DIABETES

MELLITUS IN PREGNANCY
Dr. May Nueva-Hipolito, MD, FPOGS
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PANCREAS SECOND TRIMESTER CHANGES
● Endocrine and exocrine organ ● Mild fasting hypoglycemia, postprandial hyperglycemia
● Alpha cells: glucagon and hyperinsulinemia: will facilitate the glucose transfer
● Beta cells: insulin through the placenta, via a carrier-mediated,
● Delta cells: somatostatin stereospecific, non concentrating process of facilitated
● MNEMONIC: “BIAG” (B = insulin, A = glucagon) diffusion (GLUT-1 and GLUT-3).
● Predominance: Beta cells > Alpha cells > Delta cells o In postprandial hyperglycemia, expect the sugar to
increase after eating, and in response to that, the
levels of insulin will increase.
○ “Despite the increase in insulin hindi ganun
kababa ang level ng hypoglycemia after
fasting.”
o GLUT: Glucose transporter
o Facilitated diffusion: transport through the
membrane from higher to lower concentration,
without expenditure of ATP; “kasi sumasabay lang
sa movement ng electrolytes”

Figure 1. Anatomic position of the pancreas and microscopic

From Past Trans (2019)
view of the pancreas. Facilitated diffusion is the process of spontaneous passive transport
of molecules or ions across a cell's membrane via specific
transmembrane integral proteins. Being passive, facilitated
From Lecture: Islets of Langerhans transport does not directly require chemical energy from ATP
hydrolysis in the transport step itself; rather, molecules and ions
• 75% beta cells – insulin
move down their concentration gradient.
• 20% alpha cells – glucagon
• 5% delta cells - somatostatin
● Fetal glucose levels are 80% of maternal values.
GLUCOSE METABOLISM IN PREGNANCY ● Insulin increased secretion and decreased sensitivity
o There is increase in insulin resistance which is why
EARLY PREGNANCY CHANGES they are prone to GDM in pregnancy
● Anabolic phase with increase in maternal fat stores, and ● Increased hepatic glucose production: basal endogenous
decrease in serum free fatty acid concentration, to meet glucose production increases by 16-30% in late
the increasing maternal and fetal demands of late pregnancy with increase in hepatic gluconeogenesis.
gestation and lactation. o “Yung mga na-store mo na before, eto na siya,
o “Nagpeprepare sila for lateral expenditure of narerelease na yung glucose.”
energy” ● Postprandial glucose concentrations are significantly
o “Habang lumalaki si baby, kailangan niya ng mas elevated and the glucose peak is prolonged.
madaming energy” o “So kung sa 1st trimester “ipon, ipon ipon”
● Human chorionic somatomammotropin (hCS) (AKA sa 2nd trimester “gastos, gastos, gastos”.”
Human Placental Lactogen) and cortisol lower glucose
levels and promote fat deposition. The lowering of SUMMARY OF CHANGES IN NORMAL GLUCOSE
glucose levels reaches nadir by the 12th week hence METABOLISM DURING PREGNANCY
fasting levels of 70-80mg/dL are normal. ● Increased insulin secretion
● Postprandial glucose levels are decreased that acts to ● Decreased insulin sensitivity (increase resistance)
protect the developing embryo from elevated blood ● Elevated postprandial glucose levels and prolonged
glucose levels. Hyperglycemia is toxic to the developing glucose peak (In the second trimester)
embryo in the first part of pregnancy! ● Increased hepatic glucose production (also known as
● Hormones associated with pregnancy facilitate maternal gluconeogenesis)
storage of energy in the first trimester, and assist in the ● Increased carbohydrate use (by fetus)
diversion of energy to the fetus in late pregnancy.

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● Accumulation of maternal fat stores in early pregnancy ● Type 2: Ranges from predominantly insulin resistance to
(that is later metabolized) predominantly an insulin secretory defect with insulin
● Enhanced fat mobilization in late pregnancy (thru the resistance (more common)
process of gluconeogenesis) o May problem sa end organ, hindi nagrerespond sa
● There is increase in lipolysis and liberation of free fatty insulin or may problem sa production ng insulin.
acids. ● Other types
o Genetic mutations of β cell function – MODY 1-6
POSSIBLE CAUSES OF INSULIN RESISTANCE DURING LATE (MODY = Maturity onset diabetes of the young)
PREGNANCY o Genetic defects in insulin action
● Increased blood levels of: o Genetic syndromes - eg. Down (Trisomy 21),
o Human Chorionic Somatommamotropin (hCS) Klinefelter (47 XXY), Turner (45, XO)
o Human Placental Growth Hormone (hPGH) o Disease of the exocrine pancreas - eg. Pancreatitis,
o Cortisol cystic fibrosis
o Progesterone ○ “Kapag may problem sa exocrine pancreas,
o Estrogen maaapektuhan din ang insulin; kapag
“All stated above are responsible for increasing the blood namaga ung exocrine pancreas,
glucose levels and increasing insulin resistance in magkakadikit naman sila, wala namang
pregnancy; pregnancy is actually diabetogenic.” firewall, wala naman na hindi magspread
yung inflammation dun sa Langerhan’s
● hCS, produced only by syncytiotrophoblasts, is the most cells, syempre affected din yung endocrine
abundant secretory product of the placenta. It has a part ng pancreas”
strong lipolytic and anti-insulin action, so that: o Endocrinopathies - Cushing syndrome,
o Maternal plasma glucose levels are increased pheochromocytoma (tumor located in the adrenals)
o Plasma free fatty acids are increased (accelerated o Drug or chemical induced - eg glucocorticoids
starvation) (chronic intake of steroids), thiazides (diuretics), β
o Insulin secretion is increased with the resistance to adrenergic agonists
endogenous insulin o Infections - congenital rubella, CMV, coxsackievirus
o Increased circulation of free fatty acids may aid in ● Gestational Diabetes Mellitus
the increase of tissue resistance to insulin Table 1. White Classification of Diabetes Complicating
Pregnancy (Nice to know daw).
● Reduction of maternal insulin receptor sites and glucose
transport, caused by hCS and hPGH, is a suggested
mechanism for the increasing insulin resistance through
pregnancy.
o “Kaya itong mga diabetic patients ay ineencourage
magpapayat, kasi para mag-increase ang
sensitivity/mag-decrease ang insulin resistance
because kapag may increase levels ng fat,
nagiincrease din ang insulin resistance.”

