DIABETES IN PREGNANCY
Peggy Foster, RN, MSN
April, 2008
Incidence of Diabetes 18.2 million people—6.3% of Population—Up from
16 million in 1995 and Increasing in Younger people
Prevalence-- Higher in American Indians and Non-Hispanic Blacks
Diabetes in Pregnancy--CHO intolerance onset in Pg
Affects about 4 % of all pregnant women 1-14 % of pregnancies risk fetal macrosomia and risk future diabetes When GDM adequately treated Perinatal mortality
rate equivalent to that observed in normal pregnancies
Type I Diabetes Results from the body’s failure to
produce insulin Occurs more commonly in < 30 y/o
Type II Diabetes Results from Insulin resistance—body
fails to properly use insulin Occurs more commonly in > 30 y/o
PRE-DIABETES
Condition that occurs when blood glucose levels are >normal, but not high enough for the Dx of Type II Diabetes
SYMPTOMS OF DIABETES Frequent urination Excessive thirst Extreme hunger Unusual weight loss Increased fatigue Irritability Blurry vision
DIAGNOSIS OF DIABETES
FBS Normal Levels < 100 mg/dL Pre-Diabetes levels 100-125 mg/dL Diabetes 126 mg/dL or > OGTT—Oral Glucose Tolerance Test Normal Levels < 140 mg/dL Pre-Diabetes 140 – 200 mg/dL Diabetes 200 mg/dL or >
DIAGNOSIS (cont’d) Hgb A1C-- Glycated (Glycosylated)
hemoglobin Normal levels < 6 How works—Hgb (protein) binds with
glucose blood glucose binds (glycates) with Hgb
molecules--glucose-- glycation— A1C Since RBC’s (Hgb) live 2-3 months—the
A1C reflects glucose over the lifespan of RBC
Blood Sugar affected by:
Stress-- Exercise-- Infections-- Diet—Carbohydrates
Fat
Protein
COMPLICATIONS OF DIABETES
Heart Disease and Stroke ↑Cholesterol Kidney Disease Eye Neuropathy Foot Problems Skin
CARBOHYDRATE COUNTING Calories from CHO, Protein and Fat CHO—biggest effect on Blood Sugar--
Within 2 hours after eating CHO, most changed to Blood Sugar—Protein and Fat much less effect
BASAL-BOLUS INSULIN THERAPY
Basal Insulin—keeps some Insulin in body system at all times—Long Acting Insulin (i.e. NPH or Glargine)
Boluses given with meals and snacks to cover Blood sugar peak times—Rapid Acting Insulin (i.e. Regular, Aspart, Lispro, Glulisine)
BASAL-BOLUS INSULIN
Long acting given in a.m. and p.m. Rapid Acting (or in combination with
Mid-acting) given just before meals/snacks/bedtime
Blood sugar checked 2 hours PP
MATERNAL COMPLICATIONS IF UNTREATED
Preterm Labor Preeclampsia Operative Delivery Type II Diabetes
FETAL OUTCOMES IF Untreated Abortions Congenital Malformations-- Cardiovascular (Transposition or Great
vessels, ASD, VSD, Hypoplastic Left Heart)-- CNS (Anencephaly, Myelomeningocele,
Holoprosencephaly, Microcephaly)-- Skeletal (Caudal regression syndrome, Spina bifida)-- Genito-urinary (Potter’s, Polycystic kidneys,
Double ureter)-- Gastrointestinal (TEF, Bowel atresia, Imperforate anus) Stillbirths
PATHOPHYSIOLOGY—NORMAL PREGNANCY First Trimester
In early Pg-- estrogen and progesterone affect Beta cell hyperplasia and insulin secretion
Glycogen deposits in peripheral tissues and hepatic glucose production
By end of 1st Trimester-- 10% in maternal glucose levels
Insulin dependent women therefore, normally experience periods of hypoglycemia in 1st Trimester
PATHOPHYSIOLOGY 2nd and 3rd Trimester—Diabetogenic State of Normal Pregnancy
In pregnancy there is a cellular sensitivity to insulin
As placenta grows/pregnancy advances is an Human placental lactogen, Progesterone, Cortisol, Prolactin– All are contra-insulin--Blood Sugar levels
Homeostasis requires insulin release During time when there is an maternal
glucose-- glucose supply to fetus and placenta
A woman with Insulin-dependent Diabetes cannot respond to this stress—requires insulin therapy as pregnancy advances
Pathophysiology cont’d
The’d insulin requirement (~ 30%) over pre-pregnancy is ~ equivalent to the endogenous increase in normal gestation
FETAL RESPONSE
Normal Fetal response to blood glucose levels is to secrete levels of Insulin
If glucose levels remain high, fetus then gains weight resulting in Macrosomia
Complications of FETAL MACROSOMIA
Intrapartum
• Protracted labor
• Shoulder Dystocia-- Shoulder:Hip Ratio
• Perinatal Asphyxia
• Skeletal Injuries
• risk of C/S
PP Complications—Fetal Macrosomia Mother in PP Hemorrhage Infant—Neonatal
• Hypoglycemia-usually about 3-4 hours of age
• Polycythemia • Hyperbilirubinemia • Thrombocytopenia • Hypomagnesemia
Long Term risk for childhood cancer (i.e. acute lymphocytic leukemia,
Wilms tumor) risk of adolescent obesity risk of developing Type II Diabetes at a young age
GESTATIONAL DIABETES
Who should be screened for GDM?? And What tests should be used ?
