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by: Christie Kepler
Christie Kepler
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Antepartum Assessment
Childbearing 3200
Professor Stark
Class Notes
Nurs 3200
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This 10 page Class Notes was uploaded by Christie Kepler on Sunday February 14, 2016. The Class Notes belongs to NURS 3200 at Western Michigan University taught by Professor Stark in Fall 2015. Since its upload, it has received 18 views. For similar materials see Childbearing 3200 in Nursing and Health Sciences at Western Michigan University.


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Date Created: 02/14/16
Chapter 26 : Assessment for Risk Factors in Pregnancy Assessment of Risk Factors Uteroplacental insufficiency – decline in delivery of needed substances by the placenta to the fetus, causes growth restriction, intrauterine fetal death, intrapartum fetal distress, and various neonatal morbidit. Categories of Risk Biophysical Originate within the mother or fetus and affect the development functioning of either one or both. Ex. Genetic disorders, nutritional and general health status, and medical or obstetrical related illness and medical or obstetrical related illness. Psychosocial Maternal behaviors and adverse lifestyle that have negative effects on the health of the mother Ex. Emotional distress and disturbed interpersonal relationship, inadequate social support and unsafe cultural practices, Smoking, caffeine, alcohols, drugs, psychologic status Sociodemographic Arise from mother and her family Ex. Lack of prenatal care, low income, martial status and ethnicity Environmental Include hazards in the workplace and the woman’s general environment and may include environmental chemicals Ex. Environmental chemicals, anesthetic gases, and radiation Psychologic Responses to high risk pregnancy Anxiety, low self-esteem, guilt, frustration, and inability to function, feel ambivalence, may not accept pregnancy Affects- parental attachment, accomplishment of the tasks of pregnancy, and family adaptation Antepartum Testing Begins at 32-34 weeks of gestation DMFC- Daily Fetal Monitoring Count Noninvasive, inexpensive, simple to understand, doesn’t interfere with daily routing Frequently used to monitor conditions that may affect fetal oxygenation Count once a day for 60 minutes Monitor low number of daily fetal movement- decreased motion Fetal Alarm Sign – fetal movements cease entirely for 12 hours Contraction Stress Test (CST)/Oxytoxin Challenge Test (OCT)/ NON-stress test- Required with fewer than 3 movements within 1 hour. Ultrasonography – images are reflection of the strength of sending beam, the strength of returning echo, and the density of the medium through which the beam is sent and returned Abdominal Ultrasonography- used after the first trimester, full bladder helps provide a full image of the fetus.> 1 Trimester Transvaginal Ultrasonography- probe is inserted into the vagina, removes the need for a full bladder, woman can be in a lithotomy position or with the pelvis elevatst, used to detect ectopic pregnancy, monitor developing embryo, identifies abnormalities, establish gestational age. < 1 Trimester Levels of Ultrasonography- Standard- used most frequently and can be performed by ultrasonographers. Finds fetal viability, presentation of fetus, gestational age, locate placenta, amniotic structures for malformations, amniotic fluid volume (AFV). Limited- Specific indications fetal presentation during labor and evaluating fetal heart rate (FHR) Specialized- used for suspected anatomically or physically abnormal fetus. (polyhydramnios, oligohydramnios, elevated alpha- fetoprotein (AFP) levels, a history of offspring with abnormalities. Indications for USE: First Trimester- information regards to number, size, location of gestational sacs, the presence or absence of fetal cardiac and body movements, presence of absence of uterine abnormalities, adnexal masses, and pregnancy dating. Second and Third Trimester- Fetal viability, number, position, gestational age, growth pattern, and abnormalities, AFV, Placental location and maturity, Presence of uterine fibroids or anomalies, Presence of adnexal masses, and cervical length. FHR Find as early as 6-7 weeks of gestation Fetal Death- confirmed by lack of heart motion, fetal scalp edema, maceration and overlap of cranial bones. Gestational Age Performed at 22 weeks of gestation Gestational Sac Dimension – 8 weeks/Crown-Rump Length – 7-12 weeks/Biparietal Diameter- after 12 weeks/Femur Length- after 12 weeks Fetal Growth Determined by both intrinsic growth potential and environmental factors, Requirement of assessment of fetal growth: poor maternal weight gain or pattern of weight gain, previous pregnancy of IUGR, Chronic infections, ingestion of drugs, maternal diabetes mellitus, hypertension, multifetal pregnancy, and other medical or surgical complications IUGR- Intrauterine Growth Restrictions Symmetric (fetus is small in parameters)- reflects a chronic or long-standing insult and may be caused by low genetic growth potential, intrauterine infection, under nutrition, heavy smoking, or chromosomal aberration Asymmetric (head and body growth vary)- growth suggests acute or late-occurring deprivations= placental insufficiency=hypertension +/- renal disease +/- cardiovascular disease Fetal Genetic Disorders and physical Anomalies Nuchal Translucency (NT)- Fluid in the nape of the fetal neck between 10-14 weeks of gestation to identify abnormalities Fluid Collection > 3 mm is abnormal. Low Maternal Serum marker + elevated NT = Risk of chromosomal abnormalities Trisomies 13, 18, and 21. Placental Position and Function 14-16 weeks placenta is clearly defined. 