th
From Williams Obstetrics 24 Edition.
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 From Lecture:
(gestational diabetes). Used from 1984-1994 for the management of diabetes in pregnancy
kaya hindi na siya ganun ka popular, actually hindi na siya ginagamit ng
ACOG. Recommendations of ACOG yung finafollow dito sa Philippines.
ETIOLOGIC CLASSIFICATION OF DIABETES MELLITUS

● Type 1: β-Cell destruction, usually absolute insulin
PROPOSED CLASSIFICATION SYSTEM FOR DIABETES IN
deficiency
PREGNANCY (ADA, 2012)
o Immune-mediated
● Gestational Diabetes: diabetes diagnosed during
o Idiopathic – “walang makitang reason kung bakit
pregnancy that is not clearly overt (type 1 or type 2)
nangyari”
diabetes

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 ● Type 1 Diabetes: Diabetes resulting from β-cell RISK FACTORS/ASSOCIATIONS
destruction usually leading to absolute insulin deficiency ● Obesity (increase in fats, so insulin resistance)
o Without vascular complications ● Hypertension (diabetes can cause hypertension)
o With vascular complications (specify which) ● Advanced Maternal age (≤18 y/o and ≥ 35 y/o)
● Type 2 Diabetes: Diabetes from inadequate insulin ● Non-white race (Asians)
secretion in the face of increased insulin resistance ● Family history (Type II diabetes)
o Without vascular complications ● Metabolic syndrome (Triad: Dyslipidemia, hypertension,
o With vascular complications (specify which) and abdominal obesity)
● Other types of diabetes: genetic in origin , associated
with pancreatic disease, drug induced or chemically From Past Trans (2019)
induced With pre GDM or overt diabetes, the embryo, fetus and mother
frequently experience serious complications that are caused
PREGESTATIONAL OVERT DIABETES directly by diabetes.
● Many women with GDM are likely to have type 2 The likelihood of successful outcomes with overt diabetes is
diabetes that has previously gone undiagnosed somewhat related to the degree of glycemic control or if there is
o “Diabetes na na-mask ng pregnancy” a preexisting end organ damage.
● 5 – 10% of women with GDM are found to have diabetes
immediately after pregnancy
● Criteria for Diagnosis of Overt Diabetes during pregnancy
(ADA 2012): From Lecture:
o Fasting plasma glucose of ≥ 126 mg/dL It is important to remember that whenever you encounter a
o Glucosuria certain disease that is coexistent with pregnancy, you always
○ “Sa urinalysis. Kapag sumobra, hindi kaya have to ask what is the effect of the disease in the pregnancy
ma-hold ng glucose threshold, lalabas siya and what is the effect of the pregnancy on the disease. Diabetes
sa urine” and pregnancy interact significantly, with the possible exception
o Ketoacidosis of diabetic retinopathy. The long term course of diabetes is not
○ “May ketone bodies na sa serum and urine” affected by pregnancy.
o Random plasma glucose level >200 mg/dL
o Presence of classic signs and symptoms: polydipsia, FETUS EFFECTS
polyphagia, polyuria and unexplained weight loss; Spontaneous Abortion/Miscarriage
and polyneuropathy ● Only those with HbA1c of >12% and persistently high
o High index of suspicion if with the following: fasting blood sugar of >120 mg/dL are at increased risk
○ Strong family history of diabetes for abortion
○ Previous having delivery of large infants (9 ● Women with pregestational diabetes, poor glycemic
pounds and above) control, defined by glycohemoglobin A1c concentrations
○ Unexplained fetal losses > 7 percent, was associated with a threefold increase in
○ Persistent glucosuria the spontaneous abortion rate

DIAGNOSIS OF OVERT DIABETES IN PREGNANCY Preterm Delivery
Table 2. Diagnostics for Diabetes Based on Glucose Levels. ● Fivefold increase than normal population
Measure of Glycemia Threshold ● Patients with diabetes are prone to infection
Fasting Plasma Glucose At least 7.0 mmol/L (126mg/dL)
Hemoglobin A1C (reflection At least 6.5% Congenital Malformations
of the control of sugar for ● The incidence of major malformations in women with
the past 2 months) type 1 diabetes is approximately 5% (associated with the
Random Plasma Glucose At least 11.1 mmol/L degree of control of diabetes)
(200mg/dL) plus confirmation o HbA1C <8.5% in the first trimester has a congenital
anomaly rate of 3.4% compared with 22.4% if HbA1C

is >8.5%.
PATHOPHYSIOLOGY
o Most common malformations are cardiac defects
● Type I DM
o 20-24 weeks of pregnancy - request for Fetal 2D
o Insulin deficient, secondary to the autoimmune
echo
destruction of the pancreatic islet beta cells
o One proposed mechanism for cardiac defects is that
● Type II DM
of hyperglycemia-induced oxidative stress that
o Continue to produce insulin but there is insulin
inhibits expression of cardiac neural crest migration.
resistance at the level of the end-organ receptor.

