Diabetes Mellitus During Pregnancy

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Diabetes mellitus during

pregnancy

GYNE II


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Objectives

Physiologic changes during pregnancy

Types of Diabetes during pregnancy

Pregestational diabetes1. Effects of pregnancy on diabetes

2. Effects of diabetes on pregnancy

3. Diagnosis

4. Management

Gestational diabetes


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Changes in glucose metabolism in

pregnancy

Fasting hypoglycemia due to increasedcirculatory volume

Progressive insulin resistance due to therelease of anti-insulin hormones (hPL, cortisol,PRL and placental insulinase)

Increased insulin release (double the level ofprepregnancy in the third trimester)


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Normal glucose metabolism

Glucose enters bloodstream from food source

Insulin aids in storage of glucose as fuel for cells

Insulin resistance is defined as insensitivity of cells toinsulin, therefore resulting in increased levels of insulin andglucose in the bloodstream


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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


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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


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Increased insulin resistance

Due to hormones secreted by the placenta thatare diabetogenic:

Growth hormone Human placental lactogen

Progesterone

Corticotropin releasing hormone

Transient maternal hyperglycemia occurs aftermeals because of increased insulin resistance


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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


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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


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Preexisting diabetes mellitus (DM)


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Size of the problem

Diabetes mellitus affects approximately 4

million women of childbearing age in the

United States.

90% type II and 10% type I


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Either type 1 (iddm) or type 2 (niddm)

Type 1 occurs in younger age group and end

organ complications is likely to be more.

Hence they to have increased maternal and

fetal risks

Type 2 usually occurs in obese patients and

have less maternal and fetal risks compared

to type 1. many will be using oral

hypoglycemic drugs between pregnancies

Whi i l ifi i f


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Whites prognostic classification of

DM with pregnancy

Class A1Abnormal glucose tolerance test with normal

fasting capillary (95 mg/dL) andpostprandial (120 mg/dL) glucose levelsControlled with diet alone

Class A2

Abnormal glucose tolerance test withabnormal fasting or postprandial glucoselevels Treated with diet and insulin

Background retinopathy


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Class B

Insulin-treated diabetic

Onset over age 20 yearsDuration less than 10 years

No vascular disease or retinopathy


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Class C


Onset between ages 10 and 20 years

Duration between 10 and 20 years

Background retinopathy

Class D


Onset under age 10

Duration more than 20 years


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Class F

Diabetic nephropathy

Class H

Cardiac disease

Class R

Proliferative retinopathy

Class T

Renal transplant


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Diagnosis of Diabetes

Non Pregnant

Fasting plasma BG >7.0mmol/l (126 mg/dL)

Casual plasma BG >11.1mmol/l (200 mg/dL)

Impaired Fasting Glucose FPG 6.1-7.0 mmol/l

Impaired Glucose Tolerance

normal FPG 2 h 75gOGTT test with BG 7.8 (140 mg/dL)-11.1

mmol/l (200 mg/dL)


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Effects of pregnancy on DM

Increased insulin requirements (difficult control)

More liability to fasting hypoglycemia

More liable to DKA (type I)

Nausea and vomiting may further complicate

control

Insulin requirements markedly drop after delivery


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Effects of diabetes on the mother

First trimester: miscarriage

Second trimester: polyhydramnios, hypertension

Third trimester: polyhydramnios, hypertension,preeclampsia, preterm labor (spontaneous or induced)

Delivery: increased risk of operative delivery and itsresultant complications

At all times, there is an increase risk of infection especiallyurinary tract, skin infections and monilial vulvovaginitis

Deterioration of retinopathy, gastropathy, nephropathy

and to a lesser extent; neuropathy


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Effects of diabetes on the fetus

First trimester: miscarriage, malformation

Second trimester: miscarriage (fetal demise)

Third trimester:macrosomia (due to anabolic effect of insulin)

growth retardation (in women with diabetic vasculopathy)

fetal hypoxia or even fetal death

During delivery, the baby is liable to birth trauma andasphyxia and operative delivery.