90% of cases of placenta previa diagnosed in 2 trimester- will have resolved by term. Fetal Well-being Assessment in Ultrasound of: AFV, vascular waveforms from fetal circulation, heart monitoring, Fetal Breathing Movements (FBM), Fetal urine production, and fetal limb and head movements. Amniocentesis – are safer when amniotic fluid pockets can be identified accurately Doppler Blood Flow Analysis- Study blood flow noninvasively in the fetus and placenta with ultrasound, Risk- Hypertension, IUGR, diabetes mellitus, multiple fetuses, and preterm labor , Elevated S/D ratio indicates poorly perfused placenta, exposure to nicotine increases S/D ratio Amniotic Fluid Volume – Oliohydramnios-(Decreased fluid) the absence of fluid pockets in the uterine cavity and impression of crowding small fetal parts. Congenital abnormalities, growth restriction, and fetal distress during labor Polyhydramnios (hydramnios)- increased amniotic fluid/ Large pockets of fluid, the impression of a floating fetus, and free movement of fetal limbs Amniotic Fluid Index- 10 cm -25 cm, <5 cm oligohydramnios Biophysical Profile- a noninvasive dynamic assessment of a fetus that is based on acute and chronic markers of fetal disease. Includes: AFV, FBM(Fetal breathing Movements), Fetal movements, and fetal tone determine by ultrasound and FHR reactivity determined by means of NST/ BPP of 8-10 is normal/If fetus is in a quiet sleep state, the BPP can require a long period of observation (Breathing movements, gross body movement, tone (flexion & extension, heart rate- NST, amniotic fluid volume- one or more pockets) Amniocentesis- formed to obtain amniotic fluid, containing fetal cells. Possible after 14 weeks/ Test for genetic disorders, congenital abnormalities, assessment of pulmonary maturity, and Fetal hemolytic disease RISKS: hemorrhage, infection, fetal demise, Placental Abrupto FETAL RISKS: Death, Hemorrhage, infection, injury from the needle, miscarriage or preterm labor, leakage of amniotic fluid. FOR >35 Y.o. Genetic Error Testing- High AFP may increase with multifetal- Spina Bifida, Lung maturity and Coombs Testing (Rh Compatibility) Maternal Serum Alpha-Fetoprotein (MSAFP) - screening tool for NTDs (Neural Tube Defect) in pregnancy/ Alpha-fetoprotein is produced by the fetal liver and increasing levels are detectable in serum of pregnant women from 14-34 weeks gestation, 16-18 weeks being ideal. Multiple Marker Test- to detect fetal chromosomal abnormalities, particularly Trisomy 21 (downs syndrome) / Two maternal biochemical markers- Pregnancy Placental Protein (PAPP-A) or hCG / Markers MSAFP, unconjugated estriol, HcG, & inhibin A/ Screening at 16-18 weeks of gestation/Detection rate 70-80 % Coombs Test- screening for Rh incompatibility/ Can detect other antibodies that may place the fetus at risk for incompatibility with maternal antigens/ high antibodies determine of bilirubin- fetal anemia Electric Monitoring: 3 trimester test to determine intrauterine environment to determine the timing of children for women at risk for UPI/ Gradual loss of placental function results first in inadequate nutrient delivery to the fetus, leading to IUGR=fetal hypoxia. Non-stress Test (NST) : Fetus will create fetal heart rate patterns in response to fetal movement. Common reason for FHR accelerations is quiet fetal sleep state. Disadvantages: requirement for twice-weekly testing and a high false-positive rate. > 28 weeks gestation. Absence of FHR accelerations due to fetal sleep state- give OJ or glucose increase BS. Want: REACTIVE/Contraction Stress Test- first widely used fetal assessment test/ provides early warning of fetal compromise/ identifies jeopardized fetus that was stable at rest but showed evidence of compromise after stress/ Uterine Contractions decrease is sufficient to produce hypoxia in the fetus= a deceleration in FHR/ Repetitive late decelerations (+ result) = intrauterine fetal death, late FHR decelerations in labor, IUGR, and meconium-stained amniotic fluid. WANT = Negative Chapter 27: Hypertensive Disorders in Pregnancy Maternal complication associated with hypertensive disorders include... Placental abruption/Acute respiratory distress syndrome/Stroke/Cerebral hemorrhage/Hepatic or renal failure Disseminated intravascular coagulation (DIC having lots of blood clots in arteries due to endothelial damage) Give Heparin/Pulmonary edema Perinatal complications include…Placental insufficiency leads to IUGR/Prematurity associated w/ induced birth/Hypoxia/acidosis/Placental abruption/ Most common complication of pregnancy is hypertension/2nd leading cause of maternal mentality in US is hemorrhage Classification Gestational Hypertension: onset of hypertension w/o proteinuria > wk 20 of pregnancy Hypertension: a systolic BP greater than 140 mmHg or a diastolic BP greater than 90 mmHg/Should be recorded on 2 separate occasions at least 4-6 hrs apart and w/i a one week period/Can occur any time after 20wks but usually develops at or after 37 wks of gestation. Women who have gestational hypertension do not normally have any preexisting condition and their normal BP will return 6 wks after giving birth/If proteinuria starts to develop than the dx is changed to preeclampsia Preeclampsia: pregnancy-specific condition in which hypertension and proteinuria develop after 20 wks of gestation in a previously normotensive woman. Pathology: Generalized arteriolar vasospasm/Endothelial cell damage from rushing blood leakage of plasma/Poor tissue