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● The risk of an isolated cardiac defect was fourfold higher ● Intrauterine growth restriction (IUGR)
in women with pregestational diabetes compared with o Hyperglycemia is toxic to the blood vessels à
the twofold increased risk of noncardiac defects. decreased caliber of blood vessels à decreased
nutrients going to the baby
Table 3. Congenital Anomalies in Fetuses of 91 Women with ● In GDM, the most common altered fetal growth is
Type I Diabetes between 1999 and 2004 in Norway. macrosomia, while in overt DM it is either macrosomia or
Organ System Babies affected (%) IUGR because the baby does not have a good vascular
Cardiovascular 52 supply
Musculoskeletal 12
Urogenital 9
CNS 4
Gastrointestinal 2
Chromosomal 3
Others 10
Multiorgan 8


Figure 5. Macrosomic babies.

Unexplained Fetal Demise
● “Reflection kung gaano kapanget yung uncontrolled
glucose level ng mother”
● 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

● Stillbirth without an identifiable cause is a phenomenon
relatively limited to pregnancies complicated by overt
diabetes.
● LGA, die before labor usually after 35 weeks AOG
● Hyperglycemia-mediated chronic aberrations in transport
of oxygen and fetal metabolites may account for
unexplained fetal deaths.
● Maternal hyperglycemia causes osmotically induced
villous edema led to impaired fetal oxygen transport

Figures 2-4. Upper left – atrial septal defect, upper right -
Hydramnios
spina bifida, bottom – anencephaly.
● Hydramnios is associated with diabetes is a result of
increased amniotic fluid glucose concentration.
● Hydramnios : Amniotic Fluid Index (AFI) > 24 cm; SDP > 8
From Past Trans (2019)
cm
With cardiac malformations topping the list of congenital
● Fetal hyperglycemia causes polyuria
anomalies associated with preGDM, fetal echocardiography
● Increased amniotic fluid glucose concentration
should be performed around the time when the CAS is also
● Normal AFI: 5-24
performed.
● Baby is hyperglycemic à hyperinsulinemic à spillage of
glucose to the kidney tubules à reached glucose
Altered Fetal Growth threshold à polyuria à hydramnios
● Diminished growth - congenital malformations or
advanced maternal cardiovascular disease (long standing NEONATAL EFFECTS
diabetes)
Respiratory Distress Syndrome
● Incidence of macrosomia rises significantly when mean
maternal blood glucose concentrations exceed 130 ● Insulin antagonizes cortisol-induced lecithin synthesis
mg/dL ● Decreased surfactant production by insulin
o Fetal macrosomia is secondary to fetal ● Deliver the baby as close to term as possible to prevent
hyperinsulinemia this
o Excessive somatic growth except the brain

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 ● Increased risk with duration of diabetes may be related
Hypoglycemia to oxidative stress, which plays a key role in the
● < 45 mg/dl pathogenesis of diabetic complications and preeclampsia
● Newborns of a diabetic mother experience a rapid drop
in plasma glucose concentration after delivery. Diabetic Nephropathy
● Attributed to hyperplasia of fetal β-islet cells induced by ● Pathophysiology
chronic maternal hyperglycemia. o Hyperglycemia → excessive deposition of glycogen
● Prompt recognition and treatment of the hypoglycemic to the glomerular basement membrane → BM
newborn minimizes adverse sequelae thickening → diabetic glomerulosclerosis and
papillary necrosis → albuminuria → progressive
Hypocalcemia renal destruction/deterioration → end stage renal
● Total serum Ca concentration <8 mg/dL in term disease and failure
newborns o Note: Diabetes is the leading cause of end stage
● Hypocalcemia is one of the potential metabolic renal disease!
derangements in neonates of diabetic mothers ● Clinical course
● Due to aberrations in magnesium-calcium economy, o 5 years from onset of DM → microalbuminuria (30-
asphyxia and preterm birth 300 mg/24 hours)
o 5-10 years later → overt proteinuria (>300mg/24
Hyperbilirubinemia and Polycythemia hours) with or without hypertension among those
● Fetal response to hypoxia brought about by destined to have end stage renal disease.
hyperglycemia mediated increases in maternal affinity o 10-15 years later → renal failure (indication for
for oxygen and fetal oxygen consumption. Together with dialysis)
insulin-like growth factors, this hypoxia leads to ● Microalbuminuria in early pregnancy is a very sensitive
increased fetal erythropoietin levels and red cell predictor of possible onset of preeclampsia
production.

