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WVC 2 hi-risk OB LEC

WVC 2 hi-risk OB L. Visser spring 2012

QuestionAnswer
GTPAL Gravida, term, preterm, abortion, living
Infant mortality Definition Death of live born neonate @ 20 wks gestation or more through the 1st year of life…viability is at 20 weeks.
Leading cause of infant mortality – congenital anomalies: genetic, environment, tetrogens around time of conception, chromosomal abnormality
Factors promoting prenatal health + Nutritional status; Substance abuse programs; Safer sex practices; Healthy reproductive hx; Regular pelvic exams; Tx infections i.e. STI’s; c. Importance of prenatal visits
1st pre-natal visit tests: CBC, Rh, Rubella immunity (=/> 1:16); STI’s -syphylis, gonorrhea, chlamydia, Hepatitis BsAg, HIV; Urine glucose & protein (each visit); urine C&S; Pap if indicated
Prenatal visits provide opportunity to catch problems early and hopefully, prevent poor outcomes
the number 1 factor for healthy outcomes for infants Prenatal visits
High risk pregnancy One in which life or health of mother or fetus jeopardized by disorder coincidental with or unique to pregnancy.
High risk pregnancy factors… Age <16 or >35; > gravida 5 – grand multip; Malnourish; Obese; Sub. abuse; Hemorrhage (previous pregnancy); Poverty; education; Unmarried; Unwanted pregnancy; <antenatal care; Difficulty conceiving – high tech fertility tx; Mother has medical condition or pregnancy induced disease; Infection including STI’s; Domestic violence – psych issues and trauma
Non invasive assessment of well being ***Fetal Movement Counts “Kick Counts” Quickening begins about 18/20 weeks; Several methods used…Normal = 2x q 10 min; Normal = 10-12 x q 2 hour (especially p after eating)…Call if < 3 per hour (some say 10/day)
Non invasive assessment of well being ***FHT After week 11 normal = 110-160BPM; Electronic Fetal Monitoring: Goal: Prevent intrauterine fetal death- stillbirth & Avoid unnecessary intervention & O2 to fetus
Types of Stress Tests (3) NST – Non Stress Test; CST – Contraction Stress Test; NSST – Nipple Stimulation Stress Test
NST (non stress test) (Non invasive assessment of well being): monitors fetus for accelerations of FHR in response to movement, indicating healthy fetus.
Procedure: (Vibroacoustical option) Observe: print out of fetal heart rate. Advantages: easy to perform, non invasive, inexpensive. Disadvantages: high false positive results. Interpretation: reactive pattern
CST (contraction stress test) (Non invasive assessment of well being) stimulates fetus by inducing contractions; Stable fetus, at rest, shows evidence of compromise when stressed – A decrease in uterine blood flow & decreased placental perfusion will cause a late deceleration of the FHR
Procedure: IV oxytocin
NSST ( nipple stimulated contx stress test) (Non invasive assessment of well being) Nipple massage stimulates production of oxytocin, inducing contx. Procedure: warm wash cloths on nipples. Desired outcome: negative test. Advantages: non-invasive Disadvantages: can take time, privacy, uterine issues. Interpretation: no decels w/ contx
Presence of normal biophysical activities shows CNS fully functional & Baby not hypoxemic; may be done weakly to indicate health…if things don’t look good a c-section may be scheduled. Ultrasound and external fetal monitor used.
Biophysical profile (BPP) 5 criteria (2 pts each if 1 or more episodes in 30 min., ea lasting =/> 30 sec) (normal is 8-10) Fetal breathing; Fetal movement: 3 limb movements; Fetal tone: open hand, finger to thumb extension, hand return to closed fist; BPP; Amniotic fluid volume adequate for gestational age (8-18cm).
