Diabetes Mellitus

in pregnancy
DR.Shameem R. Alaasam
 is a metabolic disorder caused by defects in insulin
secretion or action, which lead to abnormalities in the metabolism of
carbohydrates, lipids and protein .

Chronic hyperglycemia associated with diabetes causes tissue damage

in all organ systems.
TYPE 1 DIABETES
• An immune-mediated disorder characterized by destruction of the
beta cells of the pancreas, which leads to an absolute insulin
deficiency.
• Accounts for 5 percent to 10 percent of all diabetes and 1 percent of
diabetes in pregnancy.
TYPE 2 DIABETES
• Is the most prevalent form of diabetes, accounting for 90 percent to
95 percent of cases
• Is a disease of insulin resistance and relative insulin deficiency.
• Can be controlled with lifestyle modification and oral medications.
Diabetes is the most common medical complication of pregnancy.
Women can be separated into those who were known to have diabetes
before pregnancy—pregestational or overt, and those diagnosed
during pregnancy—gestational diabetes.
• The maternal metabolic adaptation is to maintain the mean fasting plasma
glucose of 74.5 ± 11 mg/dl and the post prandial peak of 108.7 ±
16.9mg/dl.
• This fine tuning of glycemic level during pregnancy is possible due to the
, as the normal pregnancy is characterized
by
Ø Increased insulin resistance and
Ø Decreased insulin sensitivity.
• A pregnant woman who is not able to increase her insulin secretion to
overcome the insulin resistance that occurs even during normal pregnancy
develops gestational diabetes.
INCREASED INSULIN RESISTANCE
Due to hormones secreted by the placenta that are “diabetogenic”:
ØGrowth hormone
ØHuman placental lactogen
ØProgesterone
ØCorticotropin releasing hormone
Transient maternal hyperglycemia occurs after meals because of
increased insulin resistance.
Relative baseline hypoglycemia
ØProliferation of pancreatic beta cells (insulin-secreting cells) leads to
increased insulin secretion.
ØInsulin levels are higher than in pregnant than nonpregnant women
in fasting and postprandial states.
ØHypoglycemia between meals and at night because of continuous
fetal draw
ØBlood glucose levels are 10-20% lower.
Pregestational diabetes
Diabetes during pregnancy can have devastating effects on both the
mother and the fetus . Women with diabetes are four times more
likely to develop preeclampsia or eclampsia than women without
diabetes. They are also twice as likely to have a spontaneous abortion.
In addition, the risks of infection, polyhydramnios, postpartum
hemorrhage, and cesarean delivery are all increased for diabetic
mothers. Similarly, diabetes can have adverse effect on the fetus,
including a fivefold increase in perinatal death and a two- to threefold
increase in the risk of congenital malformations, depending on
glycemic control
With pregestational—or overt—diabetes, the embryo, fetus, and
mother frequently experience serious complications directly
attributable to diabetes. The likelihood of successful outcomes with
overt diabetes is related somewhat to the degree of glycemic control,
but more importantly, to the degree of underlying cardiovascular or
renal disease. Thus, advancing stages of the White classification, are
inversely related to favorable pregnancy outcomes.
Fetal Effects

1.Spontaneous Abortion. Several studies have shown that early

miscarriage is associated with poor glycemic control. poor glycemic
control, defined by glycohemoglobin A1c concentrations > 7 percent,
was associated with a threefold increase in the spontaneous abortion
rate.
2.Preterm Delivery.
3.Malformations. The incidence of major malformations in women with
type 1 diabetes is doubled and approximates 5 percent and this include
cardiovascular, musculoskeletal, CNS, gastrointestinal, chromosomal
and others
4.Altered Fetal Growth.
Diminished growth may result from congenital malformations or from
substrate deprivation due to advanced maternal vascular disease.
fetal overgrowth is more typical of pregestational diabetes. Maternal
hyperglycemia prompts fetal hyperinsulinemia, particularly during the
second half of gestation. This in turn stimulates excessive somatic
growth or macrosomia. Except for the brain, most fetal organs are
affected by the macrosomia that characterizes the fetus of a diabetic
woman.
5.Unexplained Fetal Demise. The risk of fetal death is three to four
times higher in women with type 1 diabetes compared with that of the
general obstetrical population.
6.Hydramnios. Diabetic pregnancies are often complicated by excess
amnionic fluid. 18 percent of women with pregestational diabetes were
identified with hydramnios, defined as an amnionic fluid index (AFI)
greater than 24 cm in the third trimester.
Neonatal Effects.