Cardiomyopathy
● Hypertrophic cardiomyopathy that primarily affects the
interventricular septum
● 3rd trimester, the fetal interventricular septum and right
ventricular wall were thicker in fetuses of diabetic
mothers
● Request Fetal 2D echo

Long Term Cognitive Development
● IQ lower 1 to 2 points

● Autism spectrum disorders or developmental delay were
Diabetic Retinopathy
common
● “Destruction of the retina due to the sugar”

● Retinal vasculopathy is highly specific complication of
INHERITANCE OF DIABETES
both type 1 and type 2 diabetes.
● Type 1 diabetes if either parent is affected is 3 to 4 %
● Its prevalence is related to duration of diabetes (refer to
● Both parents have type 2 diabetes the risk is 40%
an ophthalmologist to note for retinopathy)
● Higher chances if father is diabetic
● Clinical course
● Breastfeeding has been associated with a reduced risk of
o Hyperglycemia induce microvascular disease →
type 2 diabetes
microaneurysm → RBC extravasation → blot

hemorrhages → leaked serous fluid will form hard
MATERNAL EFFECTS exudates (Non proliferative Retinopathy) →
Preeclampsia progressive occlusion of retinal vessels → retinal
● Hypertension with concomitant proteinuria ischemia and infarction with development of cotton
● Hypertension that is induced or exacerbated by wool exudates (Preproliferative retinopathy) →
pregnancy is the complication that most often forces compensatory neovascularization in the retinal
preterm delivery in diabetic women. surface and vitreous space (Proliferative
● Developed 3 – 4x more often in women with overt Retinopathy) → fibrous tissue formation and
diabetes retraction→ tractional retinal detachment with or
● Diabetics with chronic hypertension were almost 12x without macular edema and retinal/vitreous
likely to develop preeclampsia hemorrhages→visual impairment and blindness

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PRECONCEPTIONAL CARE
ü Weight loss
ü Exercise
ü Glucose testing
ü Treatment of hyperglycemia as appropriate
ü Strict glucose control
ü Nutritional counseling (30-35 kcal/kg/day if normal
Diabetic Neuropathy weight)
● Usually develops after 10-15 years from onset of DM ü Institute glucose testing to include fasting and 2 hr
● Peripheral and symmetrical sensorimotor diabetic postprandial values
neuropathy is uncommon in pregnancy ü Incorporate exercise regimen
ü Start or refine insulin regimen
Diabetic Ketoacidosis
● Results from an insulin deficiency combined with an ● First trimester
excess in counter-regulatory hormones such as glucagon. o Careful monitoring of glucose is essential
o Hospitalization may be necessary to individualize
Diabetic Gastropathy glucose control and education, opportunity to assess
● Diabetic gastropathy, is troublesome during pregnancy. It extent of diabetic vascular complications and
causes nausea and vomiting, nutritional problems, and precisely establish gestational age.
difficulty with glucose control. ○ Organogenesis is at 8 weeks; to avoid any
● Women with gastroparesis should be advised that this teratogenic effects on the baby
complication is associated with a high risk of morbidity o INSULIN TREATMENT
and poor perinatal outcome ○ OHA (Oral Hypoglycemic Agent) not
● Treatment with metoclopramide or H2-receptor recommended for overt diabetes except for
antagonists limited and individualized use. (hindi
kinakaya ng OHA icontrol ang sugar during
Infections pregnancy kasi nag- iincrease yung insulin
● Common infection includes candida vulvovaginitis, UTI, requirement kasi naka insulin na siya so
respiratory infection, puerperal pelvic infections nag-iincrease pa lalo yung insulin
● Almost all types of infection are increased in diabetic requirement as the pregnancy progresses)
pregnancies ○ Glycemic control
● Twofold increased risk of asymptomatic bacteriuria in • multiple daily injections
women with diabetes. • adjustment of dietary intake
● Pregestational diabetes is associated with a two- to • self monitoring of capillary glucose
threefold increase in wound complications after cesarean levels using a glucometer
delivery.

MANAGEMENT OF DIABETES IN PREGNANCY
th
● Preconceptional Care (control prior to pregnancy) FROM Williams Obstetrics 24 Edition.
o to minimize early pregnancy loss and congenital Insulin Management During Labor and Delivery
o Usual dose of intermediate-acting insulin is given at
malformations
bedtime
● ADA optimal preconceptional glucose control using o Morning dose is withheld
insulin o Intravenous infusion of normal saline is begun
o Preprandial 70–100 mg/ dl o Once active labor begins or glucose levels decrease to
o Peak postprandial values – 100-129 mg/dl <70 mg/dL, the infusion is changed from saline to 5%
● Preconceptional Care dextrose and delivered at a rate of 100-150mL/hr (2.5
o Mean daily glucose concentration: <110 mg/ dl mg/kg/min) to achieve a glucose level of approximately
o Glycosylated hemoglobin: <7 % (4 fold increase in 100 mg/dL
malformation HbA1c >10 %) o Glucose levels checked hourly using bedside meter
allowing for adjustment in the insulin or glucose
o Treatment for retinopathy (request for fundoscopy)
infusion rate
and nephropathy (request for renal function tests, o Regular (short-acting) insulin is administered by
24-hr urine collections) should be instituted intravenous infusion at a rate of 1.12 U/hr if glucose
o Folate: 400 mcg/day levels exceed 100mg/dL

