Diabetes In Pregnancy

Diabetes In Pregnancy is also known as GESTATIONAL DIABETES MELLITUS (GDP) is defined as carbohydrate intolerance of variable severity with onset or first recognition during the present pregnancy.

The entity usually presents late in the second or during the third trimester.

The potential candidates for GDM are:

(a) Positive family history of diabetes (parents or sibling). Family history should include uncles, aunts and grand parents.

b) Having a previous birth of an overweight baby of 4 Kg or more

(c) Previous stillbirth with pancreatic islet hyperplasia revealed on autopsy

(d) Unexplained perinatal loss

(e) Presence of polyhydramnios or recurrent vaginal candidiasis in present pregnancy

(f) Persistent glycosuria

(g) Age over 30 years (Obesity)

Table 1.1: Criteria for diagnosis of GDM with 100 gm oral glucose (O’Sullivan and Mahan modified by Carpenter and Coustan) and National Diabetes Data Group

GTT: Venous plasma (mg/dL)	Carpenter& Coustan	NDDG
Time
Fasting	95	105
1 hour	180	190
2 hours	155	165
3 hours	140	145

SCREENING

While some advocate screening routinely to all pregnant mothers, others reserve it only for the potential candidates.

Screening strategy for detection of GDM are;

(a) Low risk– Absence of any risk factors → blood glucose testing is not routinely required

(b) Average risk– Some risk factors → perform screening test (see below)

(c) High risk– Blood glucose test as soon as feasible.

The method employed is by using 50gm oral glucose challenge test without regard to time of day or last meal, between 24 and 28 weeks of pregnancy. 

A plasma glucose value of 140 mg percent or that of whole blood of 130 mg percent at 1 hour is considered as cut off point for consideration of a 100 gm (WHO – 75 gm) glucose tolerance test.

HAZARDS: Increased perinatal loss is associated with fasting hyperglycemia. F

Fetal anomalies are however not increased.

This is due to the absence of metabolic disturbance during organogenesis (2) Increased incidence of macrosomia (3) Polyhydramnios (4) Birth trauma (5) Recurrence of GDM in subsequent pregnancies is about 50%.

OVERT DIABETES

A patient with symptoms of diabetes mellitus (polyuria, polydipsia, weight loss) and random plasma glucose concentration of 200 mg/dL or more is considered overt diabetes.

The condition may be pre-existing or detected for the first time during present pregnancy. According to American Diabetic Association diagnosis is positive if (a) the fasting plasma glucose exceeds 126 mg/dL (b) the 2 hours post glucose (75 gm) value exceeds 200 mg/dL. (see table 1.3)

Table 1.3: Criteria for diagnosis of impaired glucose tolerance and diabetes with 75gm oral glucose (American Diabetic Association)

Plasma (mg %)
Time	Normal tolerance	Impaired glucose tolerance	Diabetes
Fasting	<100	≥100 and < 126	≥ 126
2 hour post glucose	<400	≥ 140 and <200	≥200

EFFECTS OF PREGNANCY ON DIABETES

It is difficult to stabilize the blood glucose during pregnancy due to altered carbohydrate metabolism and an impaired insulin action.

The insulin antagonism is due to the combined effect of human placental lactogen, estrogen, progesterone, free cortisol and degradation of the insulin by the placenta.

The insulin requirement during pregnancy increases as pregnancy advances. 

As more glucose leaks out in the urine due to renal glycosuria, control of insulin dose cannot be made by urine test and repeated blood glucose estimation becomes mandatory. 

With the ‘accelerated starvation’ concept, there is rapid activation of lipolysis with short period of fasting.

Ketoacidosis can b eprecipitated during hyperemesis in early pregnancy, infection and fasting of labor.

It can be iatrogenically induced by beta sympathomimetics and corticosteroids used in the management of preterm labor.

Insulin requirement falls significantly in puerperium. 

