Complications of Diabetes in Pregnancy

Dr Shihaan — Sat, 15 Nov 2008 05:15:39 +0000

Fetal and Neonatal Complications:

1)Congenital abnormalities(malformations)

i) Skeletal/CNS:

Neural tube defects excluding anencephaly

Anencephaly

Microcephaly

Caudal regression syndrome

Holoprosencephaly

ii) GIT:

Duodenal atresia

Anorectal atresia

Small left colon syndrome

iii) Cardiac:

VSD (Ventricular septal defect)

ASD (Atrial septal defect)

Cardiomegaly

Coarctation of the aorta

Transposition of the great vessels

iv) Renal:

Hydronephrosis

Renal agenesis

Ureteral duplication

v) Others

Single umbilical artery

The risk of fetal malformations is eight times higher among diabetics than in non-diabetics. It should also be noted that fetal malformations are responsible for up to 50% of perinatal deaths.

It is believed that hyperketonemia, maternal hyperglycemia, generation of free oxygen radicals,genetic factors and somatomedin inhibitors are responsible for the fetal malformations.

Caudal regression syndrome (a very rare syndrome) is seen mostly in diabetics. The is no association between chromosomal abnormalities and diabetic pregnancies (eg Down’s syndrome).

The relative risk (R.R) of the central nervous system and cardiovascular system is very high (CNS=15.5, CVS=18) .

The HbA1c values should be maintained at less than 8%. The risk of malformations is greater by three to six times when the Hb A1c values exceed 8%.

2) Fetal Macrosomia (Large baby- greater than 4.0Kg):

This can cause birth asphyxia and traumatic birth injury.eg Brachial nerve injury

Even though the perinatal mortality rate has declined over the past few decades, there is still an increased risk of birth asphyxia.

Perinatal asphyxia correlates with maternal hyperglycemia, prematurity and new onset nephropathy during pregnancy.

The incidence of fetal macrosomia is as high as 45% compared with 8% in controls.

The macrosomia in diabetic fetuses is asymmetric (decrease in head circumference over abdominal circumference) with an increase in ponderal index.

3) Hypoglycemia:

Hypoglycemia is common in the first 24 hours following delivery because the fetus continues to excrete large amounts of insulin in the immediate neonatal period. In other words, hypoglycemia (plasma glucose <35mg/dl in the neonate) is due to the persistent insulin secretion in the neonate after the maternal glucose via the placenta is discontinued.

Macrosomic babies (Large babies-greater than 4.0Kg) , growth restricted and premature babies (reduced glycogen reserves) are at increased risk of hypoglycemia .

There is a correlation between neonatal hypoglycemia and maternal hyperglycemia in labour. Hypoglycemia is less frequent among breast fed infants.

Enteral (Oral) feeding alone is sufficient in 50% of cases of hypoglycemia.

4) Hyperbilirubinaemia:

This is mainly due to the breakdown (Increased haemolysis) of large amounts of red blood cells (RBC’S- due to polycythaemia-high concentration of red blood cells) .

Hyperbilirubinaemia is also associated with fetal macrosomia, prematurity and poor maternal glycemic control.

5) Hypocalcemia:

Usually asymptomatic and resolves without treatment

6) Hypomagnesaemia:

This is also usually asymptomatic and resolves without treatment.

7) Respiratory distress syndrome:

The incidence of respiratory distress syndrome is as high as six times of normal infants.

It is thought that the high incidence of respiratory distress syndrome is due to the delay in surfactant maturation as a result of the antagonistic effect of insulin on glucocorticoids. Insulin inhibits the stimulatory effects of cortisol on lecithin synthesis.

Tests used to predict the maturation of the fetal lungs are the presence of phosphatidylglycerol in the amniotic fluid (Best predictor) and the lecithin:sphingomyelin ratio (if greater than 2.0 predicts fetal lung maturity, some centeres are more comfortable with using >3.5).

Intrauterine growth restriction (IUGR):

This can be either due to diabetic vasculopathy or to excessively tight control.

9) Spontaneous abortions:

There is an increased rate of spontaneous abortions in women who have pre-existing diabetes. Relative risk (R.R) =3 when HbA1c >14.4%.

Increased rates of miscarriage is associated with poor glycemic control.

10) Long Term Effects:

With good glycemic control the neurodevelopmental outcome is expected to be normal. There is also a negative correlation between small head circumference and intellectual development noted at age 3.A similar negative correlation has also been noted between head circumference and HbA1c levels during pregnancy.

At age 4 it is noted that children of diabetic mothers who had early IUGR are at increased risk of abnormal psychomotor development.