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 Table 4. Self-monitored capillary blood glucose goals. o Labor induction: when fetus is not excessively large
Specimen Level (mg/dL) and cervix is favorable
o Cesarean Delivery: avoids traumatic birth of a large
Fasting ≤ 95
infant
Premeal ≤100 o Increased cesarean delivery rate
1-hr postprandial ≤140 o Insulin: reducing or withholding the dose of long
2-hr postprandial ≤120 acting insulin given on the day of delivery is
0200 - 0600 ≥ 60 recommended - Insulin requirements typically drop
after delivery
Mean 100
o Laboring diabetic woman should be adequately
Hemoglobin A1 c ≤ 6% hydrated given glucose in sufficient amounts to
maintain normoglycemia
o DIET o CBGs checked frequently especially during active
○ Appropriate weight gain through labor
carbohydrate and caloric modifications ● Puerperium
based on height, weight and degree of o Women may not require insulin for 1st 24 hours or
glucose intolerance so postpartum
○ 175-g = minimum CHO per day o Infection should be detected and treated
○ CHO distributed: 3 small to moderate sized o Contraception - women should be advise to get
meals and 2 to 4 snacks pregnant to minimum of 2 years after delivery and
○ Weight loss is not recommended maximum of 5 years to minimize the complications
○ 55% CHO, 20% CHON, 25 % fats (< 10%
saturated fats) GESTATIONAL DIABETES MELLITUS
o HYPOGLYCEMIA ● Carbohydrate intolerance of variable severity with onset
○ Diabetes tends to be unstable in the first or first recognition during pregnancy.
trimester ● This definition applies regardless of whether or not
○ Average duration of hypoglycemia is 2 insulin is used for treatment
hours ● Gestational Diabetes - need for increased surveillance
○ Peak is 10 – 15 weeks AOG and further testing postpartum
● Second Trimester ● Fetal anomalies are not increased compared to patients
o Serum alpha-fetoprotein 16 – 20 weeks with pre-GDM
o Targeted sonographic examination 18-20 weeks ● Most perinatal concern in women with GDM is
(congenital anomaly scan, better at 20-22 weeks) excessive fetal growth
o Fetal echocardiography (to check for cardio ● The likelihood of fetal death with appropriately treated
congenital anomaly in the baby) gestational diabetes mellitus is not different from that of
o Goal: euglycemia through self monitoring the general population
o Increased insulin requirement due to increase in ● 50% of women diagnosed with GDM will likely develop
insulin resistance overt DM in the ensuing 20 years
● Long range complications: obesity and diabetes in the
From Past Trans (2019) offspring
Detection of fetal anomalies in obese diabetic women is more
difficult than in similarly sized women without diabetes. SCREENING FOR GDM
GDM Risk assessment: should be ascertained at the first
● Third Trimester and Delivery prenatal visit
o Fetal surveillance
○ Fetal movement counting (10 movements Low Risk
in 2 hours ; monitor at 7 months; Blood glucose testing NOT routinely required if all the
quickening at 18-20 months) following are present:
○ periodic fetal heart rate monitoring • Member of ethnic group with a low prevalence of
○ intermittent biophysical profile evaluation GDM
○ CST • No known diabetes in first-degree relatives
o initiate fetal testing at 32 to 34 weeks (ACOG,2012) • Age < 25 years
o Usually seen every 2 weeks • Wight normal before pregnancy
o 34 weeks admission is offered in insulin treated • Weight normal at birth
women • No history of abnormal glucose metabolism
o Delivery planned at 38 weeks • No history of poor obstetrical outcome

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Average Risk ● Increased body weight and calorie intake also contribute
Perform blood glucose testing at 24-28 weeks using either: to insulin resistance.
• Two-step procedure: 50g oral glucose challenge test
(GCT), followed by a diagnostic 100g OGTT for those MATERNAL AND FETAL EFFECTS
meeting the threshold value in the GCT ● Rates of fetal anomalies do not appear to be
• One step procedure: diagnostic 100g OGTT substantially increased
performed on all subjects ● BUT if the fasting blood glucose is elevated (>105mg/dl)
“All Filipinos are average risk kaya laging nagpapatest” then the unexplained fetal deaths is similar to women
with overt diabetes. Usually during the final 4 to 8 weeks
High Risk ● Fetal macrosomia: Birth Weight of ≥ 4500 grams. (prone
Perform blood glucose testing as soon as feasible, using the to shoulder dystocia)
procedures described above, if one or more of these are ● Mother prone to have hypertensive disorders and
present: increased in operative delivery and birth injury.
• Severe obesity
• Strong family history of type 2 diabetes Fetal Macrosomia
• Previous history of GDM, implaired glucose ● Primary effect attributed to gestational diabetes is
metabolism, or glucosuria excessive fetal size or macrosomia
• If GDM is not diagnosed, blood glucose testing ● Maternal hyperglycemia prompts fetal hyperinsulinemia,
should be repeated at 24-28 weeks gestation or at particularly during the second half of pregnancy. This in
any time symptoms or signs suggest hyperglycemia. turn stimulates excessive somatic growth.