Respiratory Distress Syndrome.

Hypoglycemia.
Hypocalcemia.
Hyperbilirubinemia and Polycythemia.
Cardiomyopathy.
Long-Term Cognitive Development.
Inheritance of Diabetes.
Maternal Effects

Preeclampsia. Hypertension that is induced or exacerbated by

pregnancy is the complication that most often forces preterm delivery
in diabetic women. The incidence of chronic and gestational
hypertension—and especially preeclampsia—is remarkably increased in
diabetic mothers. preeclampsia developed three to four times more
often in women with overt diabetes.
Diabetic Nephropathy. Diabetes is the leading cause of end- stage
renal disease. In general, pregnancy does not appear to worsen
diabetic nephropathy. Conversely, pregnancy in women with moderate
to severe renal impairment may accelerate progression of their disease
Diabetic Retinopathy. Retinal vasculopathy is a highly specific
complication of both type 1 and type 2 diabetes.
Diabetic Neuropathy. Peripheral symmetrical sensorimotor diabetic
neuropathy is uncommon in pregnant women. But a form of this,
known as diabetic gastropathy, is troublesome during pregnancy. It
causes nausea and vomiting, nutritional problems, and difficulty with
glucose control. Women with gastroparesis should be advised that this
complication is associated with a high risk of morbidity and poor
perinatal outcome . Treatment with metoclopramide and H2- receptor
antagonists is sometimes successful.
Diabetic Ketoacidosis. This serious complication develops in approximately 1
percent of diabetic pregnancies
Diabetic ketoacidosis (DKA) may develop with hyperemesis gravidarum, β-
mimetic drugs given for tocolysis, infection, and corticosteroids given to
induce fetal lung maturation.
The incidence of fetal loss can be as high as 20 percent with DKA.
Infections. Almost all types of infections are increased in diabetic
pregnancies. Common infections include Candida vulvovaginitis, urinary and
respiratory tract infections, and puerperal pelvic sepsis. a twofold increased
risk of asymptomatic bacteruria in women with diabetes. 5 percent of
women with diabetes developed pyelonephritis compared with 1.3 percent
of the non- diabetic population ,pregestational diabetes is associated with a two-
to threefold increase in wound complications after cesarean delivery.
 Because of the relationship between pregnancy complications and
maternal glycemic control, efforts to achieve glucose targets are
typically more aggressive during pregnancy. Management preferably
should begin before pregnancy and include specific goals during each
trimester.
Preconceptional Care

ØTo minimize early pregnancy loss and congenital malformations in

offspring of diabetic mothers, optimal medical care and education are
recommended before conception
Øoptimal preconceptional glucose control using insulin to include self-
monitored preprandial glucose levels of 70 to 100 mg/dL, peak
postprandial values of 100 to 129 mg/dL, and mean daily glucose
concentrations < 110 mg/ dL
Ø HbA1C optimal values to be < 7 percent. risk of congenital
malformations was not demonstrably higher with glycosylated
hemoglobin levels < 6.9 percent, fourfold increased risk for
malformations at levels > 10 percent.
ØIf indicated, evaluation and treatment for diabetic complications such
as retinopathy or nephropathy should also be instituted before
pregnancy.
ØFinally, folate, 5mg/day orally is given periconceptionally and during
early pregnancy to decrease the risk of neural-tube defects.
1st trimester

