LD Final
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| Fetal movement couting | kick counts- should have 4 kicks in 1 hour
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| Non Stress Testing (NST) | evaluation of FHR pattern in absence of regular uterine contractions to determine fetal oxygenation, neurologic, and cardiac functioning
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| benefits of NST | noninvasive, short, safe
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| indications for NST | fetus not moving as frequently as usual, post date, placenta may not be functioning adequately, high risk pregnancy
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| Criteria for reactive NST | 2 or more 15x15 accels in 20 minute period (10x10 ok for extreme premature)
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| Non reactive NST | no accels, one accel that meets 15x15 OR 2 or more accels that do not meet 15x15 criteria in any 20 minute period of time during a total monitoring period of 40 minutes
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| fetal acoustic stimulation test | stimulation of fetus with loud sound and identification of FHR response
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| Contraction Stress Test | determine how the fetus responds to decreased oxygen delivery during contractions; should be performed in a facility with emergency csection capability
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| benefits of CST | indirectly determines placental function and fetal oxygen reserves
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| limitations of CST | longer and more expensive than NST/FAST, invasive (requires IV with pitocin)
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| interpretation of CST | when there are 3 contractions that last 40-60 seconds during a 10 minute period the CST can be interpreted
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| negative CST | no late decels in 10 minute period
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| positive CST | late decels with 2 or more contractions in a 10 minute period
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| biophysical profile (BPP) | evaluation to determine acute and chronic developmental markers to indirectly measure fetal CNS function and oxygenation
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| scoring of BPP | 2 points for each variable: NST, fetal breathing, fetal movement, fetal tone, amniotic fluid volume
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| amniotic fluid volume - criteria for oligohydramnios | AFI <5
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| amniotic fluid volume - criteria for polyhydramnios | AFI>25
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| Biophysical monitoring techniques | daily fetal movement count, ultrasonagraphy (heart activity, gestational age, fetal growth, fetal anatomy, genetic anomalies, placental position/function), MRI
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| Biochemical monitoring techniques | alpha fetoprotein, amniocentesis, percutaneous umbilical blood sampling, chorionic villus sampling
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| alpha fetoprotein (AFP) | measured in maternal serum levels to screen for neural tube defects
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| amniocentesis | obtains amniotic fluid, which contains fetal cells
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| amniocentesis indications | genetic concerns (mom >35 yom previous child with chromosomal abnormality, family hx xsome anomalies), fetal maturity (lungs), fetal hemolytic disease, meconium
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| chorionic villus sampling | removal of small tissue specimen from fetal portion of placenta (reflects genetic makeup of fetus), used for genetic studies between 10-12 weeks of gestation
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| placental abruption | detachment of part or all of placenta from implantation site after week 20 and before birth of fetus
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| causes of placental abruption | maternal hypertension, cocaine use, trauma, cigarette use, history of abruption, preterm PROM, thrombophilias
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| clinical manifestations of placental abruption | abdominal pain, uterus tender, increased uterine tone/tetany, uterus feels firm/board like
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| management of placental abruption | csection, vag delivery if no fetal distress of if fetus is dead, blood transfusions
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| placenta previa | placenta implants in the lower uterine segment near or over the internal os of cervix (causes bleeding when cervix dilates or effaces)
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| complete/total previa | placenta totally covers the internal os
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| marginal previa | edge of the placenta is seen on transvaginal ultrasound to be 2.5 cm or closer to the internal os
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| risk facotrs for placental previa | age, prior placenta previa, drug use (smoking)
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| clinical manifestations of placental previa | PAINLESS, bright red vaginal bleeding
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| expectant management of placental previa | if fetus is <36 weeks, has normal tracing, bleeding is mild and stops and mother is not in labor- observation and bedrest, ultrasounds every 2-3 weeks, NST/BPP once or twice weekly
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| active management of placental previa | fetus >36 weeks or if bleeding is excessive/persistent 0 immediate csection
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| preterm labor | cervical changes and uterine contractions occurring at 20-37 weeks of pregnancy
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| preterm birth | occurs before completion of the 36th week of pregnancy