Oligohydrmanios amniotic fluid less than 2 cm
Polyhydramanios amniotic fluid greater than 8
Fetal heart reactivity: nonstress test (performed before BPP) reactive is a Normal result
Doppler Blood Flow Studies Doppler Velocity –ex: resistance in the arteries and vein in the umbilical cord; Abnormal flow is associated w/ placental insufficiency, maternal smoking, some chromosomal anomalies
Amniocentesis- (Ultrasound guided procedure) –transabdominal puncture of amniotic sac; fluid contains fetal cells; Done after 14-16 weeks when sufficient amnio fluid; Complications include trauma/death of fetus in 1/300 cases (Rh- incompatiabilites, gentic, lung maturity, neuro tube defects)
Biophysical profile AKA (BPP)
MSAFP also called AFP is a screening that examines alpha-fetoprotein in the mother's blood during pregnancy.
Nursing Implications for amniocentesis Void, baseline vs, FHR, prepare patient; When needle goes in, avoid valsalva; 10-20 mls withdrawn; Monitor x 30 min. FHT, contrax; Rhogam to RH- after amnio (suppress antibody formation)
Color of normal amnio fluid? clear
Amniocentisis Findings Color: yellow = Rh isoimmunization, bili green = mec. Stain, red =blood contamination
Amniocentisis Findings Fetal Lung Maturity: L/S ratio > 2:1 (protein components of lung enzyme surfactant). Lecithin/Sphingomyelin :Appears after 24 wks; @ birth ratio is >2:1; Phosphotidiglycerol: Present, Appears 35 wks + = fetal lung maturity
Amniocentisis Findings Chromosomal analysis from shed skin cells
Biochemical Assessment (Three techniques ) Percutaneous Umbilical Blood Sampling; Maternal Blood Assessment (MSAFP aka AFP); Chorionic Villus Sampling
Rh incompatibility Rh negative- mom and Rh positive baby
Urine Frequencyin pregnancy. . . til uterus out of pelvis 1st tri and after fetal head falls (lightening) last 2 weeks
Percutaneous Umbilical Blood Sampling (From fetal umbilical vein with ultrasound guidance) Can assess: CBC – determine when to transfuse in utero; Direct coombs (test for antiglobulins in RBCs used to diagnose hemolytic anemias & isoimmunizaton – Rh disease); Blood gasses; karotyping (shows chromosomes)
Nursing Implications in isoimmunizaton – Rh disease Give Rogam to Rh negative moms
Maternal Blood Assessments AFP (Alpha-Fetoprotein) Produced by fetal liver; Elevated = neural tube defects (open spinal cord); Decreased = chromosomal defect (Down’s)
Chorionic Villus Sampling determine chromosomal abnormalities; Can be performed as early as 10 wks; Removal of small tissue specimen from fetal portion of placenta while placenta is low in uterus; High risk (1/200)
Danger Signs of Pregnancy Vaginal Bleeding; Vomiting; Chills, Fever; Fluid Gush; Abd/Chest Pain; Fingers/Face Swelling; Vision change; Leg swelling or pain; Severe Headache (vaso-spasm)
Termination - prior to fetal viability (20 weeks)
Spontaneous abortion (“miscarriage”)
Elective abortion (“planned”)
Therapeutic abortion (“medical reasons”)
Lab Values in Pregnant Women Blood: CO ^ 25-50 %; BP V in 2nd tri: returns to pre-pregnant levels by 3rd tri; HR ^ by 10 BPM; Plasma volume 2400cc -> 3700 cc; Blood volume 4000 cc -> 5600 cc; FBS mg/dl 70-80 (non-pregnant) can drop to 65; Hct treat <30 ( physiologic anemia d/t expanded volume of plasma)
Most common pregnancy infection UTI (can result in early labor)
Laboratory Values in Pregnant Women: Urine GFR ^ 30-50%; Renal plasma flow ^ 25%; BUN 10-20 usual is < 15 in pregnancy; Plasma creatinine V; Bladder capacity 1330cc -> 1500cc; ureters ^; Urine glucose positive in 20%
Maternal, Fetal and Neonatal Infection: Related Nursing Implications UTI most common pregnancy infection (10%! premature del.); Uterine infections: PROM, chorioanmionitis; Neonatal infections: leading cause of perinatal infection is Grp B strep (GBS) – PCN to tx… Can be life threatening
Group B strep (GBS) can be fatal to fetus or neonate…treat with penicillin
Infections to fetus can cause physiological damage to babe during 1st trimester
SAFE antibiotics during pregnancy Amox; Ampi; Cephlosporins; PCN (pregnancy class B)
UNSAFE antibiotics during pregnancy Sulfas - near term bind bilirubin; Tetracycline- stain teeth of neonate; Quinalones – Cipro; Macrobid –near term increases risk of hemolytic dz of new born
Infection TORCH T = toxoplasmosis; O = other; R = rubella; C = cytomegalovirus; H = herpes
Toxoplasmosis infections….The cat is the only definitive host. Transmitted to humans through ingestion of raw meat (of animals who have ingested cat feces) or hand to mouth from touching used cat litter. In U.S. 50-85% pregnant women are at risk for infection. Mild sx’s of fatigue & lymphadenopathy; Tx spiramycin or sulfa – not great results; fetus: -retinal & CNS anomalies. May not be noticable at birth.