DIAGNOSIS FOR GDM Neonatal Hypoglycemia
● Two step procedure ● Neonatal hyperinsulinemia may provoke hypoglycemia
● Screening: 50 g oral glucose challenge test (OGCT) value within minutes of birth.
of ≥135 or 140 mg/dL (No fasting needed) ACOG 2013 ● Newborns had an incidence of clinical neonatal
● Confirmatory: Request for 100 g oral glucose tolerance hypoglycemia that increased with increasing maternal
test (OGTT) to confirm GDM. OGTT values
o Fasting of at least 8 hours but not more than 14
hours and after at least 3 days of unrestricted diet Maternal Obesity
and physical activity ● Maternal BMI is an independent and more substantial
o The patient should be seated and not smoking risk factor for fetal macrosomia than is glucose
during extraction intolerance
o OGTT is not requested for admitted patients because ● Higher BMI levels were associated with increasing
of restricted diet. It is requested only for OPD birthweight, regardless of glucose levels.
patients
● 100g OGTT MANAGEMENT OF GDM
o 2 or more of the venous plasma concentrations Diet
indicated below must met or exceeded for a positive
● American diabetic association (ADA) stated that the diet
diagnosis.
should consists of approximately 30 kcal/kg/day for the
○ Fasting: 95mg/dL
average patient.
○ 1 hour post prandial: 180 mg/dL
● ±5 kcal/kg/day for underweight and overweight women.
○ 2 hour post prandial: 155 mg/dL
For underweight: 35 kcal/kg/day; for overweight: 25
○ 3 hour post prandial: 140 mg/dL
kcal/kg/day
o If only one parameter is met or is exceeded, it is
● Calories should be divided between three meals and
diagnosed as impaired glucose tolerance
three snacks: 40 % carbohydrate, 20% protein and 40 %
● 75 OGTT
unsaturated fat.
o Fasting: 92 mg/dL
● Low glycemic index can decrease the need for insulin for
o 1 hour post prandial: 180 mg/dL
glycemic control in women with GDM.
o 2 hour post prandial: 153 mg/dL
● Insulin therapy is usually recommended when standard
o 2 or more of these values must ≥ for the diagnosis of
dietary management does not consistently maintain the
GDM
fasting plasma glucose at <95 mg/dL, 1-hour postprandial

plasma glucose <140 mg/dL or 2-hour postprandial
PATHOPHYSIOLOGY
plasma glucose <120 mg/dL.
● Insulin resistance caused by circulating hormonal factors:
increased maternal and placental production of hCS,
progesterone, growth hormone, cortisol and prolactin.

8

Exercise Intrapartum Management
● Appropriate exercises are those that use the upper-body ● Induction of labor
muscles (isometric exercises). This may result in lower o Diet controlled: at 41 weeks
glucose levels and reduce the likelihood of insulin o Medication controlled: by EDC (40 weeks)
therapy. ● Cesarean section if EFW >4500 grams
● Three times a week for 20 to 45 minutes. ● Frequent glucose assessment
o Every 1 hr if required medication
Glucose monitoring o Every 4 hr if diet controlled
● With a glucometer, fasting and 2-hour postprandial ● Target blood sugars 70-110 mg/dL
glucose levels should be followed daily. ● IV insulin therapy if blood sugars greater than target
● Compared to preprandial monitoring, postprandial blood sugars or with ketonuria
monitoring is associated with improvement in o IV saline infusion at 125 cc/hr unless ketonuric, then
glycosylated hemoglobin, less cesarean delivery for add 5% dextrose solution at rate to keep blood sugar
dystocia, smaller birthweights and less neonatal in target range.
hypoglycemia.
● Out patient glucose targets for GDM: Postpartum Management
o Preprandial glucose concentration of ≤ 95 mg/dL ● 75 grams OGTT at 6 to 12 weeks postpartum
o 1 hour postmeal glucose value of ≤ 140 mg/dL ● 75g OGTT for 3 years in women with history of GDM but
o 2 hour postmeal glucose value of ≤ 120 mg/dL with normal postpartum glucose screening
● “Fasting capillary glucose predicted neonatal ● Recommendations for postpartum follow up are based
complications and postprandial glucose predicted on the 50% likelihood of women with GDM developing
preeclampsia and LGA infants” overt diabetes within 20 years.
● Women with a history of GDM are also at risk for CVS
Insulin complications associated with dyslipidemia,
● Human regular insulin or rapid acting insulin analogues hypertension, abdominal obesity - Metabolic syndrome
are the preferred treatment for postprandial
hyperglycemia in pregnant women.
● The initial insulin dose for pregnancy is based on
maternal weight and can be calculated by the following
guidelines to determine total daily insulin needs:
o 0.7-0.8 U/kg actual body weight in the 1st trimester
o 1.0 U/kg actual body weight in the 2nd trimester
o 1.2 U/kg actual body weight in the 3rd trimester

Oral Hypoglycemic agent
● Glyburide

● Metformin
● “ACOG 2013 acknowledges that both oral hypoglycemic Classification of the ADA 2013
agents are appropriate, as is insulin for first line glycemic