§ REFERRAL TO A COMBINED MULTIDISCIPLINARY DIABETIC OBSTETRIC

ANTENATAL CLINIC Pregnancy outcomes are improved when women
with diabetes attend a multidisciplinary diabetic obstetric ante- natal
clinic.
§ DATING ULTRASOUND SCAN As the majority of diabetic women have
an elective delivery before term it is essential that the correct
gestational age of the pregnancy is known. Ideally a dating scan
should be performed within the first 10 weeks , Relying on ultrasound
scanning later in a diabetic pregnancy is less accurate as either fetal
growth restriction or growth promotion may be present.
SCREENING FOR DIABETIC COMPLICATIONS Diabetic micro- and
macrovascular complications increase with duration of diabetes.
v A dilated retinal examination each trimester should be performed
with referral to an ophthalmologist if retinopathy is present.
vDiabetic renal disease is more common in women with type 1 than
type 2 diabetes, and its frequency increases with increasing duration
of diabetes. Microalbuminuria and proteinuria are indicators of
diabetic renal involvement and if present, and not attributable to a
urinary tract infection, a urinary creatinine ratio or 24 h urine
collection should be performed to quantify the degree of proteinuria.
vDiabetic neuropathy also increases with duration of diabetes and is
therefore more common in women with type 1 diabetes. Autonomic
neuropathy is particularly problematic in pregnancy as it blunts the
adrenergic and metabolic response to hypoglycaemia potentially
leading to life- threatening episodes of hypoglycaemia.
v Diabetes is associated with premature cardiovascular disease. By the
age of 40 women with type 1 diabetes who have been diabetic for
more than 20 years are likely to have coronary artery calcification and
a degree of coronary artery disease (CAD), independently of any
other risk factor
ASSESSMENT AND OPTIMIZATION OF GLYCAEMIA

vThe firstHbA1c measurement taken in pregnancy provides a crude

assessment of the risk of major congenital malformations, with the
risk increasing with increasing HbA1c values.

vTo optimize maternal glycaemic control and minimize excess

maternal glucose transfer requires the maintenance of fasting
maternal plasma glucose levels below 6 mmol/l and 1 h postprandial
levels below 8 mmol/l.
vThis tight degree of glycaemic control usually requires a highly
flexible insulin regime, best suited by giving multiple injections of
short- and long-insulin injections throughout the day or an insulin
pump.
vThere is no one formula that is applicable for all type 1 or type 2
women, and the precise insulin regime and dose needed has to be
formulated on an individual basis between the women, who are often
extremely adept in doing this, and the diabetic team.
vIt is important to remind women with type 1 diabetes never to stop
their insulin if not eating because of nausea, vomiting or for any other
reason. Ketoacidosis develops more quickly in pregnancy and at
lower blood glucose levels due to enhanced maternal lipolysis.
vin type 2 diabetes there is usually sufficient insulin to prevent
ketoacidosis. However in pregnancy, due to the profound insulin
resistance and enhanced maternal lipolysis, this can occur especially
in the presence of vomiting.
Second trimester

• Repeat 24hour urine studies in women with elevated value in first

trimester or 24 hour protein or creatinine clearance less than 100ml/min
• Repeat HbA1C
• Blood urea nitrogen and creatinine
• Liver function tests
• Uric acid
• CBC count with platelet
• Assessment of fetal well being with non stress test, amniotic fluid indix,
fetal growth, and Doppler examination of the umbilical cord and middle
cerebral artery
• Detailed anatomy ultrasonogram at 18—20 week gestation
• Regular check of blood pressure.
• Fetal echocardiogram
OPTIMIZATION OF GLYCAEMIC CONTROL