Infection to fetus: Other: hepatitis Hepatitis B – High transmission rate to fetus; Infection control: bathe babies immediately. Infants born to infected moms receive immune globulin & Hep B vaccine immediately; Hepatitis C – 5% through exposure at birth
Infection to fetus Other: Syphilis (mandatory to screen in pregnancy) -Primary & secondary stages of untreated syphilis transmission rate is almost 100% resulting in abortion, hepatomegaly, skeletal deformities, splenomegaly, pneumonia, skin lesions, & later ( p 2 yrs) neurosyphilis
VDRL syphilis screening
Infection in fetus: Rubella/ German measles.. Can result in spontaneous abortion, congenital anomalies (cataracts, hearing loss, glaucoma); vaccine up to 3 months preconception or during postpartum, but never during pregnancy. Use contraception up to 3 months
Infection in fetus cytomegalovirus (CMV) Transmission is through all bodily fluids (including respiratory). Affects 1%; Can cause mental retardation or congenital deafness. Seriousness of the disease varies. 15% are gravely affected. Treatment: No vaccine. Use ganciclovir or vavlganciclovir.
Infection herpes type 1 oral; type 2 genital; may be fatal to the neonate. Cesarean indicated if mom has active lesions
Smoking Risks Growth restriction d/t vasoconstriction & “aging” placental calcifications & placental insufficiency; Smaller for gestational age, deficits in intelligence; SIDS ^ x3; low lying placenta, w/drawl sxs
Ethanol use in pregnancy No safe level of consumption. Degree of damage is r/t individual woman’s ability to metabolize alcohol in the liver, not necessarily on how much she drinks
FAS –(ARBD) 1/1000 births - craniofacial deformities, small eyes, thin upper lip, upturned nose, flat midface, low set ears, retardation-FLK… counsel and educate on effects and treatment options
FAE – (ARND) Alcohol related nerve defect. less severe than FAS.. counsel and educate on effects and treatment options
Fetal Alcohol Syndrome Manifestations Feeding problems; Distinctive facial features: thin upper lip, low nasal bridge, short nose, flat midface; Congenital heart disease; CNS dysfunction; Withdrawal sx: irritability, tremors
Alcohol Abuse and the Newborn Nursing Interventions Protect infant from injury (pressure ulcer); meds – benzodiazepines; Monitor fluid therapy; V stimuli; ) Support for parents – difficult infant; + UA report to DSHS.
Pregnancy class A- studies have been done on pregnant women and the adverse effects are known and benefit outweighs risks
Pregnancy class B- animal studies but not many studies on pregnant women
Pregnancy class c- animal studies with adverse effects on pregnant animals
Pregnancy class d- increased risk of effects
Pregnancy class x- studies show significant risks that always outweigh benefit.