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| late preterm | 34-36 weeks
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| early preterm | <32 weeks
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| low birth weight | describes only the weight at the time of birth (<2500 grams)
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| intrauterine growth restriction | inadeqaute fetal growth caused by various complications of pregnancy that interfere with uteroplacental perfusion (GDM, HTN, poor nutrition)
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| small for gestational age | less than 10th percentile for babies of that gestational age
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| risk factors for preterm labor/birth | low SES, low prepregnancy weight, smoking, alcohol, drugs, little/no PNC, uterine condiitons, previous preterm delivery, multiple gestation, hx of 2 TAB, PPROM, amnionitis, oligo, previa, abruption, incompetent cervix, PIH, fetal anomalies, IUGR, etc
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| risk factors for preterm PROM | previous preterm birth, amnionitis, mulitple gestation, abrutpion, smoking, maternal low body weight, family predisposition
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| fetal fibronectins | biomarker for preterm labor/birth- test between 2436 weeks, poor positive predictive value but used to determine who will NOT go into preterm labor
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| subjective signs of preterm labor | menstural like cramps, dull low back pain, suprapubic pressure/pain, pelvic pressure or heaviness, change in character of vaginal discharge, diarrhea
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| objective signs of preterm labor | uterine contractions- 4 in 20 min, 8 in 60 min, cervical dilation >1 cm, cervical effacement >80%, preterm PROM
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| interventions for preterm labor | tocolytics to stop contractions (terbutaline, magnesium sulfate), corticosteroids to help lung maturation, bedrest, restriction of sexual activity, activity restriction (betamethasone)
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| terbutaline | stops uterine contractions by relaxing uterine smooth muscle by stimulating beta 2 receptors in uterine smooth muscle (beta 2 agonist)
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| adverse effects of terbutaline | beta 1 stimulation (tachycardia), beta 2 stimulation (hyperglycemia)
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| contraindications to terbutaline | known or suspected heart disease, severe preeclampsia, eclampsia, pre-GDM,GDM, hyperthyroidism, migraine headaches
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| magnesium sulfate | most commonly used tocolytics, promotes relaxation of smooth muscle by competing with calcium in cells
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| betamethasone | corticosteroid that assists in lung maturation/surfactant formation
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| Induction of labor | stimulation of uterine contractions before spontaneous onset
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| indications for labor induction | pregnancy dangerous for mom/baby, health risk, pelvis adequate, no contraindications to artifical ROM, post dates and hypertension
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| bishop score | used to evaluate ability to induce, scored on dilation, effacement, station, cervical consistency, and cervix position. Score of >8 indicates that induction will be successful
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| cervical ripening agents- pharm. | prostaglandins (misoprostil, cerividil)
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| mechanical ways of cervical ripening | balloon catheter (foley), laminaria tent (seaweed), hydroscopic dilators, sex, nipple stimulation, walking
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| pitocin | synthetic oxytocin used to iduce or augment labor that is progressing slowly because of inadequate uterine contractions
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| augmentation | stimulation of uterine contractions after labor has started spontaneously but is progressing unsatisfactorily
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| how the powers affect dystocia | primary powers- hypertonic uterus/ineffective contractions, hypotonic uterus/insufficient for dilation/effacement, secondary powers compromise with lots of drugs/epidurals/exhaustion
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| how the passage affect dystocia | pelvic dystocia (contractures of pelvis tht reduce capacity), soft tissue dystocia (obstruction of birth passage by anatomic abnormality other than pelvis)
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| how the passenger causes dystocia | cephalopelvic disproportion, abnormal presentation or position, anomalies, excessive size, number of fetuses
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| how the position (maternal) can cause dystocia | recumbent and lithotomy may compromise progress
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| how the psyche can cause dystocia | psychologic responses of mother to labor r/t past experiences, prep, culture, and support system can hurt labor process- stress hormones released in response to stress can cause dystocia
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| shoulder dystocia | head is born, but anterior shoulder cannot pass under pubic arch
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| turtle sign | head goes in and out continuously
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| risk of shoulder dystocia | fetal asphyxia, brachial plexus damage, fracture, maternal blood loss, lacerations, extension of episiotomy, endometritis
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| risk factors for shoulder dystocia | maternal obesity, abnormal pelvic shape, postterm regnancy, large baby, prolonged 1st/2nd stage of labor, short maternal stature, GDM, vacuum.forceps birth, induction, increased parity, etc
