Diabetes Mellitus and

Pregnancy
By: Muhammad Ilham bin
Muntari
6th year
Group 86

CONTENT
1. PHYSIOLOGICAL CHANGES IN
PREGNANCY DUE TO DIABETES
MELLITUS
2. TYPES OF DIABETES MELLITUS IN
PREGNANCY
3. PREEXISTING DM IN PREGNANCY
4. GESTATIONAL DIABETES
5. MANAGEMENT OF DM IN
PREGNANCY
6. SOME CONCLUSIONS

1. PHYSIOLOGIC CHANGES IN
PREGNANCY DUE TO DM

Cardiovascular system
Respiratory system
Gastrointestinal system
Urinary system
Endocrine system
Genital Tract
Skin

Physiologic changes in pregnancy:

Cardiovascular
Sodium and water retention
Reduced systemic blood pressure (mean
105/60 mmHg in 2nd trimester)
Increased cardiac output (30-50% rise)
Increased blood volume (total body water
increases 40%)
Reduced systemic vascular resistance
(vasodilitation PLUS high flow, low-resistance
circuit of the uteroplacental circulation)
Increased maternal heart rate (up 15-20
beats/min)

Physiologic changes in pregnancy:

Respiratory
Mechanical changes

Diaphragm rises 4 cm
Less negative intrathoracic pressure
No impairments in diaphragmatic or thoracic
muscle motion
Lung compliance remains unaffected

Physiologic changes

Oxygen consumption increases 15-20 %

50% of this increase is required by the uterus
Progesterone directly stimulates breathing
70% of women experience dyspnea (increased
desire to breathe)

Physiologic changes in pregnancy:

Gastrointestinal
Mechanical
Pressure from growing uterus on stomach
reflux/heartburn
Pressure from growing uterus on lower portion
of colon and rectum constipation

Physiologic
Relaxation of sphincter muscle between
esophagus and stomach
Progesterone (a smooth muscle relaxant)
causes decreased GI motility and delayed
gastric emptying

Metabolic changes in
pregnancy
Caloric requirement for a pregnant
woman is 300 kcal higher than the
non-pregnant womans basal needs
Placental hormones affect glucose
and lipid metabolism to ensure that
fetus has ample supply of nutrients

Metabolic changes in
pregnancy
Lipid metabolism:
Increased lipolysis (preferential use of
fat for fuel, in order to preserve
glucose and protein)

Glucose metabolism:
Decreased insulin sensitivity
Increased insulin resistance

Metabolic changes in
pregnancy
Increased insulin resistance
Due to hormones secreted by the
placenta that are diabetogenic:

Growth hormone
Human placental lactogen
Progesterone
Corticotropin releasing hormone

Transient maternal hyperglycemia

occurs after meals because of increased
insulin resistance

Metabolic changes in
pregnancy

Relative baseline hypoglycemia

Proliferation of pancreatic beta cells

(insulin-secreting cells) leads to
increased insulin secretion
Insulin levels are higher than in pregnant
than nonpregnant women in fasting and
postprandial states

Hypoglycemia between meals and at

night because of continuous fetal
draw
Blood glucose levels are 10-20% lower

Metabolic changes in
pregnancy
Lipid metabolism
Increased serum triglyceride (300%) and
cholesterol (50%) levels
Spares glucose for fetus, since lipids do
not cross the placenta
Provides building blocks for increased
steroid hormone synthesis

2. TYPES OF DIABETES MELLITUS IN

PRGENANCY
Diabetes in
pregnancy
Pre-existing
diabetes
IDDM
(Type1)

NIDDM
(Type2)

Gestational
diabetes
Pre-existing
diabetes

True GDM

3. PREEXISTING DIABETES IN
PREGNANCY

Type 1 DM ( IDDM)
Type 2 DM (NIDDM)

Preexisting DM in pregnancy
Effect of pregnancy on pre-existing DM
Increase requirement for insulin
doses
Nephropathy , autonomic
neuropathy may deteriorate
Progress in diabetic retinopathy
(2X)
Hypoglycemia
Diabetic ketoacidosis

Preexisting DM In Pregnancy
Effect of preexisting DM on pregnancy
(1)Maternal
1. increase risk of miscarriage
2. increase risk of preclampsia
3. increase risk of infection eg
vaginal candidiasis, UTI,
endometrial or wound infection
4. increase LSCS rate

Preexisting DM in Pregnancy
(2) Fetal
1. increase risk of congenital
abnormalities
sacral agenesis, congenital heart
disease,
neural tube defects
Hba1c level
normal
<8%
>10%

Risk
not increased
5%
25 %

Preexisting DM in Pregnancy
2. Perinatal mortality (excluding
congenital abnormality ) 2 fold
increased
3. Increase risk of sudden unexplained
intrauterine fetal death.