Drug Use Risks & Appropriate Nursing Actions Teratogenic effect (prescribed, illegal, or OTC- over the counter); Know FDA Pregnancy Categories; Greatest effect between day 15-60, critical periods
Illegal drugs tend to cross placenta readily d/t low molecular wt so baby gets concentration of 50% of mom’s dose Nursing implication: stop or reduce, offer treatment at EVERY visit
Drug Dependent Mother typical profile: younger age, altered life style w/ resources going for drugs, late seeking prenatal care, alt. nutrition; causes 4-5% of fetal anomalies; Risk of HIV, Hep B&C, prostitution, STI’s
Drug Use Risks: Cocaine… Restlessness, excitement, ^ RR, cardiac & BP (d/t vasospasm); HF r/t vasoconstriction; placental abnormalities, abruptio, premature labor, fetal death, gastroschisis Infants may have cranial bleeds, emotional & learning deficits, tremors, irritability & muscle rigidity; Can be detected in mec or urine. Best is w/in 24 hours but present for 1 week. Collect all meconium, if ordered. Need about 5 cc.
Drug Risk Use: Meth ^ RR, HR & BP (d/t vasospasm); HF r/t vasoconstriction; placental abnormalities, abruptio, premature labor, death, gastroschisis; cranial bleeds, learning deficits, tremors, irritability & muscle rigidity
Drug Risk Use: Marijuana Marijuana/Hashish: short term memory loss in adults & < intelligence in kids, IUGR (Intra uterine growth restriction), SGA
Drug Risk Use: Narcotics - fetal opiate dependence Small for gestational age Drug Dependent Infant..Manifestations of withdrawal
LGA OR SGA or AGA large is >90% small is < 10%.... Appropriate for GAgestinal between 10% & 90%
Nursing Interventions for Substance Abuse and the Newborn Prevent overstimulation – possible seizures – dark, quiet environment; Supportive care – swaddle, hold firmly, pacifier; Meds as ordered; Small frequent feedings
Pregnancy causes significant metabolic changes…Hormonal changes of pregnancy results in insulin resistance; Purpose of insulin resistance is to prevent glucose from dropping to dangerous levels. HPL (human placental lactogen) < effects of maternal insulin; Estogren is an insulin antagonist; Progesterone may < insulin effectiveness; Cortisol ^ gluconeogenesis causing maternal hyperglycemia
-Gestational Diabetes- GDM first show signs of DM during pregnancy are called gestational diabetics; Incidence is 7% of all pregnancies; likely revert to non diabetic; 40% of GDMs will develop DMII later in life
Why screen for diabetes? To prevent macrosomia, LGA, neonatal hypoglycemia, hyperbilirubinemia, polycthemia, shoulder dystocia and traumatic birth injury
GDM screen between weeks 24 & 28 wks. Measures FSBS after 50 gr. of oral glucose challenge – is a random test, no preparation, commonly called the One Hour Glucola Screen; Screen sooner if have risk factors (1st prenatal visit)
GDM risk factors (BMI> 25, Fam Hx, multip, prev. GDM or LGA baby, American Indian or Hispanic)
GDM glucola test Results: normal <140. If over 140, will do diagnostic test of 3 hour GTT – glucose tolerance test. Prep for 3 hour GTT – fasting (some use a special diet for 3 days before)
Glucose tolerance test (GTT) Draw FBS. Pt. drinks 100 gr. of glucose & blood is drawn Q1hr for 3 hrs after glucola. If 2 or more values are elevated, pt. has GDM. FBS< or equal to 95; 1 hour >180; 2 hr > 155; 3 hr >140
GDM most are controlled with Diet controlled… GDM Blood sugar goals – FBS 60 – 95 mg/dl; 2 hour PP < 120
GDM Blood sugar goals – FBS 60 – 95 mg/dl; 2 hour PP < 120; Most will be diet controlled. If unable to control BS with diet and exercise, will need hyperglycemic agents.