perfusion 1/3 of eclamptic seizures happen after birth (usually w/i the first 48hr postpartum) Magnesium sulfate is the drug of choice in the prevention and tx of seizure activity caused by severe preeclampsia or eclampsia (usually given IV PB) and also suppresses uterine contractions/MgSO4 causes the relaxation of smooth muscle and if toxicity occurs with it then calcium gluconate or calcium chloride can be given to counteract the MgSO4.Side effects: warmth, flushing, burning at the IV site, Mild toxicity: lethargy, muscle weakness, decreased or absent DTR’s, double/blurred vision. Higher toxicity: maternal hypotension, bradycardia, bradypnea, and cardiac arrest. Box 27-1 Risk Factors for Preeclampsia (p 657) Placental ischemia is thought to cause endothelial cell dysfunction cell impermeability, leading to intravascular protein and fluid loss and ultimately to less plasma volume. Main pathogenic factor is poor perfusion as a result of vasospasm and reduced plasma volume Decreased liver perfusion can lead to impaired liver function & elevated liver enzyme levels If epigastric or RUQ pain occur it could be due to hepatic edema and subscapular hemorrhage development (life- threatening)CNS irritability manifests as HA, hyperreflexia, positive ankle clonus, and seizures/Arteriolar vasospasms and decreased blood flow to the retina can lead to visual disturbances such as scotoma (dim vision, blind, or dark spots in vision), blurred or double vision/Table 27-4 Deep Tendon Reflexes (p 661) S&S of PreeclampsiaDecreased urine output due to blood going thru kidneys to fast to filter/Increased protein in urine . Proteinuria is defined as a concentration at or greater than 30mg/dL – greater than 1+ on dipstick (2 randon specimen w/i 6 hr) and in a 24hr specimen it is defined as 300mg. Decreased platelets which caused clotting prob/Increased Hgb/Hct (more concentrated due to plasma leakage)/Epigastric pain HELLP Syndrome: laboratory dx for a variant of sever preeclampsia that involves hepatic dysfunction, characterized by hemolysis (H), elevated liver enzymes (EL), and low platelet count (LP). Develops in the 3rd trimester or w/i 48 hrs after birth/Women w/ the disorder report a hx of Maliaise/Influenza-like symptoms/Epigastric or RUQ abd pain/N&V/HA Women w/ this may not have S&S of severe preeclampsia…A women may have hypertension but BP may be only mildly elevated in 50% of cases and proteinuria may be absent. Most women w/ HELLP are misdiagnosed. The best preeclampsia prevention methods include: Early prenatal care for the identification of women at risk and early detection of disease/Maternal Complications/Abruption Severe preeclampsia or eclampsia:DIC/Renal failure/HELLP/Fetal Effects: Uteroplacental insufficiency, IUGR, Fetal hypoxia Eclampsia: the onset of seizure activity or coma in a woman w/ preeclampsia, w/ no hx of preexisting pathology, which result in seizure activity. Nursing Actions after a Convulsion: Assess status of woman’s Airway. Breathing, and Pulse, Suction secretions from her glottis to clear the airway, insert oral airway, and administer oxygen at 10L/min by non-rebreather mask, IV infusion is not in place, insert one with 18gauge needle Chapter 28: Antepartum Hemorrhagic Disorders Miscarriage (Spontaneous Abortion): A pregnancy that ends as a result of natural causes before 20weeks of gestation Possible causes of early miscarriage: Chromosomal abnormalities (50%)/Endocrine imbalances (luteal phase defects, hypothryroidism, DM w/ high glucose levels)/Systemic disorders (lupus)/Immunologic factors (antiphospholipid antibodies) Genetic factors/Infection is not a common cause of miscarriageThe dx of the type of miscarriage is based on S&S Types of Miscarriages (Pg 672 Table 28-1) Threatened Spotting of blood w/ cervical os closed / Mild uterine cramping/ Inevitable & Incomplete (both exhibit these S&S) Moderate to heaving bleeding w/ an open cervical os open/ Tissue present w/ bleeding/Mild to severe uterine cramping, Trip to the ER Inevitable – is often accompanied by rupture of membranes and cervical dilation Incomplete – involves the expulsion of the fetus w/ retention of the placenta Complete: Cervix has closed after all fetal tissue was expelled/Slight bleeding may occur/Mild cramping may be present Missed: Fetus has died/ Products from conception are retained in utero for several weeks/Uterus stops increasing/decreasing in size May be no bleeding or cramping/Cervical os remains closed/Recurrent (habitual)/3 or more spontaneous pregnancy loses before 20 wks of gestation/Prenatal chromosomal abnormalities is another “possible cause”/Septic/ Fever and abdominal tenderness/ Vaginal bleeding (slight to heavy)/ Malodorous (foul smelling) Premature Dilation of the Cervix: passive and painless dilation of the cervix (usually btwn 16-20wks – 2nd trimester) Management of Incompetent Cervix Placement of a cerclage (suture is placed around the cervix beneath the mucosa to constrict the internal os of the cervix until 37 wks gestation)/Prophylactically a cerclage is place btwn 11-15 wks of gestation/ Cerclage placement is offered if cervical length falls to less than20-25mm before 23 to 24 wks/ After it is inserted, intercourse should be avoided until after a postoperative check/Tocolytics may be prescribed to prevent uterine contractions and further dilation of the cervix/ Monitor for signs of preterm labor, ROM, and infection Ectopic Pregnancy: a fertilized ovum is implanted outside the uterine cavity and is also the leading cause of infertility. Ectopic pregnancies are classified by site of implantation: Tubal/Ovarian/ Abdominal (fetal