Current Updates in Management of High Risk Pregnancy

Obesity and Gestational Diabetes

Irwan T Rachman
(email: irwantaufiqurrachman@yahoo.co.id)

Division of Maternal Fetal Medicine

Department of Obstetrics and Gynecology
Sardjito Hospital - Yogyakarta
Continuing of Care
 Pyramid of Prenatal Care
Pyramid of traditional prenatal
care New pyramid of prenatal care

*The
Ministry of Health in the UK issued a
Memorandum on Antenatal Clinics
Maternal Mortality

Source: Annual death rate per 1000 total births from maternal mortality in England and
Wales (1850–1970) (Registrar General Reports)
 Continuing of Care
11-13 20-22 37-38 41
weeks weeks weeks weeks

Low Risk PPK1

PPK2

High Risk
PPK3
 11-13 20-22 37-38 41
weeks weeks weeks weeks

First Scoring Kehamilan dgn

Prenatal Diabetes

PPK 1
Visit Two of the following condition:
1) Age younger than 25 years old
2) Not a member of an ethnic group with
increased risk for type 2 DM (Hispanic,
African, Native American, South or East
Asian, or Pacific Islander ancestry)
3) BMI <25; normal weight at birth
4) No history of abnormal glucose

PPK 2
tolerance
5) No history of poor obstetric outcomes
6) No first degree relatives with DM
One High risk factor for pre-eclampsia
1) Pre Gestational Diabetes
2) Severe obesity
3) Strong family history of type 2 diabetes
4) Previous history of GDM, impaired
glucose metabolism, or glucosuria

PPK 3
 Diabetes Mellitus
• The most common medical complication of
pregnancy
• Diabetes in pregnancy: Type 1, Type 2, or
gestational diabetes mellitus (GDM)
• As the incidence of type 2 DM increases, cases of
GDM have grown also
• 4-5% of pregnancies are complicated by DM; In
90% of diabetic pregnancies, the cause is GDM.
• 0,5-1% of pregnancies are complicated by
pregestational DM (diagnosed prior to
pregnancy)
 Comparison of Type 1 and Type 2
Diabetes Mellitus

Note: The fasting plasma glucose test is preferred. An initial abnormal value must be confirmed on a different day, by repeat
fasting glucose level, plasma glucose level after glucose load, or random plasma glucose level if symptoms are present. Adapted
from Position Statement: Standards In Medical Care in Diabetes. Diabetes Care 2009;32(S1):S13-S61.
 Overweight and Obesity
• are defined as abnormal or excessive fat
accumulation that presents a risk to health.
Obesity Prevalence in World
 Carbohydrate Metabolism Changes
during Pregnancy
• In the fasting state, maternal serum glucose is lower in
pregnancy than in the non-pregnant state (55 to 65 mg/dL),
whereas free fatty acid, triglyceride, and plasma ketone
concentrations are increased.
– A state of relative maternal starvation exists in pregnancy,
during which glucose is spared for fetal consumption and
alternate fuels are used by the mother.
• GDM is similar to type 2 DM
– increased pancreatic secretion cannot over-come decreased
insulin sensitivity of maternal target tissues.
– Increased metabolism in pregnancy also increases insulin
clearance.
– These changes are due to the effects of estrogen, progesterone,
cortisol, prolactin, and human placental lactogen.
 Diagnosis and Screening
• Diagnosis of type 1 and 2 DM before
pregnancy is by standard criteria:
– two abnormal fasting glucose levels >126 mg/dL
or a random glucose level >200 mg/dL
– Classic symptoms are polydipsia, polyuria, and
polyphagia. Clinical signs include weight loss,
hyperglycemia, persistent glucosuria, and
ketoacidosis.
 Universal screening for GDM
• Patient history, clinical risk
factors, or laboratory
testing.
• Performed: at 24 to 28
weeks
– Note: if strong risk factors
such as obesity, family history,
or a personal history of GDM
are present, screening can be
performed at the first visit.
Note: Patients who meet all low-risk criteria and have no
high-risk factors may forgo oral glucose challenge testing if
appropriate.
Gestational Diabetes Risk Assessment:
Low Risk
• Age younger than 25 years old
• Not a member of an ethnic group
with increased risk for type 2 DM
(Hispanic, African, Native
American, South or East Asian, or
Pacific Islander ancestry)
• BMI <25; normal weight at birth
• No history of abnormal glucose
tolerance
• No history of poor obstetric
outcomes
• No first degree relatives with DM
High Risk
• Severe obesity
• Strong family history of type 2
diabetes
• Previous history of GDM, impaired
glucose metabolism, or glucosuria
 Screening
• 50 g oral glucose challenge is consumed, followed by serum
glucose measurement at 1 hour (Note: no fasting or dietary
preparation is required)
– Serum glucose >140 mg/dL identifies 80% of GDM.
– Serum glucose >130 mg/dL identifies over 90% of GDM.
– Serum glucose >200 mg/dL diagnoses GDM without additional testing.
• If the screening test is positive, then a diagnostic 3-hr glucose
tolerance test (GTT) should be performed with 100 g oral glucose
after at least 8 hr of fasting
• With abnormal fasting or any other two abnormal values, the
diagnosis of DM is confirmed.
• In patients at high risk for GDM with a normal GTT, a follow-up GTT
can be performed at 32 to 34 weeks to identify later-onset
diabetes.
 Criteria for Diagnosis of Gestational Diabetes
from Oral Glucose Tolerance Testing

