pregnancy outcomes.


1. Pregnant women with diabetes that developed during pregnancy (gestational diabetes), whose sugar level does not exceed normal limits, can give birth on time without increasing the risk of fetal death. The exception is:
a. Pregnant women with gestosis.
b. Pregnant women with pyelonephritis.
with. Pregnant women who gave birth to a dead child in the past.
2. Establishing the optimal delivery time for patients with insulin-dependent diabetes mellitus (IDDM) mainly depends on the condition of the fetus, the degree of maturity of the fetal lungs and the presence of complications in the mother.
Please note:
a. Increased risk of fetal death in patients with diabetes with a gestational age of more than 36 weeks.
– In the presence of diabetes with vascular lesions.
– With insufficient supervision.
– With polyhydramnios.
– With a macrosomia of the fetus.
– With hypertension caused by pregnancy.
b. Fetal lung ripening delay in diabetes without vascular disorders.
with. Accelerated ripening of the fetal lungs in the presence of vascular lesions, especially if there is a fetal growth retardation.

It should be remembered: routine early delivery of pregnant women with diabetes is currently considered illogical it does not reduce perinatal mortality. There is no reason to terminate the pregnancy before the expected term of delivery in the absence of complications of the disease.

Early delivery may be indicated in the following cases:
a. At 38-40 weeks in the presence of a “mature” cervix to reduce the incidence of fetal macrosomia and related complications (high risk of brachial dystocia with a fetal weight of more than 4200 g). With delivery up to 38 weeks, fetal lung maturity should be assessed.
b. In the presence of pregnancy complications:
– Fetal growth retardation.
– Preeclampsia.
– Increasing polyhydramnios.
– Fetal distress.

1. Diabetes mellitus is not an indication for cesarean section, which is performed according to strict obstetric indications.
2. It is better to wait for the development of spontaneous labor.
3. If necessary, early delivery, the choice, if possible, should be made in favor of childbirth by intravenous drip infusion of oxytocin.
It should be borne in mind that the stressful effects of labor excitement violate the compensation of diabetes, therefore, in the absence of effective contractions after sufficiently active labor, it is necessary to opt for caesarean section.
4. The management of labor through the natural birth canal with the spontaneous development of labor or after labor is possible under the following conditions:
a. The normal size of the pregnant pelvis.
b. Fruit weight less than 4250 g
. C. Lack of fetal distress.
d. The presence of monitor control of the fetus.
e. Stable compensated diabetes.

1. In childbirth and after them, effective control of blood sugar is necessary, which helps to prevent excessive secretion of insulin in the fetus and to avoid hypoglycemia in the newborn.
2. You should not allow the development of ketoacidosis, since it indicates an insufficient supply of carbohydrates to the body, replenishing the energy costs of the mother.
3. In labor, only short (fast-acting) insulin is used.
4. The choice of delivery management scheme is determined by the type of diabetes (gestational or IDDM), the quality of glycemia correction, the stability of the course, the presence of hypoglycemic reactions.

Scheme N 1.
a. The diet and selected single doses of insulin are left unchanged before childbirth, but women should not eat from midnight on the eve of delivery.
b. The sugar content is determined early in the morning on the day of the planned birth and is urgently determined in pregnant women with spontaneous labor.
with. A 5% glucose or dextrose solution is injected intravenously at a rate that provides 5 to 10 g glucose per hour.
Purpose of infusion:
– Prevention of ketonuria and dehydration associated with compliance with a pregnant fasting regimen.
– Prevention of intrapartum acidosis and hypoglycemia in a newborn.
– Helps maintain normal intravascular volume, minimizing the risk of maternal hypotension.
Short (fast-acting) insulin is administered continuously intravenously, while adequate control of blood sugar can be achieved at a rate of administration of 0.25-2.0 U / h. Preparation of a solution for iv insulin infusion: 25 units of simple insulin is dissolved in 500 ml of isotonic (0.9%) sodium chloride solution, which provides a concentration of 1 unit in 20 ml of solution. The introduction of 0.25-2.0 U / hour is achieved at an infusion rate of 5-40 ml / hour (2-12 drops per minute). You can initially enter intravenously 0.02-0.05 U / kg of insulin, which for a patient with a body weight of 80 kg will be 1.5-4.0 U of insulin, if an elevated fasting blood sugar level is determined.
The action of insulin with a / in the introduction is shorter than with a / to the introduction.
The onset of action is after 15 minutes. The end of the action is in 0.5-1 hour.
The total amount of fluid entering the body during each hour, including dextrose solution, insulin solution and oxytocin solution (in saline) during labor excitation should average 75-150 ml / hour.
During childbirth, it is necessary to monitor:
1. The blood sugar level every 30 minutes to maintain it at a level of 3.3 – 5.5 mmol / l (at stable rates – after 1-2 hours).
2. The presence of ketone bodies in the urinary spot.
and. The presence of ketonuria with normoglycemia indicates a lack of glucose intake.
b. The presence of ketonuria with hyperglycemia indicates a lack of insulin.