Complications of pregnancy in preexisting DM

Maternal:
Increase insulin requirment
Hypoglycemia
Fetal:
Infection
Congenital abnormalities
Ketoacidosis
Increased neonatal and perinatal
Deterioration in retinopathy mortality
Increased proteinuria+edema
Macrosomia
Miscarriage
Late stillbirth
Polyhydramnio
Neonatal hypoglycemia
Shoulder dystocia
Polycythemia
Preeclampsia
jaundice
Increased caesarean rate

Maternal hyperglycemia
|
Fetal hyperglycemia
|
Fetal pancreatic beta-cell
hyperplasia
|
Fetal hyperinsulinaemia
|
Macrosomia,organomegaly,
polycythaemia, hypoglycemia,

4. GESTATIONAL DIABETES
Definition
Carbohydate intolerance of variable
severity first recognised during the
present pregnancy.
This includes women with preexisting
but previously unrecognised diabetes

GDM: Risk factors

Maternal age >25 years
Body mass index >25 kg/m2
Race/Ethnicity
Latina
Native American
South or East Asian, Pacific Island ancestry

Personal/Family history of DM
History of macrosomia
Polyhydramnios
Previous unexplained stillbirth

Gestational Diabetes (GDM)

GDM: Screening
Screening test
50 gm 1-hour glucose
challenge test (GCT)

Screening thresholds
130mg/dL: 90% sensitivity
(23% screen positive)
140mg/dL: 80% sensitivity
(14% screen positive)

If patient screens
positive, she goes on to
take a 3-hour glucose
tolerance test (GTT)

GDM: Diagnosis
Fasting blood glucose >126mg/dL or
random blood glucose >200mg/dL
100 gm 3-hour glucose tolerance test
(GTT) with 2 or more abnormal values
Carpenter and
Coustan

National Diabetes
and Data Group

Fasting

95 mg/dL

105 mg/dL

1 hour

180 mg/dL

190 mg/dL

2 hour

155 mg/dL

165 mg/dL

3 hour

140 mg/dL

145 mg/dL

Gestational diabetes
Clinical significance of GDM
1. High incidence of macrosomia, and
adverse pregnancy outcomes,
2. A significant proportion(30%)
identified as GDM in fact have DM
before pregnancy

Gestational diabetes
Women with glucose intolerance just
above normal range are at low risk
for pregnancy complications, those
with more severe glucose intolerance
approaching the criteria of diabetes
are at risk of neonatal complications

Fetal complications
Macrosomia (>4 kg)
risk is 16-29% as compared to 10% in
control
Increase in caesarean delivery,
intrumental deliveries ( forceps/vacuum),
birth trauma, such as brachial plexus
injuries , clavicular fractures
Increase in neonatal hypoglycemia (24% ),
hyperbilirubinemia, hypocalcemia,
polycythemia
Children are at risk of type 2 DM and
obesity in life

Maternal complications
Increase risk of hypertensive
disorders
Increase risk of caesarean and
intrumental deliveries
Increased Risk (40-60%) of
developing type 2 DM within10-15 yr.

5. MANAGEMENT OF DM IN
PREGNANCY
Nutrition therapy
Home self glucose monitoring
Medical therapy if glycemic control
not achieved with diet/exercise
Subcutaneous insulin
Oral hypoglycemic agents (Glyburide,
Metformin)

Antenatal monitoring

Management:
Glycemic control
Significant benefit of insulin therapy
Prior to insulin use, perinatal
mortality was 65%
After introduction of insulin
therapy, perinatal mortality
declined to 5%

Management:
Glycemic control
Glycosylated Hemoglobin A1C (Hgb A1C)
level should be less than or equal to 6%
Levels between 5 and 6% are associated with
fetal malformation rates comparable to those
observed in normal pregnancies (2-3%)
Goal of normal or near-normal glycosylated
hemoglobin (Hgb A1C) level for at least 3
months prior to conception