control in women with GDM”
Normal Impaired fasting Diabetes
Obstetrical Management
glucose/glucose Mellitus
● No consensus regarding the value of timing of
tolerance
antepartum fetal testing, it is typically reserved for
women with pre GDM because of ↑ stillbirth rate. Fasting < 100 mg/dL 100-125 mg/dL ≥ 126 mg/dL
● INSULIN treated women offered inpatient administration 2 hour < 140 mg/dl ≥ 140-199mg/dL ≥ 200 mg/dL
after 34 weeks’ gestation and fetal heart rate monitoring Hemoglobin <5.7 % 5.7-6.4% ≥ 6.5%
3x a week. A1C
● According to ACOG:
o No evidence based recommendation can be made Contraception
regarding delivery timing in women with GDM ● Barrier Methods
o Cesarean delivery should be considered in women o Include condoms, diaphragm, cervical cap and
with GDM whose fetuses have a sonographically spermicides, are well suited for women with prior
estimated fetal weight ≥ 4,500grams. GDM because of their lack of systemic side effects or
influence on glucose tolerance.
● Intrauterine Device
o Prone to infection
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 o Very effective and reversible contraceptive method • Antenatal assessments with NST or BPP weekly from
without metabolic disturbances and therefore is an 32 to 36 weeks, then twice weekly until delivery.
ideal contraceptive women. Start earlier if diabetes is poorly controlled.
o WHO Medical Eligibility Criteria for Contraceptive
use report does not consider prior GDM as a INTRAPARTUM MANAGEMENT
contraindication to IUD prescription. • Trial of labor unless clinical or ultrasound EFW >
● Combination Oral Contraceptives 4500 grams
o Low dose COC can be prescribed taking into account • Delivery at 39 weeks or prior to 39 weeks if
that the absolute risks increase with age. pulmonary maturity documented by amniocentesis.
o “Bawal if magbreastfeed” • IV insulin therapy to maintain blood sugar between
● Progestin-only oral contraceptives 70-110 mg/dL
o Contain low dose norethindrone, levonorgestrel or • IV dextrose solution if blood sugars fall < 70 mg/dL
desogestrel or development of ketonuria.
o They are well-suited for those with type 1 DM where • For scheduled CS, administer the dose of long acting
estrogen-containing methods are contraindicated insulin PM and withhold the AM short acting dose.
and for women with prior GDM who often have • Monitor blood glucose hourly
several cardiovascular risk factors
● Long acting Progestins POSTPARTUM MANAGEMENT
o Use is still limited • Reduce the antepartum insulin dose by half and
● Sterilization administer it with the resumption of oral intake
o Operative sterilization is an excellent choice for
• Supplement breastfeeding mothers with extra 500
women who are no longer desirous of subsequent kcal compared to nonpregnant levels
child bearing
• Postpartum evaluation

• Contraception
SUMMARY
• Breastfeeding
PRECONCEPTIONAL CARE
• Weight loss REFERENCES
• Exercise 1. Lecture recordings
• Glucose testing 2. PPT
• Treatment of hyperglycemia as appropriate 3. William’s Obstetrics 24th Edition
• Strict glucose control 4. 2019 trans
TRANSCRIBERS
PRENATAL CARE 1. TRANS GROUP: 19A
• DIET 2. SUBTRANSHEAD: Daniela Marquez
o 55% carbs, 20% protein, 25% fat with less
than 10% as saturated fat Just 8 more weeks til sem break and 8 more months until
• GLUCOSE CONTROL your very first white coat. You got this, doc! Konti nalang! J
o Fasting: ≤ 95 mg/dL #RoadtoClerkship #LABAN2020
o Premeal: ≤ 100 mg/dL
o 1hr postprandial: ≤ 140 mg/dL
o 2hr postprandial: ≤120 mg/dL
o 0200-0600: ≥ 60mg/dL
o Mean (average): 100 mg/dL
o HbA1C: ≤ 6 %

ANTEPARTUM MANAGEMENT
• Insulin therapy adjusted by weight and pregnancy
trimester as guided by glucose monitoring.
• Viability/dating scan
• Fetal surveillance and antepartum testing
• Alpha-fetoprotein screening at 16 to 20 weeks
• Detailed anatomic survey at 18-20 weeks
• Fetal echocardiogram at 20-22 weeks
• Serial ultrasounds for growth in the second and third
trimester.

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 PAST E (2019) cms, 50% effaced, head at station 0, with intact bag of waters.
1. A 35 – year- old primigravid consulted you for her first What should be included in the intrapartum management of this
prenatal visit. She was diagnosed with Type 2 Diabetes patient?
Mellitus 2 years ago and was maintained on Metformin for A. Frequent glucose assessment: every 4 hours
blood sugar control. After delivery her newborn will be at B. May use oxytocin in augmenting the labor as long as
risk for having: the baseline CTG of the patient is category I
A. High total serum calcium C. May opt to do outright cesarean section
B. High glucose concentrations D. All of the above
C. Hypotrophic cardiomyopathy
D. High bilirubin load 8. Who among these gravid patients can use metformin to
achieve good glycemic control?
2. The best time to perform screening of Gestational Diabetes A. FBS = 7.2 mmol/L
Mellitus B. RBS = 13.9 mmol/ L
A. 20 – 24 weeks C. 100g OGTT result = FBS : 5.4 mmol/L , 1st hour : 10.3
B. 24 – 28 weeks mmol/L, 2nd hour: 8.9 mmol/L; 3rd hr: 8.1 mmol/L
C. 28 – 32 weeks D. All of the above
D. Anytime during pregnancy
9. The incidence of stillbirth is highest in pregnancies
3. A 27 year old G1P0 24 weeks AOG by amenorrhea had her complicated by which of the following?
first consult with Dr. Idea. Her father is a known diabetic. What A. Overt diabetes
examination should Dr. Idea request for to know if the patient B. Gestational diabetes
has diabetes mellitus? C. Overt diabetes and hypertension
A. 50g OGCT D. Gestational diabetes and hypertension
B. Hba1c
C. FBS 10. Insulin maintain the fasting plasma glucose at ≤ ___mg/dl or
D. 100g OGTT the 2 hours post prandial plasma glucose ≤ _____ mg/dl therapy
is usually recommended when standard dietary management
4. 100 g OGTT prerequisites does not consistently
A. Overnight fast for 4 to 18 hours A. 90, 140
B. After 3 days at least of unrestricted physical activity B. 90, 120
C. Unrestricted diet ≥ 120 g/d of at least 3 days C. 95, 140
D. May be seated or standing up but should not smoke D. 95, 120