3. Respiration, pulse, body temperature, fetal heartbeat (monitoring), fluid balance, blood electrolytes.

Scheme N 2 (less reliable).
and. In the evening, the woman receives a light dinner in accordance with the diet prescribed for diabetes.
b. In the morning on the day of delivery, before breakfast, instead of the usual dose, 5-10 IU of simple (short) insulin is administered intravenously.
with. Next, continuous intravenous administration of insulin.
d. The initial infusion rate is 1 U of insulin and 5 g of glucose per hour.
Preparation of a solution for iv insulin infusion:
5 U of simple insulin is dissolved in 500 ml of 5% glucose solution, which provides a concentration of 1 U of insulin and 5 g of glucose in 100 ml of p- pa
Blood glucose is monitored every 30
minutes – 1 hour, keeping it at a level of 3.9-6.8 mmol / L. The level of glucose in the blood remains within the specified limits at a rate of administration of 0.25-2 U / hour, which corresponds to 25-200 ml of solution (8-60 drops / min.).
During childbirth, anesthetics, oxytocin, and other drugs are administered in glucose-free solutions. Monitoring the condition of the mother and fetus is the same as in scheme N 1.

Scheme N 3 (use undesirable).
and. An intravenous infusion of 5% glucose solution is carried out at a rate of 100 ml / hour (30 drops / min.), Changing it depending on the level of sugar in the blood.
b. The introduction of subcutaneous small doses (4-8 IU) of short (fast-acting) insulin every 4 hours, if such a need is confirmed by indicators of blood sugar.
with. Monitoring blood glucose every 30 minutes – 1 hour.


Option N 1
1. In the morning immediately before the operation, the blood sugar level is determined and further maintenance is carried out according to schemes N 1 or N 2. 2. The blood sugar level
is determined every 30 minutes.

Option N 2 (use is undesirable)
1. Blood sugar level is checked one hour before the operation, then half of the next dose of short (fast-acting) insulin is administered.
2. With the beginning of anesthesia, they start drip infusion of a 5% glucose solution, adding to the solution:
a. 1 PIECE of insulin for every 4 g of glucose with glycemia of 8.3 mmol / L
(6 PIECES of insulin in 500 ml of 5% glucose solution).
b. 1 PIECE of insulin for every 3 g of glucose with glycemia from 8.3 to 11 mmol / l
(8 PIECES of insulin in 500 ml of 5% glucose solution).
with. 1 PIECE of insulin for every 2 g of glucose with glycemia above 11 mmol / L (12 PIECES of insulin in 500 ml of 5% glucose solution).


1. After the birth of the placenta, an important source of antagonistic action against insulin is eliminated – placental lactogen, whose half-life is 20-30 minutes.
2. Basically, the antagonistic effect of placental lactogen on insulin activity ceases within 2-3 hours, after which the puerpera may develop hypoglycemia, therefore:
a. After birth, glucose infusion should be continued under the control of frequent (after 0.5-1 hours) blood sugar determinations.
b. Depending on the level of glycemia, insulin administration either stops or decreases its dose.
with. The introduction of glucose is carried out until its increasing or stable level is registered.
d. If there is a need for a fasting regimen associated with operative delivery, then parenteral nutrition is carried out by the drip of a 5% glucose solution in a volume of up to 1-2 liters.
3. The amount of insulin that will be needed to treat the mother in the first days after birth is determined based on the results of determining the blood sugar level (glycemic profile).
and. Typically, the dose of insulin is less than that used during pregnancy and is approximately 60% of the dose of insulin used before pregnancy.
b. Starting from the 5-6th day of the postpartum period, the dose of insulin often needs to be increased, however, it usually does not reach the prenatal level or even the level before pregnancy.