Treatment goals: Entire Team Care—Woman-Family-MD-RN-RD-SW
GDM Screening
Low risk—Screening not Required IF:
-- < 25 years
-- If low risk race or ethnic group
-- Normal pre-pregnancy weight and
weight gain during pregnancy
-- No history of abnormal blood glucose
-- No prior poor OB history
GDM Screening (cont’d) High risk—Screen ASAP and @ 24-28 weeks
gestation --Overweight/Obese --Hx of Glucose Intolerance -- Family Hx of Diabetes--1° Relative -- Black, Latino, Native American, Asian, Pacific Islander, or Indigenous Australian -- Current glycosuria
Target Glucose Levels to Minimize Macrosomia
Fasting ≤ 95 mg/dl 1 hour Post Prandial ≤ 140 mg/dl 2 hour Post Prandial ≤ 120 mg/dl Pre Prandial 60-100 mg/dl
Total Calories in the Euglycemic Diet 40 % CHO 40% Fat and 20% Protein PERCENT OF IDEAL
BODY WEIGHT 80- 120 %
121-150 %
> 151 %
TOTAL
CALORIES 30 Calories/Kg
Present Pg Weight 24 Calories/Kg PPW
12-15 Calories/Kg PPW
DIABETIC MEDICATIONS
Insulin—Acts to glucose into cellsTypes: Regular, Semilente, Lispro, Aspart, NPH, Lente, Glargine, PZI, Ultralente, Detemir
Many new Oral Hypoglycemics—act differently in system--sometimes given in combination with each other and with Insulin
INSULIN PUMPS
Set to deliver Basal Rate and Boluses at designated times
Advantages—continuous, covers meal times, snack times, prevents nocturnal hypoglycemia and “dawn” phenomenon
Disadvantages—not allow for exercise induced hypoglycemia, varied meal times or varied calorie meals and varied metabolism in relation to CHO, Fat, Protein intake
IDEAL PREGNANCY TREATMENT PRE-CONCEPTION COUNSELING Normal body weight Normal blood sugars Hb A1C -- maintained b/w 5-6 End organ evaluation Folic acid supplementation
Diabetic Care in Hospital Goal to maintain BS 75-100 mg/dL IV access Mainline IV Normal Saline 2nd IV--Sugar Line D5/LR (30 mL/hr) as
maintenance IV Insulin 250 Units/250 cc and Flush tubing
(Insulin binds to Plastic tubing) Piggy back Insulin into D5/LR line as close
to Hub as possible Blood sugar finger stick every hour and
adjust insulin infusion according to MD Orders
Diabetic Keto-Acidosis in Pregnancy Definition--Hyperglycemia causes osmotic
diuresis with ↑ loss of water and electrolytes Results in: Hypovolemia which leads to Hypoperfusion of tissues, and Acidosis (lactic) Diagnosis of DKA: Blood Glucose > 300 HCO3 > 15 pH < 7.3
Contributing Factors to DKA Stress Infection Emesis Steroid Administration Beta Adrenergic agonists (Brethine) Non-compliance Insulin Pump Failure
Signs & Symptoms’s DKA N&V Abdominal pain Polyuria Polydypsia Dehydration Fruity breath Kussmaul Respirations Leg Cramps ∆ Mental status Labs: ↑ BUN, ↓ Creatinine Clearance, ↑
WBC’s, ↑ Bands
TREATMENT GOALS DKA
1. Rehydrate
2. ↓ Acidosis
3. Normalize Blood Glucose
4. Maintain Normal Electrolytes (Potassium)
DKA Rx in Pregnancy Baseline Vital Signs, Temp Fetal Assessment—Often Late Decels Verify patient weight Labs: CBC, Renal panel, Arterial Blood Gas, Cath
Urine for U/A, Blood Glucose Stat and q 1 h Foley with Urimeter Hourly I&O NO Steroids Not rehydrate Too fast—Cerebral Edema if ↓
Glucose too rapidly Watch Potassium as Diurese
What’s in our future--NOW ??
Continuous glucose monitoring with computerized dosing of Insulin from pump
Glucose Sensor--Tiny sterile flexible electrode inserted just under the skin
Alternative methods to give Insulin-- Dermal Applications, Nasal Insulin, Insulin tablet and pulmonary delivery