Time since 100 gr Modified O’Sullivan Carpenter and Coustan

Glucose Load (hour) Scale Scale

Fasting > 105 > 95

1 > 190 > 180

2 >165 > 155

3 > 145 > 140

Note: Values are plasma glucose levels in mg/dL. Adapted from O'Sullivan JB, Mahan CM. Criteria for the oral
glucose tolerance test in pregnancy. Diabetes 1964;13:278-285; and Carpenter MW, Coustan DR. Criteria for
screening tests for gestational diabetes. Am J Obstet Gynecol 1982;144:768-773
 Maternal Complications of DM
• Maternal complications are increased with diabetes.
• Diabetic ketoacidosis (DKA) is a potentially life-threatening
metabolic emergency for both mother and fetus.
– In pregnant patients, DKA can occur at lower blood glucose
levels (i.e., <200 mg/dL) and more rapidly than in nonpregnant
diabetics.
– Fetal mortality rates from 10%-30% are reported.
– About half of DKA cases are due to medical illness, usually
infection; another 20% result from dietary or insulin
noncompliance. In 30% of cases, no precipitating cause is
identified.
– Antenatal steroids for fetal lung maturity and beta adrenergic
tocolytics can precipitate or exacerbate DKA in pregestational
diabetics.
 Pathophysiology and Diagnosis
Pathophysiology:
• relative or absolute insulin deficiency. The resulting
hyperglycemia and glucosuria lead to osmotic diuresis,
promoting urinary potassium, sodium, and fluid loss.
• Insulin deficiency also increases lipolysis and hepatic
oxidation of fatty acids, producing ketones and eventually
causing metabolic acidosis.
Diagnosis:
• maternal hyperglycemia, acidemia, and serum ketosis.
• Signs and symptoms: abdominal pain, nausea and
vomiting, polydipsia, polyuria, hypotension, rapid deep
respiration, and impaired mental status (ranging from mild
drowsiness to profound lethargy)
Note: Acidosis can be defined as a plasma bicarbonate level <15 mEq/L or arterial pH <7.3. In the presence of
hyperglycemia, ketosis is presumed and can be verified by serum testing. Because pregnancy is a state of
physiologic respiratory alkalosis, profound DKA may occur at a higher pH
 Management Diabetic Ketoacidosis
1) IV Fluid Hydration
– 1 L of normal saline (NS) administered in the first hour.
– 500 to 1,000 mL/hr for the next 2 to 4 hr followed by 250 mL/hr.
– Change fluids to D5 NS when blood sugar decreases to 250 mg/dL.
2) Insulin Infusion (Rapid-Acting Insulin)
– Loading dose of 0.2 to 0.4 U/kg.
– IV infusion of 2 to 10 U/hr (double the rate if glucose level does not decrease by 25% in
first 2 hr).
– When blood sugar declines to 150 mg/dL, decrease infusion to 1 to 2 U/hr. Continue
until urine ketones are cleared.
– When the patient is able to tolerate food, start their usual insulin regimen.
3) Potassium
– If initially normal or reduced, an infusion rate up to 15 to 20 mEq KCl/hr may be
required; if elevated, wait until potassium levels decrease into the normal range, then
add KCl to intravenous solution in a concentration of 20 to 30 mEq/L.
4) Bicarbonate
– Add one ampule bicarbonate (44 mEq) to 1 L of 0.45 normal saline, if pH is <7.1
 Management of Diabetes in
Pregnancy
• Ideally, preconception consultation and maintain euglycemia
before conception.
• HbA1C is helpful in evaluating recent (8 to 12 weeks) glycemic
control and assessing risk for fetal malformations.
– Note: HgbA1C >9.5% carries >20% risk of major fetal malformation.
Strict glucose control (i.e., HgbA1C <6%) during organogenesis
dramatically reduces embryopathy to nondiabetic levels. Early
nutrition consult and counseling may be beneficial.
• Blood glucose goals (Table 13-6).
– Patients should start or continue intensive glucose monitoring early in
pregnancy using a home glucometer. They should record fasting and 1-
hr (or 2-hr) postprandial blood sugar levels for each meal.
– Postprandial glycemic control correlates best with risk for neonatal
hypoglycemia, macrosomia, fetal death, and neonatal complications.
– Home monitoring records are reviewed every 1 to 2 weeks and
therapy is optimized.
 Goals for Glycemic Control in
Pregnancy
Goal Blood Sugar Values
Fasting 60-9- mg/dL
Premeal < 100 mg/dL
1 hr postpandrial <140 mg/ dL
2 hr postpandrial < 120 mg/dL
Bedtime < 120 mg/dL
02.00-06.00 60-90 mg/dL