Vascular changes, specially retinopathy, nephropathy, coronary artery disease and neuropathymay be worsened during pregnancy.

Complications of diabetes (Hyperglycemia and adverse pregnancy outcome):

Maternal

Fetal and Neonatal

MATERNAL

During pregnancy:

• Abortion: Recurrent spontaneous abortion may be associated with uncontrolled diabetes.
• Preterm labor (20%): May be due to infection or polyhydramnios.
• Infection: Urinary tract infection and vulvo vaginitis.
• Increased incidence of pre-eclampsia (25%).
• Polyhydramnios (25-50%) is a common association. Large baby, large placenta, fetal hyperglycemia leading to polyuria, increased glucose concentration of liquor irritating the amniotic epithelium or increased osmosis, are some of the probabilities.
• Maternal distress: May be due to the combined effects of an oversized fetus and polyhydramnios.
• Diabetic retinopathy, microaneurysms, hemorrhages and proliferative retinopathy. Laser photocoagulation is the preferred treatment.
• Diabetic nephropathy: May lead to renal failure.
• Ketoacidosis

During labor:

There is increased incidence of : (1) Prolongation of labor due to big baby. (2) Shoulder dystocia due to disproportionate growth with increased shoulder/head ratio. (3) Perineal injuries. (4) Postpartum hemorrhage. (5) Operative interference.

Puerperium: (1) Puerperal sepsis (2) Lactation failure.

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FETAL AND NEONATAL HAZARDS:

Fetal macrosomia (30-40%) probably results from: (a) Maternal hyperglycemia →hypertrophy and hyperplasia of the fetal islets of Langerhans → increased secretion of fetal insulin → stimulates carbohydrate utilization and accumulation of fat.

Insulin like growth factors (IGF-I and II) are also involved in fetal growth and adiposity.

With good diabetic control, incidence of macrosomia is markedly reduced.

Elevation of maternal free fatty acid(FFA) in diabetes leads to its increased transfer to the fetus → acceleration of triglycerides synthesis→adiposity.

Congenital malformation (6-10%) : is related to the severity of diabetes affecting organogenesis, in the first trimester (both in type 1 and type 2 diabetes). The factors associated with teratogenesis are multifactorial:

(a) Genetic susceptibility (b) Hyperglycemia (c) Arachidonic acid deficiency

(d) ketone body excess (e) Somatomedin inhibition (f) Free oxygen radical excess. Risks of fetal chromosomal abnormalities are not increased.

MAJOR BIRTH DEFECTS IN INFANTS OF DIABETIC MOTHERS (6-10%)

CNS and skeletal	Cardiovascula	Renal	Gastrointestinal	Others
Neural tube defectsAnencephaly   Microcephaly   Caudal regression syndromeSacral agenesis	VSD, ASD   Coarctation of aorta   Transportation of great vessels   Situs inversus   Fallot’s tetrology	Renal agenesisHydronep hrosis   Double ureter   Polycystic kidneys	Duodenal atresiaAnorectal atresia   Omphalocoele   o Tracheoes- ophageal fistula	Single umbilica l artery

MANAGEMENT:

Goal is to achieve tight control of diabetes, before the onset of pregnancy. Ideally a diabetic woman should be seen jointly by the diabetologist, obstetrician and dietitian.

Fetal congenital malformations are significantly low (0.8-2%) in women who receive pre-conceptional counseling. Women are taught for self glucose monitoring.

The patient needs more frequent antenatal supervision with periodic check up of fasting plasma glucose level which should be less than 90 mg percent. 

Maintenance of mean plasma glucose level between 105 and 110 mg/dL

It is desirable for good fetal outcome (DIPSI – 2009). The control of high blood glucose is done by restriction of diet, exercise with or without insulin. 

Human insulin should be started if fasting plasma glucose level exceeds 90 mg/dL and 2 hours post prandial value is greater than 120 mg/dL.