Oral hyperglycemic agents… -glyburide – used since 2000. Not FDA approved for use in pregnancy yet. Studies show no statistical difference in outcomes between use of insulin or use of glyburide in pregnancy. No increase in fetal anomalies or death. Maternal blood sugar is adequately controlled (currently class C). -Metformin –being used in clinical trials
Gestational Diabetes Antenatal Care & Fetal Surveillance -nutritional counseling w/ dietitian; -teach glucose monitoring & FSBS; educate re: fetal effects & increased risk of future DM; fetal movement counts; -NSTs & Ultrasound for growth in 3rd trimester; exercise; encourage breastfeeding; anticipate induction at 38-40 wks; may elect c-section if EFW 4500 gms >
Poor glycemic control in pregnancy…1st tri. ^ risks birth defects d/t uncontrolled maternal acidosis interfering w/ neurolologic development of fetus; 2nd & 3rd tri. Ketoacidosis can occur between meals; ^ risks of macrosomia..or opposite can occur: Mom w/ vascular changes r/t DM may have compromised uteroplacental circulation. < O2 to fetus may contribute to IUGR, resulting in SGA infant &/or fetal death.
Macrosomia 25-42% babies grow large in GDM because they make more insulin to deal with more glucose coming their way…Insulin acts as growth hormone.
Some oral hypo. agents are teratogenic. Up until recently, insulin has been the only agent used during pregnancy.. If DM woman on oral hypo. agent and plans pregnancy, have consult MD to probably change her medication.
Insulin dependent women are likely to need larger doses as pregnancy advances decreases need for insulin in 1st trimester…but the glucose will rise in 2nd and 3rd tri d/t HPL; Estogren; Progesterone; & ^ Cortisol
Avoid hyperglycemia: maternal acidosis causes fetal anoxia r/t inability of fetus to use O2 when acidotic (diabetic ketoacidosis)
Fetus care in Pregnant DM Mom: Recommendations –Maternal Alphafetoprotein @ 15 wks; US @ 7 wks to for viability & @ 18 wks to for abnormalities & monthly after 28 wks for AFV & growth Weekly NST’s @ 32-36 wks; Creatinine CL each trimester to determine intact vascular system (kidneys); Serial HbA1Cs; Consider steroids (lung maturity); Kick cts daily @ 24 wks; BPP; Delivery @ 36-38 wks if needed
Diabetic Intrapartum Strenous muscular contx ^ cellular use of glucose, depleting glycogen stores; Frequent fsbs used to control DM during L&D; rapid acting used.
Diabetic Postpartum: Insulin requirements fluctuate during immediate pp; Factors associated w/ delivery tend to ^ bg levels & ^ insulin requirements ( Stress, trauma, infection, surgery); Birth also reverses diabetogenic hormonal changes & V insulin requirements…higher risk of hypoglycemia during 24-48 hr after delivery; Some diabetic women may require no insulin during this time.
Diabetic Postpartum Breastfeeding: does insulin enter breast milk? Insulin does not enter breast milk; Breast feeding may < insulin requirements.
Gestational DM Usually subsides within 6 wks after delivery.
What recommendation is made to breast feeding mom’s d/t risk of hypoglycemia in the nursing infant? nurse on demand is the recommendation
Diabetic Women, Postpartum: Contraception Considerations OCs ^ blood glucose by increasing progesterone which interferes w/ insulin activity; OCs contain estrogen which ^ lipids, cholesterol & clotting; IUD = no increased risk of PID (pelvic inflammatory disease) in diabetics
How soon after birth do you check bs of babe? (30 min) Pancreas programmed to produce ^ insulin d/t maternal hyperglycemia in utereo. @ Birth glucose supply interrupted-yet neonatal pancreas continues to produce insulin @ ^ rate.
In neonate hypoglycemia treat BS less than <40 treat with D10W IV or sometimes oral. Brain damage can result from < brain glucose. Sx: tremors, jitters, lethargy, convulsions
Why do LGA babies warrant same assessment as SGA infants? babies of diabetic mom can be large or small…check blood sugar in both.