One should also bear in mind that children of diabetic parents are at increased risk of developing the same type of diabetes .(5-6% for typeI and 10-15% for type II DM).

Obstetrics complications/ complications with respect to delivery:

Diabetics are at increased risk for medical and obstetric complications such as preterm labour ,hypertension, cesarean section , obstetric trauma, periodontal disease, urinary tract infections and other infections.

1) Preterm Labour:

There is a high incidence of iatrogenic (Due to intervention by medical personnel) as well as spontaneous delivery.

Iatrogenic- 22 % versus 3% in normal

Spontaneous- 16% versus 11% in normal.

There is also an association in the incidence of preterm delivery before 35 weeks of gestation with the severity of the diabetes.

The presence of proteinuria at the onset of pregnancy is also associated with an increased incidence of preterm delivery.

Hypertensive complications are responsible for one third of all preterm deliveries in diabetic women.

2)Pre-eclampsia:

Prevalence of pre-eclampsia is 10 to 20 % compared to 5 to 10 % in non-diabetics.

Uncontrolled diabetes results in a much higher rate of pre-eclampsia.

There is also a high incidence of pre-eclampsia with the presence of proteinuria at the onset of pregnancy.

The rate of pre-eclampsia is increased even in non-hypertensives.

Important: The complications of diabetes in the pregnant mother (Impact on the mother) will be discussed in a subsequent post.

References:

Page 195 to page 197 Chapter 23 Diabetes in Pregnancy by Dr Purvi Patel 2006 .Medical Disorders in Pregnancy-An Update. Edited by Hiralal Konar and Pralhad Kushtagi. Jaypee publications. A publication by the Federation of Obstetric and Gynaecological Societies of India.

Page 248-249 Chapter 16.Medical Diseases Complicating Pregnancy . Obstetrics by Ten Teachers .Seventh edition edited by Stuart Campbell and Christoph Lees

Diabetes in Pregnancy- An Introduction

Dr Shihaan — Fri, 14 Nov 2008 01:45:48 +0000

Incidence and prevalence:

Approximately 3% of all pregnancies are affected by diabetes mellitus. Overall there has been a significant increase in the prevalence of type 2 as well as gestational diabetes, especially among Asian women.

Gestational diabetes accounts for about 90% of all cases of diabetes in pregnancy, while the remaining 10% are due to pre-gestational diabetes (This refers to women who are diagnosed to have diabetes prior to pregnancy).

Gestational diabetes refers to the onset of diabetes for the first time during pregnancy.

History of Diabetes in pregnancy

Insulin was introduced in 1921. Prior to the introduction of insulin 40% of diabetic women who became pregnant died during the pregnancy, mainly due to diabetic ketoacidosis. Prior to the introduction of insulin fetal loss was also very high (about 50%), mainly due to miscarriage ,premature labour, late intrauterine and neonatal death. As soon as insulin was introduced maternal mortality fell to between 2 and 3%. However the decline in the perinatal mortality rate was much slower, mainly due to late intrauterine death among diabetic women. This led to the policy of early induction of labour in diabetic pregnant women.

Pathophysiology of diabetes in pregnancy

Pregnancy is “an insulin resistance state”.

There is increased levels of blood insulin, glucose as well as triglycerides. The insulin resistance state is caused by high levels of circulating insulin antagonists such as cortisol,oestrogens, progesterones and other hormones produced in the placenta such as placental lactogen.

Insulin regulates the release and storage of glucose, fat and amino acids.

Diabetes complicating pregnancy (weather gestational or pre-existing), leads to an increase in the circulating concentration of all metabolic substrates that are available to the fetus (Glucose crosses by facilitated diffusion, free fatty acids cross by simple diffusion and amino acids by active transfer).

Insulin (plus other polypeptide hormones such as glucagons) cannot cross the placenta, therefore the high levels of glucose and amino acids in the fetal circulation stimulates the fetal pancreatic islets of Langerhans leading to beta-cell hyperplasia and fetal hyperinsulinaemia.

Insulin , being a major fetal growth factor can lead to fetal macrosomia (especially if the diabetes is not controlled). The combination of fetal hyperinsulinaemia (high concentration of circulating insulin) and fetal hypoxia stimulates fetal medullary and extramedullary erythropoiesis (formation of red blood cells) causing polycythaemia (high levels of circulating red blood cells) possibly due to increased erythropoietin levels.

Other complications caused in the neonate due to fetal hyperinsulinaemia include hypoglycemia, respiratory distress syndrome and jaundice.