1. Insulin treatment is not carried out
2. Management corresponds to the normal postpartum period.

Remember: 1. For pregnant women with diabetes, the exact same obstetric care is required as for healthy women, with the exception of a thorough (hard) compensation of the level of glycemia,
2. Diabetes is not a contraindication to pregnancy with the exception of:
– The presence of vascular complications,
– The labile form, resistant to insulin.
Breastfeeding should be encouraged. Consultation on contraception is needed: women with diabetes, without obesity and hypertension, have no contraindications to low-dose COCs and, especially, contraceptives containing “pure” progestogens (“mini-drank”).


1. The main metabolic symptoms.
and. The accumulation of organic acids, acetoacetate and beta-hydroxybutyrate.
b. An increase in serum acetone.
with. A sharp increase in blood glucose concentration.
2. The main life-threatening clinical symptoms:
a. Metabolic acidosis (due to hyperketonemia).
b. Hyperosmolarity (hyperglycemia and water loss).
with. Dehydration (osmotic diuresis associated with hyperglycemia and vomiting due to severe metabolic acidosis.

1. The main symptoms of DKA:
– Nausea, vomiting.
– Labored breathing.
– Decrease in mental functions, ranging from mild drowsiness to severe coma.
– Dry mucous membranes.
– Reduced skin turgor.
– Fruit breath.
– Kussmaul’s breath (quick, deep breaths).
– Blood pressure is reduced, which is accompanied by tachycardia.
– There are abdominal pains that take the character of an “acute abdomen”.
2. Laboratory signs.
– Significant hyperglycemia.
– Severe glucosuria.
– A sharply positive reaction to the presence of ketone bodies in the urine.
– blood pH below 7.3 at pCO2 40 mm Hg or lower.
– A sharply positive reaction of undiluted blood serum to the presence of ketone bodies.
The sample is put by adding 1-2 drops of serum or plasma to a crushed tablet containing nitroprusside. A sharply positive test is characterized by the appearance of pronounced purple staining.


1. Insulin.
and. Only fast-acting insulins are used.
b. Possible high dose regimen (50-100 PIECES), administered intermittently in 2-4 hours.
c. However, the regimen of low doses (6-10 units), administered by continuous intravenous infusion or intermittent i / m or s / c injection, is no less effective and less dangerous in the sense of developing hypoglycemia.
At the beginning of treatment, intravenous administration is preferred, since circulatory disorders may interfere with absorption of sc or intramuscularly administered insulin. You can start with a single injection of 6-10 IU of insulin, intravenously after which a continuous infusion of the hormone is carried out at a rate of 0.1 IU kg / h until the glycemia level drops to 13.7-14 mmol / L. If it is not possible to provide a controlled infusion rate, a reasonable alternative is i / m or s / c administration of insulin at a dose of 5-10 U / hour.
However, with this method of administration, the initial decrease in the level of glucose and ketone bodies in the blood is slower than with the on / in infusion. In addition, the effect of insulin, administered in / m or s / c, can persist for 4 hours or more after the last injection.
d. The response to treatment is assessed by indicators:
– Glucose in plasma, determined every hour before its normalization, and then every 2 hours.
– Electrolytes in serum.
– pH of the blood, as well as the level of ketone bodies, determined every 2-4 hours.
e. Dose adjustment options.
– If the plasma glucose does not decrease by 30% in the first 2-4 hours, or by 50% in 6-8 hours, then the dose of insulin should be doubled.
– If in this case hyperglycemia persists, the dose should be doubled every 2 hours.
A decrease in blood sugar of 2.8-5.6 mmol / l / hour indicates the correct dose (0.1 units kg / hour). If the rate of decline is slowed down, the dose of insulin should be doubled.
f. As soon as the plasma glucose level drops to 14 mmol / L, the insulin infusion is stopped and the infusion of 5% dextrose (glucose) is started.
g. Then, to eliminate glucosuria, small doses (10 IU) of fast-acting insulin are administered intermittently. If the plasma glucose level drops to 14 mmol / L or more, but the pH remains below 7.3, then the analysis for ketone bodies with nitroprusside should be repeated:
– If a “large” or “moderate” number of ketone bodies is detected, insulin 6 units / h together with 200 ml / h of 5% glucose solution. This delay in the clearance of ketone bodies may reflect a slower circuit than glucose.
– In case of a weakly positive or negative reaction to nitroprusside (euglycemic metabolic acidosis without ketosis), this should be considered a sign of the development of concomitant lactic acidosis requiring treatment with sodium bicarbonate.
h. Prior to stabilization of the clinical condition and the start of self-administration of food and / or liquid, intermediate-acting insulin should not be used.