Name the underlying problem in an Infant of a Diabetic Mom.. Immature reflexes; < Respiratory drive; Fx clavical, paralysis r/t nerve damage; ICP r/t head pressure; Hyperbilirubinemia r/t bruising Cyanosis; Rebound hypoglycemia; Asymmetrical motion; unresponsive pupils, vomiting, bulging fontanels, high pitched cry; jitteriness, lethargy, uncoordinated eye movement & seizure….(diabetic baby)
Definition of preterm labor: occurs btw 20 to 37 weeks of gestation…8 or more contx/hour or PROM or 2 cm dilated, 80% effaced and 8 or more contx/hr
Etiology of preterm labor (9% of US births) - 50% etiology not identified
Risk Factors for Preterm Labor Chronic pyelonephritis; Incompetent cervix; Multiple gestation; Hx premature births; sepsis/infection; Placental- previa/ abruption; Cervical surgery;
Betamethasone (Celestone) promote lung develop. Begins to be effective when given 30-32 gestation.
Fibrinectin test for preterm labor… a swab of vaginal fluid that shows a protein in the vaginal mucus
Nursing interventions/treatment for preterm labor Bed rest & hydration; Assess vitals, FHR, contx pattern, sx of infection; suppress uterine activity; support; Betamethasone (Celestone) (lung develop).
In preterm labor If membranes intact, FHT good variability, no bleeding, cervix < 3-4 cm and effacement < 50%, will try to stop labor.
Toxolytics - ritodrine or terbutaline Terbutaline: Label Change - Warnings Against Use for Treatment of Preterm Labor; Nifedipine (Ca Channel blocker); MgSO4; (preterm labor & seizure); beta adrenergic blockers- B-2 receptor sites on uterus, bronchial & bld vessels.
Before administration of tocolytics for preterm labor Assess baseline VS, FHT, HCT, serum glucose, K+, Na, Cl & CO2. Maybe an EKG; Assess: pt meets preterm labor criteria; no vaginal bleeding; afebrile
Ritodrine & terbutaline tocolytics: Ritodrine (no longer available in U.S. as of 2/09), terbutaline (‘2011 negative research),
Specifics of tocolytics & preterm labor…MgSo4, indomethacin (Indocin), nifedipine (Procardia)….Lateral recumbent; Quiet; Report P>120; Report BP < 90/60, chest pain, crackles, dyspena; < HCT (hemodilution) preceeds pulmonary edema so monitor HCT, lytes; Strict I & O. IV <100cc/hr; Prior to stopping IV meds, give po med 30 min. before d/c IV to maintain blood levels; Resp. dep. w/ MgSO4; Tachy w/ terbutaline & ritodrine
Differentiation between Hypertensive Diseases of Pregnancy Chronic Hypertension: 140/90 before 20 weeks of pregnancy (or before preg.) & persists afterward…Hypertensive disorders of pregnancy after 20 weeks gestation.
Mild preeclampsia: 140/90 or higher, or SBP >30 mmHg above first trimester baseline or DBP > 15 mmHg above first trimester baseline; 1+ proteinuria; generalized, pitting edema; progressive, excessive wt. gain
Severe preeclampsia: 2 resting BP readings 6 hr apart 160/110 or higher; 3-4+ proteinuria; massive generalized edema; oliguria; CNS irritability (headache, blurred vision, hyperreflexia).
Lab changes associated with preeclampsia –monitor Hct/Hgb, Creatinine, Plts, serum uric acid
A Variant of severe preeclampsia is HELLP syndrome (Rare (1/1000) but life threatening) - Hemolysis of RBCs Elevated Liver enzymes (liver damage) low Platelets (< 100,000); HTN leads to multi organ failure through poor perfusion to organs d/t vasospasm; DIC; RT epi-gastric pain, N&V
Tx of DIC in preeclampsia – blood products i.e. fresh frozen plasma or platelets.
Eclampsia Seizure after 20 weeks of pregnancy with pre-eclampsia and not attributable to another cause.