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Neonatal complications

After delivery, the infant of diabetic mother is liable to

hypoglycemia (due to increased fetal insulinproduction secondary to increased glucose loads fromthe mother

hypocalcemia

Polycythemia

jaundice (polycythemia)

Hypomagnesemia Respiratory distress syndrome (decreased surfactant)


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Congenital anomalies of infants of

diabetic mothers.Skeletal and central nervous system

Caudal regression syndrome (200 times increased risk)

Neural tube defects (2-10 times increased risk)

Microcephaly

Cardiac(4 times increased risk)

Transposition of the great vessels

Ventricular septal defects and Atrial septal defects Coarctation of the aorta

defects or patent ductus arteriosus

Cardiomegaly

Renal(10 times increased risk)

Hydronephrosis

Renal agenesis

Ureteral duplicationGastrointestinal(3-10 times increased risk)

Duodenal atresia

Anorectal atresia

Small left colon syndrome

Other

Single umbilical artery


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Management

Before pregnancy

During pregnancy: Medical management

During pregnancy: obstetric management Delivery

Puerperium


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Before pregnancy

Women with diabetic nephropathy (albuminuria, Creatinine >250micromol/L or impaired creatinine clearance), cardiopathy(coronary artery disease), and gastropathy should avoid pregnancy

Counsel women with proliferative retinopathy about possible

deterioration

Optimize glycemic control

Type II to switch to Insulin if not on Insulin

Stop ACE inhibitors

Assess HBA1c (


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Before pregnancy (2)

Assess fundus, urea and creatinine, protein in urine, ECG

Do laser coagulation before pregnancy if proliferative

retinopathy

FOLIC ACID 5 MG BEFORE PREGNANCY

Counsel about the need for tighter control, more frequenthypoglycemia, need for frequent maternal and fetal

monitoring and increased rate of operative delivery and

diabetes in the offspring (6% if mother has DM, 10% if father

has DM)


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Glycosylated Hemoglobin A1C (Hgb A1C) level shouldbe less than or equal to 6%

Levels between 5 and 6% are associated with fetalmalformation rates comparable to those observed innormal 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 withfetal anomaly rate of 20-25%


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During pregnancy Diet:Three meals and three snacks

30-35 Kcal/Kg ideal body weight, 25 if obese

No more than 10-12 Kg weight gain50% of energy carbohydrates (unrefined), 30% fat

and 20% proteins

Review diet history to identify major areas of

reduction of caloric intakeAlert the patients and relatives about the

possibility of hypoglycemia and measures tocounteract


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Insulin Starting dose (0.6-0.8 U/Kg body weight in 1st trimester, 0.7-0.9 U/kg body

weight in the 2nd

trimester and 0.9-1.1 U/kg body weight in the 3rd

trimester)

Which types of insulin to give (short acting and intermediate [long acting stoppedbefore pregnancy])

Dosage schemes twice daily or three times or four times. The more frequent, thetighter the control but increased inconvenience and less compliance

Glycemic targets

Fasting: 60 90 mg/dL

Preprandial: 80 95 mg/dL

Postprandial: < 120 mg/dL

Monitoring of glycemic control (clinically by symptoms of hyper andhypoglycemia, glucose profile weekly, HBA1c every 1-2 months)

Glucose profile is home based assessment of glucose 7 times/day; fasting, 2 hafter breakfast, before lunch, 2h after lunch, before dinner, 2 h after dinner andat midnight. This should be done weekly or at any time glucose control is

suspected. Dose adjustment is undertaken according to the profile


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Diabetic Ketoacidosis

5-10% of pregnant Type 1 pts

Risk factors

New onset DM

Infection

Steroids

B mimetics

Fetal mortality 10%


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Management

Assess BG, ketones electrolytes

Insulin

0.2-0.4U/Kg loading and 2-10U/h maintenance

Begin 5% dextrose when BG is 14 mmol/l

Potassium replacement

Rehydration isotonic NaCl Replace Bicarb and phosphate as needed


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Obstetric management

First trimester:

aggressively manage nausea and vomiting Ultrasound (viability, nuchal fold thickness)

Second trimester:

Anomaly scan 16-20 w

Fetal echo 24-26 w

Third trimester

Serial assessment of fetal growth

Serial assessment of fetal wellbeing (start at 32 weeks)