deformity is high) Most common types of problems include…Facial or cranial symmetry/ Joint deformities/ Limb deficiencies/ Central nervous anomalies S&S (3 classic symptoms) Abdominal pain (dull, lower quadrant pain)/Delayed menses/ Abnormal vaginal bleeding that occurs appox 6-8 wks after last norm menstrual period Other S&S: If not dx until after rupture, referred shoulder pain may be present/Also one-sided lower quadrant acute pain/Shock/Faintness and dizziness r/t bleeding in the abd cavity/Syncope (passing out) Medical Mgmt Most important screening tools are …Quanitative beta-hcg levels (>1500 there is an increased chance of ectopic pregnancy)/Transvaginal ultrasound/Progesterone levels are drawn to see levels (<5ng/ml suggest ectopic preg)/Methotrexate is given to dissolve the tubal pregnancy (stops rapidly developing cells) Surgical Mgmt Salpingectomy: surgical removal of fallopian tubes If a woman desires future fertility, a salpingostomy can be performed instead (surgical unblocking of a blocked fallopian tube) Placenta Previa: placenta is implanted in the lower uterine segment such that it’scompletely or partially covers the cervix or is close enough to the cervix to cause bleeding when the cervix dilates or the lower uterine segment effaces. Complete – covers the entire internal cervical os Marginal – edge of the placenta is seen on transvaginal US to be closer to the internal cervical os Risk Factors Previous hx/ Advanced maternal age/Multiparity/ Hx of prior curettage suctioning/Smoking (leads to decrease in uteroplacental oxygen S&S Painless, bright, red blood during 2nd or 3rd trimester of pregnancy/ Vital signs are normal/ Clinical presentation and decreased urinary output may be better indicators of acute blood loss than vital signs alone/Fundal ht is greater than expected gestational age/Fetal mal-presentation is common/ Maternal and Fetal Complications : Major maternal complication is hemorrhage/ Development of an abnormal placental attachment/ If excessive bleeding can’t be controlled then a hysterectomy may be necessary/Greatest risk of fetal death is caused by preterm birth Other fetal risks include: Still birth/Malpresentation / Fetal anemia/ If less than 34 wks gestation, antenatal corticosteroids should be administered Expected Mgmt Less than 36 wks gestation and has normal FHR, and mild bleeding (<250ml) and no labor (observation & bedrest) Large bore IV access initiated immediately/ Lab (Hgb, hemocrit, platelet count and coagulation studies) /Type screen blood sample/ If less than 34 wks then antenatal corticosteroids should be administered / IF, bleeding stops – bedrest and 15-30 mvmt 4x/day/ Pelvic rest/ US performed q2-3wks / Fetal surveillance includes NST, BPP (biophysical profile) 1-2x wkly MgSO4 is given for tocolysis Active Mgmt : Beyond 36 wks or excessive bleeding immediate C-Section is indicated Asymptomatic women whose placenta lies 2cm from the cervical os can labor safely. C-section –maternal vitals assessed frequently for decreasing BP, increasing pulse, chg in level of consciousness and oliguria.Continuous FHM to assess fetus for hypoxia Placental Abruption (Abruptio Placentae): detachment of part or all of a normally implanted placenta from the uterus. Separation occurs in the area of ductus basalis after 20 wks of gestation and b4 birth of infant. Incidence and Etiology Maternal hypertension – chronic or pregnancy related is most consistent identified risk factor for abruption. Other risk factors include: Cocaine – causes vascular disruption in placental bed/ Blunt force trauma bc of motor vehicle accidents/ Maternal battering/ History of cig smoking/ Previous hx of abruption/ Preterm PROM/ Presence of inherited thrombophilias Clinical Manifestations Separation – partial or complete Bleeding from placental site may dissect and flow out of the vag C-section – blood clot will be attached posterior surface of placenta Classic symptoms: Vag bleeding, abd pain/ Uterine tenderness/ Contractions/ Maternal hypovolemia and coagulopathy(due to blood loss) Mild to severe hyprtonicity/ Pain is mild to severe & localized in one region of the uterus or diffuse over uterus board-like abdomen/ Couvelaire uterus – purple or blue uterus and contractility is lost/ Positive apt test (blood in AF)/ Decrease in Hgb, hct, coag factor levels/ KB test – determine presence of fetal to maternal bleeding this test helps to guide Rh immune globulin therapy in Rh neg women Maternal and Fetal Outcomes Hemorrhage, hypovolemic shock, hypofibrinogenmia, and thrombocytopenia/ Renal failure and pituitary necrosis form tissue ischemia/ Rare cases – Rh neg women become sensitized if fetal-to-maternal hemorrhage occurs Diagnosis (clinical) US exam/ Hypofibrinogenemia and evidence of DIC supports dx/ Confirmed after birth by visual inspection of placenta Suspected in women who experience sudden onset of intense, localized pain/ Physical exam – abd pain, tender uterus, contractions/ Increased fundal ht – indicative of concealed bleeding/ Abnormal clotting studies (fibrinogen, platelet, PTT) Expectant Mgmt Depends of severity of blood loss and fetal maturity status/ Cord Insertion and Placental Variations Succenturiate placenta: (rare) placenta is divided into 2 or more separate lobes This increases the risk for postpartum hemorrhage Clotting problems Disseminated vascular coagulation (DIC): consumptive coagulopathy—pathologic form of clotting that is diffuse and consumes large amt of clotting factors causing widespread external and internal bleeding or both Never a primary problem but results from some prob triggered by clotting cascade. Chapter 