Complications of pregnancy Part 3 Diabetes

Disorders of carbohydrate metabolism, Cause: Partial or complete lack of insulin secretion by beta cells of the pancrease, GDM: 9.2% Prevalence 50% of women with GDM will develop type 2 DM later in life

Skeletal, cardiac muscles, & adipose tissue require insulin to carry glucose across cell membrane, Without insulin, glucose accumulates in the. blood which results in hyperglycemia, Body attempts to dilute the glucose by increasing thirst (polydipsia), Fluid is draw from intracellular spaces into vascular bed, results in dehydration at cellular level But fluid volume excess in vascular compartment, Kidneys excrete large volumes of fluid including glucose (polyuria/ glucosuria), Without glucose the cells starve, weight loss occurs, The body begins to metabolize protein and fat to meet energy needs, Metabolisim of fat results in ketosis

Type 1, Type 2, Gestational Diabetes

Deendent on insulin, Prone to ketoacidosis, Assoicated with autoimmune destruction of beta cells, Not often obese

Hyperglycemia develops gradually, Obese, abdominal obesity, Usually sufficient insulin to prevent ketosis, Frequently occurs in women who had gestational diabetes, May be diet controlled

Onset: During Preganancy, Exogenous insulting may or may not be required, Glucose regulation returns to normal after girth, At risk for type 2 later in life, Accounts for 90% of cases of DM during pregnancy

Obesity (>90kg or 198lbs), Previous birth of large infant (>4000g) Chronis hypertension, Maternal age older than 25, Family history of DM, Gestational DM previous pregnancy, Fasting serum glucose >140mg/dl or random serum glucose >200mg/dl

Increased SAB, PIH, UTI, Polyhydramnios, Ketoacidosis, Difficult labor R/T macrosomia Injury to birth canal C/S PPH

Congenital anomalies, neural tube and cardiac defects, Macrsomiam birth injury, IUGR- intrauterine growth restriction, Preterm birth and PROM, Respiratory distress syndrome, Hypoglycemia, Perinatal death ***Fewer fetal effects seen with good maternal control of hyperglycemia!!

Glucose travels across the placental barrier without difficulty, If woman is hyperglycemic, so is baby, Maternal insulin does NOT cross the placenta the fetus produces insulin by 10ths GA, Exessive fetal blood sugar stimulates excessive production of insulin, a growth hormone

If vascular impairment is severe placental perfusion is decreased, Supplies of glucose & oxygen are decreased, Result intrauterine growth restriction

During pregnancy high levels of glucose were provided by mother, Hyperplasia of pancreas’s occurs, At birth maternal glucose supply stops, Fetus continues to produce insulin, Rebound effect, hypoglycemia, What is newbor blood glucose? above 45 general rule

Fetus who experiences recurrent hypoxia compensates by production of more RBCs to carry oxygen, After birth, excess erythrocytes are broken down, results in elevated bilirubin

Infants of diabetic moms have delayed prodction of surfactant (lube of lungs), Lecithin/ Sphingomyelin (L/S) ratio and presence of phosphatidylglycerol (PG) should be done before C/S to evaluate lung maturity

Used to evaluate fetal lung maturity, LS: Stabilize neonatal alveoli to prevent collapse on expiration, Lecithin in amniotic fluid is less than the amount of Sphingomyelin until 26 wks, At 30-32wks the two lipids are equal in value, At 35 wks Lecithin levels rise sharply, Normal value 2:1 or greater, Requires 3cc of amniotic fluid for test, Fetuses of insulin dependent moms develop RDS at higher rates. The L/S rations should be 3.5:1 or greater

Similar to preexisting DM except:, No increase in SAB, No increase in congenital anomalies. Why? organogenesis, 1st trimester

Diet: Nutritional counseling 2200-2400 cal/day, Exercise: Contraction skeletal muscles increases glucose uptake, Blood glucose monitoring: Fastion (no food for 4 hrs) and postprandial (2hrs after a meal) usually 4-6 times/ a day. GOAL: Fsting<95 and postprandial <120, HbA1c last 4-8wks, RBCs life for 3 months sugar sticks to them, values: 6=135, 7=170, 8=205, 9=240, 10=275, 11=310, 12=345, Fetal surveillance: Maternal AFP (alpha-fetal protein) to screen for neural effects, kick counts, ultrasound, biophysical profile, NST(non-stress-test)

Need to maintain rigorous control during pregnancy!, May require more frequent injections Most regimen require 3 injections: 1. Regular (short acting) & NPH AC breakfast 2. Regular before dinner 3. NPH at bedtime, Insuling needs increased markedly in 2nd and 3rd trimesters, May require an insulin drip during labor

To prevent hypoglycemia eat meal within 30 min of administration, What needle and syringe?, What route?, What angle of injection?, Insery and withdraw quickly, Is aspiration necessary?, Injection slowly allow tissue exp. 2-4 secs, Common sites include upper thigh, abdomen, upper arm

Those identified at risk should be screened with GCT, Done at 24-28 gestation, Woman does NOT need to fast, Drinks 50g or oral glucose solution, 1hr later blood sample is taken, if blood glucose ≥140mg/dL, a 3hr oral glucose tolerance tests is ordered (gold standard for Dx)

No longer required to have a high carb diet, Fast after midnight day of test, Fasting blood level is draw in AM, Ingests 100g of oral glucose solution., Blood drawn at 1,2,3 hrs, DX is positive if fasting is abnormal or 2 or more of the draws are elevated: Fasting>95 1hr>180 2hr>155 3hr>140

Treat at once to prevent damage to the maternal brain and fetus, S&S: shakiness, tremors, sweating, pallor, cold, clammy skin, disorientation, hunger, blurred vision, headache, 15g of carbs (glucose tabs, 1/2cup juice/soft drink, 6 saltines