Start earlier at 28 w if growth restriction is suspected (women withvascular disease, nephropathy or hypertension)

Women with poor control and IUGR are likely to have abnormal resultsof tests of fetal wellbeing


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Delivery

If everything is OK, deliver at 38-40 weeks Route of delivery depends on fetal size, past obstetric

performance and associated factors

Keep a high threshold for CS

Vaginal delivery should be conducted by a seniorobstetrician trained to deal with accidents such as shoulderentrapment

Women with proliferative retinopathy should not beardown

If preterm termination is required and corticosteroids aregiven to accelerate lung maturation, an increased insulinrequirement over the next 5 days should be anticipated, andthe patients glucose levels must be closely monitored

Fluid and insulin management during


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Fluid and insulin management during

and after delivery Stop subcutaneous insulin once labor starts 5% dextrose at 100 ml/hour

50 unit short acting insulin/500 cc normal saline(2-3 units/hour)

Measure capillary glucose hourly and serumglucose/4 h

Maintain glucose


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NEW BORN MANAGEMENT

SERIALLY ASSESS CAPILLARY GLUCOSE OF THE

NEONATE ESPECIALLY IN THE FIRST 12 HOURS.

REPLACE GLUCOSE IF THE GLUCOSE LEVEL IS

LESS THAN 45 MG/DL

IF THE HEMATOCRIT VALUE EXCEEDS 70,

EXCHANGE TRANSFUSION

SERIALLY MONITOR BILIRUBIN LEVEL


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Gestational diabetes mellitus

Definition Glucose intolerance of variable severity first diagnosed in Pregnancy

Prevalence 2-4%

Risk Factors

A family history of diabetes, especially in first degree relatives

Prepregnancy weight more than 90 kg.

Age >29 years

A previous large baby (>9 pounds [4.1 kg])

History of abnormal glucose tolerance

A previous unexplained perinatal loss or birth of a malformed child

Polycystic ovary syndrome

Glycosuria (repeated twice) at the first prenatal visit

Current use ofglucocorticoids


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Effects on the mother and fetus

Increased liability to infections Preterm labor

Polyhydramnios

Preeclampsia Operative delivery

All the effects of DM on the fetus exceptanomalies (why???)

GDM is liable to recurrence 50-60% of women with GDM will develop type II

DM later in life


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GDM IS ASYMPTOMATIC. IT IS

DETECTED BY SCREENING


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Screening approaches

Universal screening at 24-28w

Screening high risk only

Screening most women with few exception at

24-28w and earlier screening of women with

risk factors


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Criteria for avoiding laboratory screening forgestational diabetes

All criteria must be met for a patient to be considered low-riskand glucose testing avoidedAge less than 25 years

Prepregnancy Body mass index of 25

No prior history of glucose intolerance (GDM, DM, IGT, or IFG)

No prior history of obstetric outcomes associated with GDM(macrosomia, stillbirth, polyhydramnios, malformations)

No known diabetes in a first-degree relative


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Risk Factors A family history of diabetes, especially in first degree relatives

pre-pregnancy weight more than 90 kg or more

Age >25 years

A previous large baby (>9 pounds [4.1 kg])

History of abnormal glucose tolerance

A previous unexplained perinatal loss or birth of a malformed child

Polycystic ovary syndrome

Glycosuria (repeated twice) at the first prenatal visit

Current use ofglucocorticoids


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Criteria of the 1h, 50 g tolerance screening

1h >140 = GDM

1h


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Medical Management

Diet

Insulin (indications)

Oral hypoglycemic agents (promising)

Peripartum management. Insulin can usually

be withheld during labor delivery

Infusion of normal saline is usually sufficientto maintain normoglycemia.


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Obstetric Management

Similar to third trimester management of DM except: noneed to deliver at 38 weeks if controlled diabetesespecially on diet alone

Antepartum fetal surveillance restricted to those withpoor control, those on insulin or other associatedobstetric factors that will necessitate fetal monitoringsuch as preeclampsia, hypertension or abnormal fetalmovements

Do not forget

Perform OGTT at 6 weeks to confirm disappearance ofimpaired glucose tolerance


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Thank you

Diabetes Mellitus During Pregnancy

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