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