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| Interventions for shoulder dystocia | GET HELP!, Mcrobert's maneuver, suprapubic pressure, gaskin maneuver (hands and knees), ruben's maneuver (suprapubic, intravaginally), wood screw maneuver
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| prolapsed umbilical cord | occurs when the cord lies below the presenting part of the fetus
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| risk factors for cord prolapse | iatrogenic (artificial ROM), long cord, malpresentation, transverse lie, unengaged presenting part
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| risk of prolapsed cord | fetal hypoxia resulting from prolonged cord compression (occlusion of blood flow for more than 5 minutes)- can result in CNS damage or death of the fetus
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| interventions for cord prolapse | call for help!, do not attempt to put cord back inside uterus, keep hand in place, lift fetal head off the cord, monitor fetal heart tones, immediate csection, hand must stay in place until baby is delivered and cord is retrieved through uterus
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| complications of infants of diabetic mothers | congenital anomalies, macrosomia, birth trauma, perinatal asphyxia, stillbirth, preterm birth, respiratory distress syndrome, hypoglycemia, hypoclacemia, hypomagnesemia, cardiomyopathy, hyperbilirubinemia, polycythemia
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| what causes congenital anomalies in infants of mothers with DM? | fluctuations in BG levels and episodes of ketoacidosis early in pregnancy are believed to cause congenital anomalies
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| macrosomia- patho | mothers pancreas cant release enough insulin to meet demands, maternal hyperglycemia results in increased amounts of glucose crossing placenta and stimulates fetal pancreas to release insulin --> results in excessive fetal growth
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| physical characteristics of macrosomia | round, cherubic face, chubby body, flushed complexion, large internal organs and increased body fat
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| perinatal asphyxia/oxygen deprivation in fetus of DM mother | normally maternal blood is more alkaline than fetal blood that contains CO2 waiting to be removed. When mother is hyperglycemic and gets ketoacidosis, blood becomes more acidotic than fetal blood and little exchnge of CO2 and O2 occurs, causing hypoxia
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| reason for respiratory distress syndrome in infants of DM mothers | high fetal serum levels of insulin and or glucose can delay surfactant production
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| L/S ratio in DM mothers | 3:1
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| hypoglycemia (infant) | infant blood glucose level less than 40. Caused by hyperinsulinemia. Regulation of insulin can take a few days. Signs= jittery, apnea, tachypnea, cyanosis
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| hyperbilirubinemia | increased total serum bilirubin (commonly due to polycythemia, esp. in DM babies)
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| pathologic jaundice | occurs within 24 hours of birth, lasts for longer than 10 days in term infant and 21 days in preterm
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| risk factors for pathological jaundice | mother with DM, hemolytic disease of newborn, delayed cord clamping, altered hepatic clearance
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| kernicterus | encephalopathy caused by neonatal hyperbilirubinemia. Basal ganglia and other areas of brain and spial cord are infiltrated with bilirubin, can result in death
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| Chronic Hypertension | hypertension that is present before pregnancy or develops before 20 weeks of gestation; also, htn that lasts more than 6 weeks postpartum
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| gestational hypertension (PIH) | onset of hypertension without proteinuria after week 20 of pregnancy
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| risk factors associated with PIH | first pregnancy or pregnancy of new genetic makeup, history of vascular disease, multiple gestation, women age <20 or >40, primigravida, morbid obesity, multiple gestation
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| pre-eclampsia | pregnancy specific syndrome in which hypertension and proteinuria develop after 20 weeks of gestation in a previously normotensive woman
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| risk factors for preeclampsia | primigravidity, multifetal pregnancy, morbid obesity, <20 yo, >40 yo
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| preeclampsia patho | vascular remodeling to inc capacity of vessels of uterus does not occur, dec placental perfusion adn hypoxia occur, placental ischemia causes endothelial cell dysfunction, generalized vasospasm,poor tissue perfusion in all organs, inc BP, protein loss
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| diagnosis of preeclampsia | 0.3 g protein or greater in 24 hr period, +2 or greater on urine dipstick, increased blood pressure
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| mild preeclampsia | elevated blood pressure (>140 S, >90 D), .3 g protein, +2 urine dip
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| severe preeclampsia | BP >160 S >110 D, proteinuria 5 g, 3+ urine dip, oliguria, CNS changes (vision, HA, scotomata, mental status), pulmonary edema, epigastric/RUQ pain
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| HELLP Syndrome | variant of severe preeclampsia that involves hepatic dysfunction. Hemolysis, Elevated Liver enzymes, Low Platelet count
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| eclampsia | onset of seizure activity or coma in a woman with preeclampsia with no history of preexisting pathology that could result in seizures
