Summary DIABETES MELLITUS Williams Obstetrics 25th Chapter 57

o Preterm delivery
DIABETES MELLITUS PREGESTATIONAL DIABETES MELLITUS
Williams Obstetrics 25th  Maternal and perinatal risks: increase
Chapter 57  Prognostically bad signs of pregnancy
o Ketoacidosis
OUTLINE o Pyelonephritis
o Pregnancy induced hypertension
DIABETES MELLITUS ....................................................................... 1
o Poor clinic attendance or neglect
PATHOPHYSIOLOGY...................................................................... 1
PREGESTATIONAL DIABETES MELLITUS ....................................... 1  Vasculopathy
o
PREPREGNANCY CARE ................................................................. 1 Retinopathy
ANTEPARTUM CARE ......................................................................
o 1 Nephropathy
DELIVERY .......................................................................................
o 2 Hypertension
CONTRACEPTION .......................................................................... 2
GESTATIONAL DIABETES ................................................................ 2  Poor glucose control
CONSEQUENCES ........................................................................... 2
SCREENING AND DIAGNOSIS........................................................ 2 PREPREGNANCY CARE
ANTEPARTUM MANAGEMENT ....................................................... 3
SURVEILLANCE OF MATERNAL DIABETES ................................... 3 Objectives
DELIVERY ....................................................................................... 4 1. Assess for maternal vasculopathy by an ophthalmological
POSTPARTUM CARE...................................................................... 4
evaluation, electrocardiogram and 24-hour urine collection
for creatinine clearance and protein excretion.
DIABETES MELLITUS 2. Improve maternal glucose control (target glycosylated
 Complicates approximately 7% of all pregnancies hemoglobin 7% or lower with normal range 6% or lower) to
o T/N: The concept of getting at least 1500 kcal needed reduce the risk of fetal malformations and miscarriage;
dies, pregnant women need 2000 kcal. Basically, the assess for hypoglycemic awareness.
thinner the pregnant woman, the higher kcal allowance in 3. Provide contraceptive counseling
her diet. 4. Educate the patient and her partner about the
management plan for diabetes in pregnancy
Gestational Diabetes Pregestational Diabetes 5. Determine rubella immune status and check thyroid
Mellitus (90%) Mellitus (10%) function studies
 Carbohydrate intolerance  Both type 1 and type 2 6. Begin folic acid supplementation to reduce risk of fetal
 Detected for the first time diabetes mellitus neural tube defects
during gestation  Type 2 Diabetes - most
common form of Detection and Evaluation of Malformations
pregestational diabetes 1. Identification of women at greater risk; maternal
mellitus glycosylated hemoglobin levels in the first trimester
T/N: Caudal regression 2. Noninvasive aneuploidy screening and MSAFP (maternal
syndrome – babies born serum α-fetoprotein)
like a mermaid to a mother 3. Ultrasonography at 13-14 weeks to detect to detect
with diabetes mellitus anencephaly
4. Comprehensive ultrasonography at 18-20 weeks with
PATHOPHYSIOLOGY careful study of cardiac structure, including great vessels
 Maternal hyperglycemia
 Glucose crosses the placenta by facilitated diffusion ANTEPARTUM CARE
 Maternal hyperglycemia produces fetal hyperglycemia Regulation of Maternal Glycemia

First Trimester  Target capillary glucose levels in pregnancy:
Mean level 100 mg/dl
 Maternal hyperglycemia increases the risk for abnormal fetal
organogenesis Before breakfast <95 mg/dl
 Major fetal malformations: 6-10% of pregnancies Before lunch, supper, bedtime <100 mg/dl
complicated by pregestational diabetes 1 hour after meals <140 mg/dl
 Poorly controlled patients: 25% risk for fetal maturation 2 hours after meals <120 mg/dl
2am – 6am >60 mg/dl
Later Gestation  Glycosylated hemoglobin levels in each trimester target is
 Chronic Fetal Hyperglycemia 6% or less
o Fetal hyperinsulinemia
o Excessive fetal growth Insulin Therapy
o Delayed fetal pulmonary maturation  Multiple insulin injections
o Poorly controlled diabetes mellitus o Prandial insulin (Insulin Lispro or Insulin Aspart) with
o Fetal hyperinsulinemia meals, snacks
o Hypoxia and lactic acidosis o Basal insulin (Neutral Protamine Hagedorn [NPH])
o Intrauterine fetal death o Before breakfast (two-thirds of total NPH dose) and at
 Diabetic vasculopathy affect placental function, increases the bedtime (one-third of total NPH dose)
risk for:  If well controlled on insulin Glargine or Detemir, may
o Fetal growth restriction continue these basal insulins
o Preeclampsia

Obstetrics: Diabetes Mellitus • 1 of 4