29: Endocrine and Metabolic Disorders in Pregnancy Diabetes Mellitus: refers to a group of metabolic diseases characterized by hyperglycemia (high BS) resulting from defects in insulin secretion, insulin action, or both. Hyperglycemia causes hyperosmolarity of blood which attracts intracellular fluid into the vascular system resulting in dehydration and expanded blood volume (BV)/ Polyuria (kidneys job), glycosuria, polyphagia and polydipsia occur/ Body compensates for inability to convert carb (glucose) into energy by burning proteins (muscle) and fats./ End products are ketones and fatty acids produces ketoacidosis and acetonuria/ Weight loss due to fat and muscle breakdown Tissue bkdwn causes starvation and compels person to become ployphagic/ Structural chgs affect in particular the heart, the eyes, they kidneys, and the nerves/ This results in premature atherosclerosis, retinopathy, neuropathy, and nephropathy Classification 90% of all pregnant women with diabetes have GDM/ Type 1 is insulin deficient : caused by pancreatic islet beta cell destruction – prone to ketoacidosis/ Type 2 is insulin resistant: cause is unknown – undiagnosed for years due to hyperglycemia levels slow rise/ other risk factors for type 2 include: aging, sedentary lifestyle, family hx, genetics (strong genetic predisposition), puberty, hypertension, prior gestational diabetes Whites Classification Priscilla White – physician that worked w/ diabetic pregnant women in the ‘40’s. System was based on dx, duration of illness, and presence of vascular disease Class A-C have good pregnancy outcomes as long as blood glucose levels are well controlled Class D thru T (D, F, R, T) have poorer outcomes bc of already developed vascular damage. Metabolic Changes Glucose = fuel for fetus is transported across the placenta (glucose levels in fetus are proportional to maternal levels) Insulin does NOT cross the placenta/ During 10th wk – fetus begins secreting own insulin at levels adequate to use the glucose obtained from mother maternal glucose levels rise and fetal glucose levels increase resulting in increased fetal insulin secretion Early pregnancy women are prone to hypoglycemia : Normal insulin production/ Increased tissue response to insulin (glucose store)/ Blood glucose levels (70-120) Later pregnancy women are prone to ketoacidosis ketones in blood which results from hyperglycemia leads to metabolic acidosis Diabetogenic effect happens : Rising levels of hormones act as insulin antagonist/ Insulin resistance is a glucose-sparing mech that ensures an abundant supply of glucose for the fetus/ Insulin requirements increase gradually in 18-24wks to 36wks. For non-breastfeeding moms the pre-preg insulin-carb balance returns w/i 7-10 days For breastfeeding moms insulin requirements remain low during lactation (lactation uses maternal glucose) A glucose test is taken during the 28th wk of pregnancy Pre-gestational Diabetes Mellitus: may have type 1 or type 2. Type 2 is more common – almost all women that are PDM are insulin dependent. They fall into White’s classification system classes B thru T. Maternal Risk and Complications Early loss (spontaneous abortion) happens in 1st trimester/ Fetal macrosomia (birth wt more than 4000g-4500g or in the90th percentile)/ Stores a lot of fat due to large amts of glucose from mom having a lot of insulin/ Gestational hypertension/ Pre- term labor (PTL)/ Increased risk of c-section/ Hydramnios (excess AF accumulation)/ Develops in 3rd trimester/ Increased risk for infection insulin moves glucose in to cellsglucose in urinebacteria love glucose and warm, moist places / Women w/ nephropathy and hypertension in addition to diabetes are at an increase to develop preeclampsia Fetal/Neonatal Risks and Complications Respiratory distress immature respiratory system / Still birth/ Early loss/ Congenital abnormalities (most important cause of perinatal loss)/ Anomalies commonly seen affect the cardiovascular, CNS, and skeletal systems Common birth injuries associated w/ diabetic preg are: Brachial plexus palsy/ Facial nerve injury/ Humerus or clavicle facture/ Cephalhematoma Differentiation Hypoglycemia (insulin shock) Hyperglycemia (diabetic ketoacidosis Irritability Thirst Hunger N&V Sweating/nervousness Abdominal pain Personality change Constipation/increased urination Weakness/fatigue Drowsiness Headache Headache Diplopia Dim vision Rapid pulse Weak, rapid pulse Shallow respirations Rapid breathing Pallor, clammy skin Flushed, dry skin Dizziness Fruity breath (acetone breath odor) Urine – neg for sugar & acetone Urine – positive for sugar and acetone Target Blood Glucose Levels during Pregnancy (Euglycemia) Time of Day Target Plasma Glucose Level (mg/Dl) Pre-,meal or fasting >65 but <95 Post-meal (1 hr) <130-140 Post-meal (3hr) <120 Care Mgmt (Antepartum) Routine prenatal lab work/ Baseline renal function – 24hr urine collection for total protein excretion/ Creatinine clearance UA – for UTI infection/ Thyroid function tests if there is thyroid disease present/ Hgb A1C: measured to assess the glycemic control over a period of time (4-6wks)/ Levels >6 indicate glucose during the previous4-6wk/ Fasting blood sugar is done antepartum/ Daily bath that includes good perineal care and foot care/ Diet/ Obese women w. BMI > 30, caloric intake should be 25kcal/kg/day / Large bedtime snack is preferred (25g carb w/ protein and some fat) to help prevent hypoglycemia and starvation ketosis during the night. Ideal diet consists of: 55% carbs / 20% protein/ 25% fat w/ <10% for sat fat/ Simple carbs limited/ Complex carbs are high in fiber bc starch and protein in