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