Risk Factors for acquiring hypertensive disorders of pregnancy hypertension before pregnancy; GDM or DM; high BMI; multiple gestation; Hispanic ethnicity
Nursing implications for preeclampsia, eclampsia, gestational and transient hypertension Conservative treatment : bed rest; antihypertensives – labetalol
Labor implications for preeclampsia, eclampsia, gestational & transient HTN… Assess VS & BP q 15 min when critical, then 1-4 hr; Status can change quickly; BP (= perfusion); Assess edema -I & O (qhr if on Mag), daily wt; CNS irritability- HA, vision changes, DTRs; proteinuria (dip urine); EFM; CBC; epigastric pain (d/t < liver perfusion); Seizures; Bedrest. Lie on left side; adequate fluid & protein intake; LFT & kidney labs
Who gets MgSO4 everyone with PIH…prevents seizures and can stop labor at higher doses…monitor labs (MGSO4 level 4-7)
MgSO4 -used to prevent seizures..SE: CNS depressant. May have to stabilize & deliver preterm if severe or C-section (if unable to tolerate labor) Monitor serum levels 4-7; deep tendon reflexes (hypo or hyper) & RR & Kidney function
Pre-adminstration of MGSO4 IV slow push – (piggybacked); Anti-HTN If DBP > 110; Absence of deep tendon reflexes* early indication impending MgSO4 toxicity (assess baseline and withdraw MGSO4 if loss of reflexes)
How long after PIH must a woman be watched for at least 24 hrs
MgSO4 therapeutic range 4-7; Serum Creatinine: as serum levels approach 1 mg/dl the kidney does not excrete magnesium so monitor Mag levels
MgSO4 given as seizure prophylaxis… interferes w/ release of acetylcholine @ synapses (V neuromuscular irritability; V cardiac conduction; V CNS irritability); V RR; Monitor Mag levels Q 6hrs (range= 4 -7); I&O 30 ml/hr; Continue MgSO4 postpartum for 12 – 24 hours, as ordered; Assess for abruptio placenta.
Antidote for MgSO4 is calcium gluconate: keep @ bedside (give IV push, slowly over at least 3 minutes)
Problems w/ force of labor (4) Hypotonic; Hypertonic; Uncoordinated; Other
Dystocia Dysfunctional Labor Patterns or difficult Labor
Hypotonic labor – not enough contx strength: Cause… Analgesic before 3-4 cm dilation; Cephalopelvic disproportion (CPD); Stretched uterus (polyhydramnios, grand; multip)… , ^ chance of infection if ROM…Tx – oxytocin, nipple stim., shower, positioning
Hypertonic labor – Resting tone > 15 mmHg, measured w/ IUPC; Tachysystole- >5 contx in 10 min; Causes: infection/chorioamnionitis; zero relaxation of myometrium; more than one area in uterus being stimulated; Tx: Monitor, turn mom to L side, O2 & hydrate; Rest uterus w/ morphine or Terb. Off label; Stop oxytoxin or start small amount; Assess cervix for rapid dilation; Reassure mom/breathing to cope; Quiet environment
Effect of hypertonic labor (when uterus does not relax between contx, < O2 to placenta may result. This can bring about hypoxic fetus.).
Uncoordinated labor (contx not following one pacer) Tx - Oxytocin used to regulate, or other non-pharm. methods to stimulate contractions
Other factors associated with uterine dystocia Extension or military position of fetal head; Rigid cervix; Maternal exhaustion; Primigravida
Prolonged Labor: Prolonged Latent phase: Greater than 20 hours –options for Tx : Supportive Tx w/ rest; glucose to combat fatigue; relaxation techniques; reassurance; tx pain – narcotics; induce
Prolonged labor: prolonged active phased: Protracted Freidman’s curve; Labor Arrest: 2 or more hours w/ no progress in labor…TX: C/sec
the “4 P’s” preparation, powers, pelvis, psyche
Prolonged labor or arrest of descent: Minimal or no descent p 1 -2 hours of pushing , Anticipate Post Partum Hemorrhage, prepare for shoulder dystocia… Tx – c-sec
Precipitate Labor (emergent situation) (Don’t stop birth ) < 3 hrs; Risk fetal subdural hemorrhage;; Risk of moms laceration & hemorrhage… monitoring/communicate w/ MD; stay w/ pt.; Encourage panting w/ contx, side lying; guide fetal head during birth
Inversion of Uterus (Emergency) Cause: may be fundal pressure & traction applied to cord.
