H:\Capp Diabetes In Pregnancy 04 08 3 With Monitoring[1]
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H:\Capp Diabetes In Pregnancy 04 08 3 With Monitoring[1]

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    H:\Capp Diabetes In Pregnancy 04 08 3 With Monitoring[1] H:\Capp Diabetes In Pregnancy 04 08 3 With Monitoring[1] Presentation Transcript

    • 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 g lucose
      •  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 1 st Trimester-- 10%  in maternal glucose levels
      • Insulin dependent women therefore, normally experience periods of hypoglycemia in 1 st Trimester
    • PATHOPHYSIOLOGY 2 nd and 3 rd 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 cells
      • Types: 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
      • 2 nd 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
      • Rehydrate
      • ↓ Acidosis
      • Normalize Blood Glucose
      • 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