foods help regulate blood glucose levels Insulin Therapy 3-7wks insulin demands are increased and decrease by 7-15 wks / Type 1 Common prescribed dose in 0.7units/kg in 1st trimester/ 2nd and 3rd trimester – insulin resistance dose must be increased/ Insulin requirements plateau at 35wk and drop significantly after 38wks Types of Insulin Type of Insulin Generic (trade) Name Onset of Action (min/hr) Peak of Action (min/hr) Duration of action Rapid-acting Lispro (Humalog) 15min 30-90min 4-5hr Aspart (Novolog) 15min 1-3hr 3-5hr Short-acting Humulin R 30min 2-4hr 5-7hr Novolin R 30min 2.5-5hr 6-8hr Intermediate-acting Humulin NPH 1-2hr 6-12hr 18-24hr Novolin N 1-5hr 4-20hr 24hr Humulin Lente 1-3hr 6-12hr 24hr Novolin L 2-5hr 7-15hr 22hr Long-acting Humulin Ultralente 4-6hr 8-20he >36hr Glargine (lantus) 1hr None 24hr Unused vials of insulin should be store in the refrigerator until exp date is reached/ Should not be frozen/ Can be stored at room temp for 1 month and should not be stored in direct sunlight/ Reg insulin can be mixed in syringe w/ NPH or ultralente (long-acting)/ Once mixed it can be used or stored – if used later it must be rotated 20x before use/ Glargine is administered at bedtime (can NOT be mixed w/ any other insulin)/ Prepared syringes are stable for 2wks in fridge/ Abdomen is preferred site due to best absorption site: Other site are upper outer arm (not deltoid), the thighs, and buttocks/ Each injection should be one inch from previous injection site and used no more than once in 30 days Treatment of hypoglycemia 4oz of unsweetened OJ / 4oz of regular soda/ 5-6 hard candies/ 8oz of skim milk/ 2-3 glucose tabs/ Rest for 15 min then recheck blood sugar Intrapartum Normal saline or lactated ringer solution is administered with continuous insulin PB (ONLY rapid or short-acting insulin can be admin IV)/ Determinations of blood glucose levels are made q hour and fluid and insulin are adjusted to maintain blood glucose levels at less than 140mg/dl./ Continuous FHM is necessary/ C-section should be scheduled/ No morning insulin given day of surgery Postpartum Insulin requirements decrease substantially / Possible complications include: Preeclampsia or eclampsia, Hemorrhage (overdistended uterus), Infection (endometritis), Breastfeeding women are increased risk for hypoglycemia, mastitis, and yeast infections, Transdermal contraceptives are not recommended for women >90kg Gestational Diabetes Mellitus: More likely to occur among Hispanic, Native American, Asian, and African American women than in Caucasian women./ Women at high risk for developing GDM should have a glucola screening at the 1st prenatal visit and again at 24-28 wks if the initial screen is negative/ Glucola screening consists of 50g oral dose of glucose followed by a plasma glucose measurement 1hr later. (No fasting is needed)/ 130-140 is considered a positive screen and should be followed by a 3hr oral glucose tolerance test (OGTT) –avoid caffeine/ OGTT requires fasting glucose level: Negative = <130- 140, Positive = > or equal to 130-140 3hr OGTT , Neg = no GDM, Positive for GDM = fasting 95, 1hr – 180, 2hr – 155, 3hr – 140 Care Mgmt (antepartum) Tx begins immediately/ Education, teaching, participation, and adherence/ Maintain a good blood glucose level/Diet & Exercise/ Standard diabetic diet: 30kcal/kg/day/ Carb intake is restricted to 50% of caloric intake/ Exercise (aerobic exercise w/ resistance training) – 30 min/ Glyburide is a good drug to give during GDM because only minimal amts cross the placenta to the fetus Hyperemesis Gravidarum: Vomiting during pregnancy the becomes excessive enough to cause weight loss, electrolyte imbalance, nutritional deficiencies, and ketonuria Happens during the 1st trimester to nulliparous women who have increased wt, and have a hx or migranes, a multiple gestation preg, have a gestational trophoblastic disease, or are carrying a fetus w/ an abnormality such as triploidy or trisomy 21./ Carrying a female fetus  more likely to have hyperemesis gravidarum Complications accompanying hyperemesis gradvidarum include: Esophageal rupture/ Deficiencies in vit k and thiamine resulting in Wernicke encephalopathy/ Fetal/neonatal complications/ SGA / LBW / Prematurity/ 5-min APGAR scores of <7 Etiology May be related to high levels of HCG and estrogen/ May be associated w/ hyperthyroidism/ Gastric dysrhythmias, esophageal reflux, and reduce gastric motility may also contribute to this prominent puking Clinical Manifestations Dehydration/ Significant wt loss/ Dry mucous membranes/ Decreased BP/ Increase HR/ Poor skin turgor/ Can’t keep clear liquids down Treatment Vitamin B injections/ Phengren or Zofran which is given sublingually/ IV or TPN/ I&O/ Wt assessment/ Avoid odors and progressive diet Hyperthyroidism: over production of a hormone (levothyroxine) caused by Grave’s disease Clinical manifestations Heat intolerance, diaphoresis/ Tachycardia/ Fatigue, anxiety, emotional liability Treatment Primary tx is drug therapy w/ PTU/ Starting dose is 100-150mg q8hrs/ Clinical improvement w/i 2wks/ Required to be taken for 6-8wks/ Med can be discontinued by 32-36 wks of gestation/ Propranolol and atenolol can be used in severe cases of hyperthyroidism/ In severe cases a subtotal thyroidectomy can be done during the 2nd trimester Maternal Side effects Pruritus, skin rash/ Drug-related fever/ Hepatitis/ Bronchospasm/ Lupus-like syndrome/ Most severe side-effect is agranulocytosis (fever and unexpected sore throat) Hypothyroidism: Not enough thyroid hormone is produced Severe hypothyroidism is associated w/ infertility and increased risk of miscarriage. Cause