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| postpartum hemorrhage | loss of 500 ml or more after vag birth, loss of 1000 ml after csection, 10% change in hematocrit from labor admin values, early is w/in 24 hr, late is 24 hr-28 days
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| causes of PP hemorrhage | tone (uterine atony), trauma (lacerations, episiotomy, hematomas, inversion, rupture), tissue (retained placenta), thrombin (coagulopathies)
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| hypovolemic shock assessments | rapid shallow respirations, rapid/weak/irregular pulse, decreasing blood pressure, cool/pale/clammy skin, decreasing urinary output, altered LOC, mental status change, dec CVP, poor turgor, dry MM
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| interventions for hypovolemic shock | restore circulating blood volume (IV crystalloids, pRBCs), treat underlying cause of hemorrhage, oxygen per nonrebreather mask 10-12 L
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| drugs to stop PP hemorrhage | methergine, hemabate
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| uterine atony | marked hypotonia of uterus, results in brisk venous bleeding, impaired coagulation
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| risk factors for uterine atony | high parity, hydramnios, macrosomic fetus, multifetal gestation, uterine atony in previous pregnancy, overstretched uterus (poorly contracts after birth)
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| subinvolution | failure of uterus to return to pre-pregnancy state
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| signs and symptoms of subinvolution | boggy uterus, reddish/brown oozing from vagina/irregular heavy vaginal bleeding in 6 weeks PP, low persistent backache, abdominal pain or tenderness, fatigue, foul smelling discharge d/t infection, persistent low grade temperature
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| risk factors of subinvolution | retained placental fragments, pelvic infection
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| complete inversion of uterus | large, red, rounded mass protrudes 20-30 cm outside introitus
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| causes of uterine inversion | traction on cord before placenta separates, fundal implantation of placenta, manual extraction of placenta, short umbilical cord, uterine atony, leimyomas, abnormally adherent placental tissue
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| signs and symptoms of uterine inversion | large PP hemorrhage 800-1800 ml, shock, pain, absence of palpable fundus
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| idiopathic thrombocytopenia purpura | autoimmune disorder in which antiplatelet antibodies decrease lifespan of platelets, can cause severe hemorrhage after csection, vag delivery, cervical lecerations
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| von willebrand disease | hereditary bleeding disorder, factor VIII deficiency and platelet dysfunction
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| disseminated intravascular coagulation | pathological clotting throughout body, coagulation proteins and platelets used up, normal coagulation disrupted, bleeding occurs in skin, GI tratc, resp. tract, etc
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| risk factors for DIC | placenta abruption, placenta previa, severe preeclampsia, HELLP syndrome, hemorrhage, amniotic fluid embolism, septic abortion, massive hemorrhage
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| DIC lab markers | PT prolonged, PTT normal/shortened, fibrinogen decreased, platelets decreased, fibrin split products increased, coagulation factors decreased
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| manifestations of DIC | severe bleeding, shock, dyspnea, hemoptysis, acute renal failure
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| thrombophlebitis | inflammation of superficial deep veins
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| risk factors for venous thrombosis | varicosities, immobility, obesity, advanced maternal age, smoking
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| s/s thrombosis | pain, tenderness in lower extremity, warmth, redness, swelling, tenderness over vein, positive homan's sign
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| treatment of superficial venous thrombosis | NSAIDs, rest, elevation of extremity, stockings, moist heat
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| treatment of DVT | anticoagulants (heparin), bed rest, elevation, analgesia
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| pulmonary embolism | complication of DVT, clot breaks off to pulmonary artery, causes cough, dyspnea, shallow/rapid breathing, adventitious lung sounds
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| tx for PE | IV heparin, oxygen, blood products, etc
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| puerperal infection | infection of genital tract or a would that occurs 28 days after miscarriage, induced abortion, childbirth, or csection (100.4 x2 consecutive days during first 10 days PP)
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| endometritis | infection of decidua (pregnancy endometrium)
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| risk factors for endometritis | prolonged labor, prolonged ROM, multiple vag exams, internal monitors, maternal DM, manual removal of placenta
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| endometritis s/s | fever, uterine tenderness, foul lochia, leukocytosis, bacteremia
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| UTI risk factors | urinary catheterization, frequent pelvic exams, epidural anesthesia, hx of UTI
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| s/s UTI | dysuria, frequency, urgency, urinary retention, hematuria, pyuria, CVA tenderness
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| mastitis prevention | support breasts, comfort, promote brestfeeding, prevent cracked nipples
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