2. Liquids.
and. In most patients, the total fluid deficiency is approximately 6 liters and rarely exceeds 10 liters.
b. Since dehydration is a consequence of osmotic diuresis, water loss is relatively greater than salt loss, therefore, in the absence of hypotension, these losses should be replenished with a hypotonic solution in the form of a 0.45% sodium chloride solution.
– Do not prescribe glucose solutions to patients with hyperosmolar coma.
– Do not prescribe hypotonic solutions unless patients have a hyperosmolar, hypernatremic coma.
In patients in a state of shock, the most important task is to increase the intravascular volume, so they should be given an isotonic (0.9%) sodium chloride solution. For the 1st hour of treatment, 1 liter of liquid should be administered, for the next 2 hours another 1 liter, then inject it at a speed of 300-500 ml / hour.

The total amount of fluid in the first 12 hours is about 5 liters.
with. After 4-6 hours or earlier, if the blood glucose level drops to 14 mmol / L or lower, the saline infusion should be replaced with an infusion of 5% glucose in order to prevent hypoglycemia and reduce the likelihood of developing cerebral edema due to a rapid decrease in plasma glucose below 14 mmol / l (the level at which ketone bodies disappear).

3. Sodium bicarbonate.
and. Since acetoacetate and beta-hydroxybutyrate are metabolizable anions, their oxidation, under conditions of suppression of further production by insulin, leads to the formation of sodium bicarbonate, due to which its concentration in serum changes towards normal even without the introduction of alkaline solutions.
b. An objection to the routine use of sodium bicarbonate is that a rapid increase in arterial blood pH can cause:
– An excessive decrease in cerebrospinal fluid pH and a concomitant deterioration in central nervous system function.
– A shift in the hemoglobin dissociation curve due to alkalization of the blood can limit the oxygen supply to the tissues.
with. Sodium bicarbonate should be administered only to patients with severe metabolic acidosis at a blood pH of 7.1 or lower and a level of bicarbonate of less than 5 meq / l. In such cases, 88 meq (7.4 g) of sodium bicarbonate is added to 1 liter of hypotonic saline or 132 meq (11.0 g) if the pH is less than 7.0. Sodium bicarbonate should only be added until the pH, measured every 2 hours, remains below 7.25. In order to exclude the possibility of cell dehydration due to the infusion of a hypertonic solution, it is important to add bicarbonate specifically to the hypotonic (0.45%), and not to the isotonic (0.9%) sodium chloride solution.

4. Potassium.
and. Despite the decrease in potassium reserves in the body due to ketonuria and repeated vomiting by 5-10 meq / l, its concentration in the blood serum is within normal limits or even increased due to its transition from the intracellular space to the extracellular space, which accompanies an increase in the concentration of hydrogen ions ( decrease in pH).
b. With the correction of acidosis and stimulation of glucose uptake by cells, the serum potassium level decreases, therefore, 3 hours after the start of treatment, potassium chloride (if there is no anuria) should be added at a dose of 40 meq per liter (3.0 g / l) of intravenous fluid. In total, 120-160 meq / l (9.0-12.0 g / l) of potassium is usually administered in the first 12-18 hours. In a few patients (less than 5%) who have hypokalemia from the very beginning, potassium (40-60 meq / l or 3.0-4.5 g / l) is added to the first portions of the injected fluid.
with. ECG monitoring may help determine hypo- or hyperkalemia, but this should not replace serum potassium measurements at intervals of 2-4 hours.



1. With a short coma:
a. The skin is pale, moist.
b. The tongue is wet.
with. Tachycardia.
d. Blood pressure is normal or slightly elevated.
e. The breath is ordinary.
f. There is no smell of acetone from the mouth.
2. As the coma deepens:
a. Sweating stops.
b. Breathing becomes shallow.
c. Blood pressure decreases.
d. Bradycardia is possible.
e. Changes in the neurological status are increasing: nystagmus, anisocoria, meningism, pyramidal signs, after a period of increase tendon and abdominal reflexes are inhibited.
3. Treatment.
and. Begin with immediate intravenous jet administration of 60-80 ml of a 40% glucose solution.
b. In the absence of effect, intravenous drip infusion of a 5% glucose solution is carried out, which lasts for hours and days.
with. 30-60 mg of prednisolone, 4-5 ml of ascorbic acid are added to the dropper.
d. Glycemia should be maintained at 8.32-13.87 mmol / L. With its further increase, insulin in small doses (4-8 units) is fractionally administered.