by an iodine deficiency (rare) S&S Wt gain / Lethargy/ Decreased exercise capacity/ Cold intolerance/ Moderately symptomatic women suffer from -constipation/ -hoarseness/-hair loss/ -brittle nails / -dry skin Untreated mothers are at increased risk for: (levothyroxine is given as tx)/ Miscarriage/ Preeclampsia/ Gestational hypertension/ Placental abruption/ Preterm birth and still birth Maternal Phenylketonuria: recognized cause of mental retardation, is an inborn error of metabolism caused by an autosomal recessive trait that creates a deficiency in the enzyme phenylalanine hydrolase Impairs body’s ability to metabolize the amino acid phenylalanine which is found in all protein foods Individuals w/ this disorder have: Hypopigmentation of hair, eyes, and skin bc phenylalanine inhibits melanin production/ Damage can be prevented or minimized by dietary restriction of phenylalanine before and during pregnancy Exclude these from your diet: Meats, milk, eggs, nuts and wheat products Chapter 32: Mental Health Disorders and Substance Abuse in Pregnancy Risk factors for depression : Previous depression/ Lack of support/ Stressful life events/ Partner problems/ Hx of PMS Treatment No psychotropic meds approved in pregnancy/ Self-help strategies/ Making time for self/ Positive relationship w/ caregiver Anxiety Disorders Most common mental disorders Phobias: irrational fear of ppl, objects, events, or situations Panic disorders: unprovoked episode of intense fear that develop w/o warning and are not r/t any specific event OCD Symptoms include: recurrent, persistent, and intrusive thoughts that cause anxiety which a person tries to control by repetitive behaviors PTSD: acute emotional response to a traumatic event or situation such as sexual abuse Signs include: irritability, outburst of anger, Avoidance of stimuli, Difficulty sleeping, Numbing, Difficulty concentrating Hypervigilance, over startle reflex Substance Abuse: refers to continued use of substances despite related problems in physical, social, or interpersonal areas. Any use of alcohol or drugs during pregnancy is considered abuse. Dual diagnosis: coexistence of substance abuse w/ another disorder (ie. Major depression + and anxiety disorder) Risk Factors Smoking  which causes low birth wt, prenatal death and spontaneous abortions, preterm births, placental problems (abruotio placentae), SIDS, r/t the # of cigs smoked/ Hx of childhood sexual or physical abuse/ Spouse who abuses substances/ Socioenvironmental risk factors include: Unstable home environment/ Preg women are more vulnerable to: Unemployed, Unmarried, Experiencing psychiatric disorders, Barriers to Treatment Fear of losing custody of child/children or criminal prosecution/ Unknowledgeable about the effects of what substances can do to their baby/ No insurance Commonly Abused Drugs Nicotine and Caffeine/ Nicotine has additive substances that cause physical and psychological dependence Smoking decreases placental perfusion/ Oxygen carrying capacity of hgb is decreased when carbon monoxide is passed thru the placenta/ Nicotine cause vasoconstriction/ Caffeine can produce anxiety and sleep disturbances Alcohol : Causes feeding problems, vomiting, and FTT, Facial abnormalities, Cardiac abnormalities, Skeletal (joints), Mental retardation microcephaly, Hyperactivity, Growth retardation/ Cocaine: Hypertension (hypertensive crisis), Abruption of placenta (extreme pain), Prematurity in baby, Neonate is hyper-reactive to environmental stimuli, Irritable, Tremulousness and poor feeding. Polydrugs : Intrauterine asphyxia, Intrauterine infections, Small for gestational age or large for gestational age r/t drugs, Low APGAR scores, Neonatal abstinence syndrome, Mood Disorders, PPD (postpartum depression): intense and pervasive sadness w/ severe and labile mood swings and is more serious and persistent than baby blues, Occurrence is higher in young women w/ lower educational attainment and those receiving Medicaid, Inability to provide care, Insomnia Risk Factors Prenatal depression, Low self-esteem, Stress of child care, Previous hx of PPD, Difficult infant temperament, Postpartum blues, Single status, Low socioeconomic status, Unplanned or unwanted pregnancy, Life stress Treatments for PPD (non-pharmacological), Yoga, Massage, Relaxation techniques, Psychotherapy, Social support group, Sensory interventions (music therapy and aromatherapy), Behavioral interventions such as breathing exercises and progressive muscle relaxation, Cognitive intervention such as positive self-talk training, reframing and redefining, and reassurance to help women learn to change the way she feels about herself, Exercise is always helpful for some to let go of unwanted energy Chapter 33: Labor and Birth Complications Preterm Labor: Cervical chgs and uterine contractions occurring between 20-37wks of pregnancy Preterm Birth: Any birth that occurs before the completion of 37wks of pregnancy Late preterm: Any birth that occurs between 34-36wks of gestation Late preterm infants are at risk for early death and long term health problems compared to full term infants Very preterm: born before 32wks Extremely preterm: born before 28wk Non-Hispanic black women have the highest incidence of having preterm labor Hispanic women are next ,Non-Hispanic white women have the lowest rate of preterm birth Risk Factors for Spontaneous preterm labor Genital tract infection, Non-Caucasian race, Multifetal gestation, 2nd trimester bleeding, Low pregnancy wt, HX of previous spontaneous preterm birth, Dehydration, Constipation or bowel upset, #1 risk factor for PTL is a previous PTL