ØBy the start of the second trimester in non-diabetic pregnancies

there is a fall in fasting glucose and a rise in postprandial glucose
values. By the middle of the second trimester maternal insulin
resistance starts to increase due to high concentrations of circulating
maternal fatty acids and placental hormones. By term, in non-diabetic
women, insulin secretion has to increase 2–3 fold to control blood
glucose levels postprandially.
ØWomen with diabetes who start pregnancy well- controlled may not
need to increase their overall insulin dosage until after 20 weeks’
gestation, prior to this they may actually need to reduce their insulin
due to nausea and decreased food intake.
ØAfter this time insulin requirements begin to rise usually doubling or
trebling by term.
ØThe diabetic nurses should ensure that the women have the
knowledge and confidence to increase their insulin in response to
their glucose monitoring readings.
 ‫جوة كلة خرط‬

ØWomen with type 2 diabetes are usually insulin resistant prior to

pregnancy. For those women taking oral hypoglycaemic agents during
the first trimester by the second trimester when insulin resistance
increases further these drugs are usually unable to secrete sufficient
insulin to achieve adequate glycaemic control.
ØBy the end of pregnancy daily insulin doses in women with type 2
diabetes may exceed 300 units a day.
ØToday some centers are prescribing Metformin in addition to insulin
in the management of obese type 2 diabetic women.
Third trimester

• Evidence on serial ultrasounds of a rising abdominal circumference

percentile in relation to the head circumference or bi-parietal
diameter is indicative of accelerated fetal growth. This pattern of fetal
growth is seen in association with poor maternal control and fetal
hyperinsulinaemia.
• Growth ultrasonogram to assess fetal size every 4 -6 weeks from 26-
36 weeks' gestation in women with overt preexisting diabetes
• Growth ultrasonogram for fetal size at least once at 36 - 37 weeks'
gestation for women with GDM
• Screening for renal, cardiovasculer, CNS and retinopathy.
OPTIMIZATION OF GLYCAEMIC CONTROL

• During the third trimester maternal insulin resistance continues to

increase along with insulin requirements. Achieving good glycaemic
control tends to become easier as the insulin resistance protects
women from severe hypoglycaemic episodes.
• When glucocorticoid steroids are required for lung maturation insulin
requirements over the next 72 hr may need to double.
• All pregnant women with diabetes should be made aware early in pregnancy that
it is potentially harmful to the baby for the pregnancy to go beyond term.
• The risk of late unexpected stillbirth among women with diabetes is
approximately fourfold higher than for the non- diabetic population and it is for
this reason that most authorities advocate delivery between 38 and 39 weeks.
• Induction at 38 weeks’ gestation in a nulliparous type 1 woman is often slow or
unsuccessful. Caesarian section following failed induction is therefore high among
type 1 diabetic women
• Labor induction may be attempted when the fetus is not excessively large and the
cervix is considered favorable . Cesarean delivery at or near term has frequently
been used to avoid traumatic birth of a large infant in a woman with diabetes.
delivary
• While there is not an absolute right or wrong way to give insulin
during this period it is usual to start an intravenous insulin sliding
scale with a 5% glucose insulin infusion during active labour and
during an operative delivery, and that is continued after delivery until
the mother starts taking meals. During this time hourly blood glucose
monitoring should be done. Once delivered the insulin dose must be
halved.
• As most pregnant women prior to delivery are taking a night time
long-acting basal insulin and quick-acting bolus insulin with their
evening meal, women being admitted for a planned induction should
be encouraged to take their normal insulin doses the night before.
Once admitted they should continue with their short-acting bolus
insulin to cover meals only switching to an intravenous insulin sliding
scale once in labour or a decision has been taken to perform a
Caesarean section.
• Ideally elective Caesarean sections should be planned for early
morning, with the women instructed to take their normal bolus
insulin with their evening meal and two thirds of their usual basal
insulin the night before admission. Once on the ward an intravenous
insulin sliding scale can be started, with the dose adjusted
downwards straight after delivery,
Puerperium

• Often, women may require virtually no insulin for the first 24 hours or
so postpartum. Subsequently, insulin requirements may fluctuate
markedly during the next few days. Infection must be promptly
detected and treated.
• Counseling in the puerperium should include a discussion of birth
control. Effective contraception is especially important in women with
overt diabetes to allow optimal glucose control before subsequent
conceptions.