1. Since fetal hyperinsulinism can block the effect of cortisol on surfactant function with a high incidence of SDR, the main principles of the approach to the management of a pregnant woman with diabetes are reduced to monitoring the blood sugar level of a pregnant woman, especially in the third trimester, and its correction.
2. Prevention and correction of diabetic fetopathy include the following points:
a. Planning for conception in the most favorable period with the somatic and psychological well-being of the parents.
b. The need for counseling and subsequent metabolic control of the disease before conception:
– achievement of normoglycemia through insulin therapy
– serial determination of glycosylated hemoglobin several months (2-4) before the planned conception (goal – achievement of normal numbers: 3-6 molar%)
3. Pregnant in the first trimester must be informed:
a. About the risk of congenital malformations of the fetus (with compensation for diabetes, the risk does not exceed that in healthy women).
b. On the relationship of the outcome of pregnancy with the timeliness and adequacy of insulin and diet therapy.
with. About the risk of developing diabetes in a child: with uncompensated diabetes in a pregnant woman – up to 9% in adulthood.
In order to reduce the likelihood of developmental abnormalities (neural tube defects), folic acid is prescribed in a dose of at least 0.8 mg / day (with a history of defect – 4 mg / day).
4. In the second trimester of pregnancy.
and. The need for insulin is increasing, the harmful effects of maternal ketoacidosis on the fetus (antenatal death) are increasing. In this case, the concentration of a-fetoprotein in the blood of a pregnant woman can serve as a prognostic test if, with a gestational age of 16-18 weeks, the level of a-fetoprotein decreases significantly (2.5 times).
b. Ultrasound at 18 weeks, eliminating up to 95% of large
abnormalities of the central nervous system, skeleton, gastrointestinal tract and urinary tract (for the heart – at 22 weeks).
5. In the III trimester of pregnancy.
and. The need for nsulin is increasing again. In connection with these, at 26-28 weeks, repeated ultrasound is required, a clear monitoring of blood sugar levels.
b. Determine the risk of preeclampsia.

1. The main clinical and metabolic signs of diabetic fetopathy:
macrosomia, malformations and RPS, SDR, hypoglycemia, hyperglycemia, hypocalcemia, hypomagnesemia, hyperosmia, acidosis, dyselectrolythemia, neurological disorders.
2. Assessment of the condition of the newborn.
and. Determination of blood glucose at birth, then every hour for 3 hours, then after 3 hours, after 6, after 12 hours and then after 26 and 48 hours
b. Determination of hematocrit and hemoglobin 1 h after birth and 24 h
. Signs with which hypoglycemia is associated:
– Large body weight at birth (hypotrophy is not excluded).
– Moon-shaped face.
– Pseudo-obesity.
– Hypertrichosis (upper edge of the auricle).
– Pastosity.
– Swelling on the legs and lower back.
– An increase in parenchymal organs.
– Polycythemia (hematocrit greater than 0.65 and hemoglobin greater than 220 g / l).
– Hypodynamia, hypotension, hyporeflexia.
– Apnea, tachypnea.
– SDR, shock.
d. The diagnosis of hypoglycemia is established when the glucose level in the blood of a full-term newborn is less than 2.22 mmol / l (less than 1.65 mm / l for premature infants).
3. Management of newborns with hypoglycemia.
and. 2 ml / kg of a 10% glucose solution is injected intravenously at a rate of 1 ml / min (glucose solutions of higher concentration are not used), then they switch to a drop infusion of glucose at the rate of 6 mg / kg / min, only 75 ml / kg on the first day of life under monitoring blood sugar every 30 minutes until normalization.
b. If glucose levels do not normalize, medications are prescribed that increase blood sugar:
Glucagon 0.1-0.3 mg / kg 2 times a day. It is used only in combination with intravenous glucose infusions in connection with a possible ricochet phenomenon (hypoglycemia at the end of glucagon action).
Glucocorticoids are prescribed for children who have resistance to intravenous glucose infusions.
The dose for hydrocortisone is 10 mg / kg per day.
with. In premature infants with hypoglycemia and intrauterine hypotrophy, glucose infusion is combined with its oral administration and, if possible, enteral feeding begins early.

Leave a Reply

Your email address will not be published. Required fields are marked *