Hgb A1C concentration near 10% is

associated with fetal anomaly rate of 2025%

Management:
Glycemic Control
Blood glucose goals during pregnancy
Fasting < 95mg/dL
1-hr postprandial < 130-140mg/dL
2-hr postprandial am < 120mg/dL
2 am < 120mg/dL
Nocturnal glucose level should not go below
60 mg/dL
Abnormal postprandial glucose
measurements are more predictive of
adverse outcomes than preprandial
measurements

Management:
Nutrition
Caloric requirements:
Normal body weight - 30-35 kcal/kg/day
Distributed 10-20% at breakfast, 20-30% at
lunch, 30-40% at dinner, up to 30% for snacks
(to avoid hypoglycemia)

Caloric composition:
40-50% from complex, high-fiber
carbohydrates
20% from protein
30-40% from primarily unsaturated fats

Management:
Subcutaneous Insulin Therapy
Insulin requirements increase rapidly,
especially from 28 to 32 weeks of
gestation
1st trimester: 0.7-0.8 U/kg/d
2nd trimester: 0.8-1 U/kg/d
3rd trimester: 0.9-1.2 U/kg/d

Management:
Subcutaneous Insulin Therapy

Regular insulin = Humalog, Novalog

Management:
Oral Hypoglycemic Agents
Glitazones (Avandia, Actos)
Sensitize muscle and fat cells to accept insulin more
readily
Decrease insulin resistance

Sulfonylureas
Augment insulin release
1st generation
Concentrated in the neonate hypoglycemia

2nd generation (Glyburide)

Low transplacental transfer

Biguanide (Metformin, aka Glucophage)

Increases insulin sensitivity
Crosses placenta

Management Summary:
Pregestational Diabetes
Referral to perinatologist and/or
endocrinologist
Multidisciplinary approach
Regular visits with nutritionist
Hgb A1C every trimester
Fetal Echocardiogram
Level II ultrasound
Opthamologist
Baseline kidney and liver function tests

Management Summary:
Pregestational Diabetes
Optimize glycemic control frequent
insulin dose adjustments
Type 1: often have insulin pump
Type 2: subcutaneous insulin

Fetal monitoring starting at 28-32 weeks,

depending on glycemic control
Ultrasound to assess growth at 36 weeks
Delivery at 38-39 weeks

Management Summary:
GDM
Begin with diet / walk after each meal
If borderline/mild elevations, consider
metformin (start at 500 mg daily)
Counsel about increased PTD rates
Unlikely pre-existing DM

If elevations start out moderate to

severe or metformin fails, proceed to
subcutaneous insulin therapy
NPH (long acting)
Humalog/Novalog (short acting)

Management Intrapartum
Attention to labor pattern, as
cephalopelvic disproportion may indicate
fetal macrosomia
Careful consideration before performing
operative vaginal delivery
Hourly blood glucose monitoring during
active labor, with insulin drip if necessary
Notify pediatrics if patient has poorly
controlled blood sugars antepartum or
intrapartum

Management Postpartum
For patients with pregestational diabetes,
halve dose of insulin and continue to
check blood glucose in immediate
postpartum period
For GDM patients who required insulin
therapy (GDMA2), check fasting and
postprandial blood sugars and treat with
insulin as necessary
For GDM patients who were diet controlled
(GDMA1), no further monitoring nor
therapy is necessary immediately
postpartum

Management Postpartum
For all GDM patients, perform 75
gram 2-hour OGTT at 6 week
postpartum visit to rule out
pregestational diabetes
Most common recommendation is for
primary care physician to repeat
2-hour OGTT every three years

6. DIABETES MELLITUS &

PREGNANCY; SOME CONCLUSIONS

Diabetes and Pregnancy

Conclusion
(1)Preexisting DM in pregnancy
() Good glucose control is important
for decreasing morbidities
() Insulin is still the gold standard of
treatment in pregnancy
() Increasing evidence for clincial
effectiveness for treatment with
oral hypoglycemic agents

Diabetes and pregnancy

conclusion
(2) Gestational diabetes
no consensus
The morbidities increases as glucose level
approaching the diagnosis as DM
Possible that treatment improves
outcomes
Overlap with preexisting DM, esp type2
Long term implication for health of the
mother and baby