From: Metger BE, et al. Summary and Recommendation of the 5th International Workshop-Conference on
Gestational Diabetes Mellitus. Diabetes Care. 2007; 30(2): 5251
 GDM Management
• Consists of: diet and exercise. If good glucose
control is not achieved, oral hypoglycemic
agents or insulin are then prescribed.
– Women with newly diagnosed GDM are started on
a diabetic diet of 1,800 to 2,400 kcal/day.
– Moderate exercise can improve glycemic control
in GDM. Patients are encouraged to maintain a
consistent level of activity throughout pregnancy
provided there are no complications (e.g., preterm
labor).
Oral Hypoglycemic Agents or Insulin?
• Oral hypoglycemic agents: when dietary efforts fail.
– Glyburide: increasing tissue insulin sensitivity and has
minimal placental transfer. The starting dose is usually 2.5
mg PO at bedtime or 2.5 mg PO twice daily, titrated to a
maximum dose of 10 mg PO twice a day.
• Four to twenty percent of patients will need additional therapy
with insulin, particularly if fasting blood sugars are high.
• Side effects: hypoglycemia, nausea, heartburn, and allergic skin
reactions.
– Metformin is also safe and effective; about one half of
patients on metformin will require insulin as well
Oral Hypoglycemic Agents or Insulin?
• Insulin therapy can improve glycemic control for
GDM.
• Different types of insulin are combined to
maintain even control through day and night
• Neutral Protamine Hagedorn (NPH) insulin is an
intermediate-acting insulin given in the morning
and at night, with peak activity at 5 to 12 hr.
• Rapid-acting insulin (e.g., Humalog or Novolog) is
administered with meals because its onset is 5 to
15 minutes and peak activity occurs at 2 to 4 hr
 Types of Insulin for People with
Diabetes
① Rapid-acting: Usually taken before a meal to cover the blood
glucose elevation from eating. This type of insulin is used with
longer-acting insulin.
② Short-acting: Usually taken about 30 minutes before a meal to
cover the blood glucose elevation from eating. This type of insulin
is used with longer-acting insulin.
③ Intermediate-acting: Covers the blood glucose elevations when
rapid-acting insulins stop working. This type of insulin is often
combined with rapid- or short-acting insulin and is usually taken
twice a day.
④ Long-acting: This type of insulin is often combined, when needed,
with rapid- or short-acting insulin. It lowers blood glucose levels
when rapid-acting insulins stop working. It is taken once or twice
a day
 Types of Insulin for People with
Diabetes
Type Brand Name Onset Peak Duration
Rapid-acting Humalog 10-3- min 30 min – 3 3-5 hours
Novolog hours
Apidra
Short-acting Regular (R) 30 min – 1 2-5 hours Up to 12 hours
hours
Intermediate- NPH (N) 1.5-4 hours 4-12 hours Up to 24 hours
acting
Long-acting Lantus 0.8-4 hours Minimal peak Up to 24 hours
Levemir
 Calculation and dose distribution for
initial insulin management in pregnancy
 Fetal Monitoring