5. According to O’Sullivan, there is a need to evaluate GDM 11. Mrs Concepcion’s pregnancy was complicated with
patients postpartum based on the 50% likelihood of women Gestational Diabetes Mellitus and required insulin to achieve
with gestational diabetes developing overt diabetes within the good glycemic control. She is currently on her 6th week
ensuing postpartum. Which of the following is true regarding
A. 10 years postpartum management of patients with GDM?
B. 15 years A. Request for 75 g OGTT 6 – 8 weeks postpartum for
C. 20 years classification of glucose metabolism post delivery
D. 25 years B. Advise breastfeeding because it can help patients
achieve better glycemic control
6. The most important perinatal concern in gestational diabetes C. Intrauterine device should not be offered to
mellitus postpartum GDM patients
A. Increase in the incidence of fetal anomalies D. All of the above
B. Greater risk of fetal death
C. Excessive fetal growth 12. Which is true regarding fetal demise in patients with type I
D. All of the above DM?
A. Hypoglycemia-mediated chronic aberrations in
7. A 33 – year – old G2P1 (1001) 40 weeks AOG based on early transport of oxygen and fetal metabolites may account
ultrasound consulted at the emergency room for labor pains. for unexplained fetal deaths. Fetuses have elevated
She was diagnosed with gestational diabetes mellitus at 26 lactic acid levels
weeks AOG and was started on Insulin at 29 weeks AOG. Her B. It is unexplained because common factors such as
recent biometry done at 39 weeks AOG revealed that the abruption, obvious placental insufficiency, fetal growth
sonographic estimated fetal weight was 4,500 grams. She was restriction or oligohydramnios are not identified.
received at the ER by Dr. Nazareno who did an internal C. These infants are typically appropriate for gestational
examination which showed a cervix that was dilated to 5 to 6 age and die before labor, usually after 35 weeks AOG

11
 D. All of the above should be done. Which of the following statements is true
regarding detection of fetal anomalies?
13. The incidence of major malformations in women with type I A. The accuracy of sonographic fetal anatomical
diabetes mellitus is approximately evaluation is not diminished by concurrent maternal
A. 3% obesity
B. 5% B. Maternal serum alpha fetoprotein determination
C. 8% should be completed early between 12 and 16 weeks in
D. 10% mothers with overt diabetes
C. Sonographic anatomical evaluation is best performed
14. Who among the following patients is considered high risk for at 18 – 20 weeks’ gestation
GDM? D. None of the above
A. 29 yo, G2P1 (1001), 15 weeks AOG with 1 elevated
value in her 75 g OGTT done in her previous pregnancy 19. Summary of changes in normal glucose metabolism in
B. 31 y/o, G2P0, 20 weeks AOG with 1 spontaneous pregnancy
abortion at 11 weeks A. Enhanced fat metabolism in late pregnancy
C. 33 y/o, G2P1 (1001) 28 weeks AOG with 1 elevated B. Increased insulin sensitivity
value in her 100 g OGTT in her previous pregnancy C. Decreased insulin secretion
D. 26 y/o, G2P1 (1000), first baby died of measles at 2 D. Elevated postprandial glucose levels and shortened
months 2 glucose peak

15. Which nutrition therapy? is true regarding glucose 20. The genetic syndromes associated with Diabetes Mellitus
monitoring in patients with gestational diabetes mellitus on A. 45,XO
medical B. Trisomy 13
A. Women using daily blood-glucose self- monitoring C. Trisomy 18
had significantly lower macrosomic infants and gained D. Cushing Syndrome
less weight after diagnosis
B. Preprandial surveillance for gestational diabetes has ANSWERS: DBDBC-CCCCD-BBBAA-DACAA
been shown to be superior to postprandial surveillance
C. ACOG recommends 5 times daily glucose monitoring
performed fasting, either 1 or 2 hours after each meal
and at bedtime.
D. All of the above

16. Patient MNH, 31 years old G1P0 26 weeks AOG consulted Dr
Vidanes for her first prenatal check-up. She is asymptomatic
with normal vital signs and good fetal heart tones. She has no
medical co morbidities, no known allergies. Her father is a
known diabetic. 100 g OGTT revealed the following results:
results. FBS 7.22 mmol/L; 1st hour 10.3 mmol/L; 2nd hr 8.3
mmol/L ; 3rd hr 7.2 mmol/L. Interpret the results.
A. Normal
B. Impaired Fasting Glucose
C. Gestational Diabetes Mellitus
D. Overt Diabetes

17. What might be said about a pregnancy complicated with
overt diabetes that has a baby with a sonographic estimated
fetal weight of 5000 grams at 38 weeks?
A. This increases the mother’s risk for shoulder dystocia
B. The baby is at risk for neonatal hypercalcemia
C. The mother probably had an excellent glycemic
control
D. All of the above

18. Patient MNH was diagnosed with Type 2 Diabetes Mellitus 3
years ago. She is currently pregnant and was told by Dr. Vidanes
that her baby is at risk of having fetal anomalies so screening

12