Maternal and fetal stress, uterine over-distention, allergic response, and a decrease in progesterone are other factors that could play a part in initiating PTL S&S of PTL Uterine activity, discomfort, or vaginal discharge, Spontaneous preterm births (75%) occur following early initiation of labor process, Indicated preterm births (25%)occur as a means to resolve maternal or fetal risk r/t continuing the pregnancy Major risk factors associated w/PTL and PTB are: Biomedical Marker, Fetal fibronectin: glycoprotein “glue” found in plasma and produced during fetal life has been found during the 2nd trimester and early 3rd trimester to be related to placental inflammation thought to be one of the causes of PTL, Interventions (reduce neonatal morbidity and mortality), Transfer of the mother to hospital equipped to care for her preterm infant, Giving antibiotics during labor to prevent neonatal group B strep, Administering glucocorticoids to woman in labor (reduce incidence of resp distress syndrome, intraventricular hemorrhage, and necrotizing enterocolotis The dx of PTL is based on 3 major dx criteria: Gestational age between 20-37wks, Uterine activity, Progressive cervical chg (effacement 80% or cervical dilation of 2cm), A pregnant woman 30wk gestation w/ irritable uterus but no document cervical chg is not in PTL, Suppression of Uterine Activity Tocolytics: medications given to arrest labor after uterine contractions and cervical chg have occurred. Goal: to delay birth long enough to institute interventions that reduce neonatal morbidity and mortality MgSO4 (IV admin): most common used relaxes smooth muscle (uterus) and also helps prevent seizures in preeclampsia Side effects of MgSO4 Hot flushes, sweating, burning at IV site, N&V, dry mouth, drowsiness, blurred vision, diplopia, HA, dizziness, lethargic Low resp rate, pulmonary edema, chest pain, sever hypotension, low urine output (25-30ml/hr), extreme muscle wkness magnesium sulfate toxicity, and discontinue for any of the following adverse effects: loss of deep tendon reflexes, urinary output less than 30 mL/hr, respiratory depression less than 12/min, pulmonary edema, and/or chest pain Terbutaline (subQ): most commonly administered beta adrenergic agonist used for tocolysis. Inhibits uterine activity and causes bronchodilation Side effects of Terbutaline Tachycardia, chest discomfort, palpations, tremors, HA, N&V, hypotension, hyperglycemia, hypokalemia BP less than 90/60, chest pain, MI, pulmonary edema Fetal S&S: tachycardia, hyperinsulinemia, hyperglycemia Nifedipine: CCB that can suppress contractions (inhibits CA+ from entering smooth muscle cells Side effects of Nifedipine : HA, flushing, dizziness, and nausea, hypotension, reflex tachycardia Indomethacin: NSAID that has been shown to suppress PTL by blocking the production of prostaglandins Side effects of Indomethacin : In them mother side effects are uncommon, Fetal side effects are a major concern Constriction of the ductus arteriosus, Oligohydramnios, Neonatal pulmonary hypotension Betamethasome (antenatal glucocorticoid - IM): stimulates fetal lung maturation by promoting release of enzymes that induce production of release of lung surfactant Used: to prevent or reduce the severity of neonatal respiratory distress syndrome by accelerating fetal lung maturity between 24-34wks of gestation Side effects: Pulmonary edema (if given w/ beta adrenergic medications)/ Increases glycogen depletion and hyperglycemia Antenatal glucocorticoids have been shown to: Reduce the incidence of respiratory distress syndrome/ Intraventricular hemorrhage/ Necrotizing enterocolitis Death in neonates w/o increasing risk of infection, Premature Rupture of Membranes: spontaneous rupture of the amniotic sac beginning before the onset of labor, Preterm PROM: membranes rupture before 37wks of gestation which results from: Weakening of amniotic membranes caused by inflammation, stress from uterine contractions, or other factors that cause increased uterine pressure, Chorioamnionitis :( most common maternal complication) bacterial infection of the amniotic cavity, Other maternal complications include: Placental abruption, sepsis, and death Fetal complications include: Intrauterine infection, Cord prolapse, Umbilical cord compression associated w/ oligohydramnios, Placental abruption Prior to 20wks – pulmonary hypoplasia Dystocia- Long, difficult, or abnormal labor caused by various conditions associated with the five factors affecting labor: Ineffective uterine contractions or maternal bearing-down efforts (the powers), Alterations in the pelvic structure (The passage), Fetal causes, including abnormal presentation or position, anomalies, excessive size, and number of fetuses (the passenger), Maternal position during labor and birth, Psychologic responses of the mother to labor related to past experiences, preparation, culture and heritage, and support system. These factors are interdependent. Hypertonic Uterine Dysfunction- Anxious first time mother who is having painful and frequent contractions that are ineffective in causing cervical dilation or effacement to progress TX; Rest and relaxation Hypotonic Uterine Dysfunction- initially makes normal progress into the active phase of the first stage of labor but then the contractions become weak and inefficient or stop altogether. CPD and malpresentation are common causes. CPD- Cephalopelvic Disproportion- is disproportion between the size of the fetus and the size of the mother’s pelvis. CPD the fetus cannot fit through the maternal pelvis to be born vaginally.


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