• Fetal monitoring is not required for GDM-A1

diabetics.
– They are not at increased risk for fetal demise before
40 weeks' gestation.
• Women with GDM-A2 (i.e., on medication)
require antenatal testing similar to that
recommended for pregestational DM
– twice weekly NSTs or BPP from 32 to 34 weeks until
delivery)
– Delivery by 40 weeks' gestation is recommended.
 Pregestational DM Management
• Diet: 1,800 to 2,400 kcal daily (20% protein, 60% carbohydrates,
and 20% fat)
• Continued on their normal prepregnancy insulin regimen while
initial blood sugar monitoring is performed. Monitoring and goals
are the same for GDM and pregestational DM
• The American Diabetes Association recommends insulin for
pregnant women with DM and for women with DM considering
pregnancy.
– Patients taking oral hypoglycemic agents (except glyburide) or a 70/30
(NPH/regular) mixed insulin regimen are switched to NPH and a rapid-
acting insulin analog.
– Patients with type 1 DM usually require 50% to 100% increased insulin
doses in the second half of pregnancy.
– Type 2 DM insulin dosing is frequently more than doubled in
pregnancy
 Fetal Assessment And Monitoring For
Pregestational Diabetes
• First trimesterearly dating sonogram to confirm GA and document fetal viability.
• Second trimester: Offer maternal serum AFP screening for neural tube defects
(either alone or as part of aneuploidy screening if desired by the patient; see
Chapter 12).
– Ultrasonography at 18 to 20 weeks is recommended for complete anatomy evaluation.
– Fetal echocardiography is also recommended at 19 to 22 weeks for pregestational diabetics.
• Third trimester:
– Twice weekly antenatal testing should be initiated for all diabetic pregnancies starting at 32 to
34 weeks' gestation.
– Patients with comorbidities or very poor glycemic control may start assessment as early as 28
weeks.
– Serial USG exams for fetal growth should be considered at 28-30 weeks and again at 34-36
weeks. Earlier assessment and umbilical artery Doppler velocimetry may be required to assess
for IUGR in patients with microvascular disease
 Labor and Delivery in Diabetic
Pregnancies
• Timing of delivery in an insulin-requiring diabetic patient should consider
maternal glycemic control, maternal comorbidities, estimated fetal
weight, antenatal testing, and amniotic fluid volume.
– In many patients with well-controlled DM, labor may be induced safely at 39-
40 weeks.
• Amniocentesis for fetal lung maturity is recommended before elective
delivery for gestations of <39 weeks. Amniocentesis may need to be
repeated until 39 weeks or fetal lung maturity is achieved, or until delivery
for other obstetric indications (e.g., nonreassuring fetal testing).
• Tests for fetal lung maturity include the following:
– Fluorescence polarization. Maturity suggested by >55 mg surfactant/g
albumin
– Lecithin/sphingomyelin ratio. Maturity suggested by L/S ratio of >U.0
– Phosphatidylglycerol. Maturity suggested by positive test.
Congenital Malformations Associated
with Maternal Diabetes
Congenital Malformations Associated
with Maternal Diabetes
Congenital Malformations Associated
with Maternal Diabetes
 Congenital Malformations Associated
with Maternal Diabetes
Maternal diabetes has toxic effects on the development of the embryo and
significantly increases the risk of congenital malformations in humans. The incidence
of fetal structural defects caused by maternal pregestational diabetes is three- to
fourfold higher than that caused by non-diabetic pregnancy. The congenital
malformations associated with diabetic pregnancy arise before the seventh gestational
week. Diabetic embryopathy can affect any developing organ system, including the
central nervous system (CNS) (anencephaly, spina bifida, microcephaly, and
holoprosencephaly), skeletal system (caudal regression syndrome, sacral agenesis,
and limb defects), renal system (renal agenesis, hydronephrosis, and ureteric
abnormalities), cardiovascular system (transposition of the great vessels, ventricular
septal defects, atrial septal defects, coarctation of the aorta, cardiomyopathy, and
single umbilical artery), and gastrointestinal system (duodenal atresia, anorectal
atresia, and small left colon syndrome). Pregnant women with fetuses with diabetic
embryopathy may have chronic or unrecognized hyperglycemia and elevated levels of
glycerated hemoglobin. This review emphasizes the necessity to consider
hyperglycemia-induced teratogenesis during genetic counseling of parents with
prenatally detected fetal malformations. Successful preconception counseling for
women with diabetes mellitus and metabolic control will reduce birth defects and
maternal morbidity. [Taiwanese J Obstet Gynecol 2005;44(1):1–7]
 Obesity and Risk GDM
Twenty studies were included in the meta-analysis.
The unadjusted ORs of developing GDM were
• 2.14 (95% CI 1.82–2.53), 3.56 (3.05–4.21), and
8.56 (5.07–16.04) among overweight, obese, and
severely obese compared with normal-weight
pregnant women, respectively.
• CONCLUSIONS — Our findings indicate that high
maternal weight is associated with a substantially
higher risk of GDM
Email: irwan.taufiq@gmail.com
Source:
https://www.dropbox.com/sh/879s17iaprzi8fk/AAD86rfdWtUhewIRokPX
uXyta?dl=0

TERIMA KASIH