Abruptio Placenta (1:75-90 births) 15% of all perinatal deaths…( Associated with: cervical ripening agents & Pit, trauma, pre-eclampsia, eclampsia, cocaine, multiparity) premature sep. of placenta. (painful) uterus/abdomen & vaginal bleeding (concealed bleeding possible); Rigid abdomen; Shock-diaphoretic; Nonreassuring fetal signs; Sudden onset, continuous contx, or irritable pattern
Treatment for abruptio placenta – depends on maternal & fetal status, usually prepare for C/S & treat blood loss.. Tell patient what is going on; Observe for shock; Monitor VS, FHR; Assess for DIC*, infection, anemia
Possible Emergency: Macrosomia (Fetal weight greater than or equal to 4500 gms ) risk is shoulder dystocia – might see “turtle sign”; Sequelae –Erb’s palsy, hypoglycemia, rescusitation; when stuck, useMc Robert’s position OR - Hands & knees position
McRoberts maneuver: Lower bed flat; Grab legs back as far back as they will go; Pressure over symphysis pubis, rotates shoulder under symphysis (suprapubic pressure)
DIC Disseminated Intravascular Coagulation Bleeding & clotting occur simultaneously; Microemboli everywhere use up all clotting factors..Then start bleeding everywhere; Give platelets fast! (probable renal damage & Long recovery)
Placenta Previa (incidence <1%) . Risk Factors (Older mothers; Multips; tobacco use)…Placenta attaches low in uterus, either near or covering the cervical os…. manifestations (HEMORRHAGE W/O PAIN.) Painless bright red vaginal bleeding (may be intermittent); Abdomen is relaxed, non tender, normal tone; Most are discovered on US & > 90% will “migrate” by end of 2nd tri, as uterus enlarges..
Placenta Previa Types (3) Total – completely covers cervix; Partial – partial covering of cervical os; Low lying – near to cervical os
Treatment for placenta previa (Do not do vaginal exams on known or suspected previas ) Tx/Varies from bed rest to immediate C-section, may need blood transfusion. Observe for hemorrhage. If hemorrhaging, prepare to treat for shock; Weigh pads, vitals & FHR. Be ready for emergency c-section;
Amniotic Fluid Embolism (1:15,000 – 1: 20,000)…Description: as placenta separates there is a possibility of amniotic fluid with debris, entering maternal circulation. High mortality – 61%. …Manifestations V LOC, RR distress, Circulatory collapse, hemorrhage, corpulmonale, DIC; Confirm diagnosis –other pos. for resp. arrest? (epidural?); O2; lat –side; IV fluids to dilute; Blood replacement; c-sec; Catheterize, shock
Ruptured Uterus (Rare).. May be spontaneous or d/t trauma or med., May be caused by obstruction or weakness of uterine wall, Scars may cause weakness. (previous c/s), Fetus & amniotic sac may be expelled into peritoneal cavity. S&SX: Ab. pain; Hemorrhage; Shock; Abrupt reversal in station; Fetal Distress Tx: Change position; Correct hypotension; Elevate legs; ^ rate of IV; DC oxytocin ; O2 @ 10-12 L/min; C-sec if not fully dilated
Prolapsed Cord (Directly after ROM, gravity moves cord down ) contributing factors: Unengaged presenting part, Breech or transverse, Long cord (> 40 )... Manifestations: . gush amniotic fluid causes cord to descend..TX: PREVENT HYPOXIA ( > 5 min = CNS damage); W/ sterile gloved hand hold presenting part off cord and stay there until delivery; Sims position or Trendelenburg or knee chest; C-section
0+ reflex means impending MGSO4 toxicity
Meconium Stain Definition – fetal defecation while in utero. May occur in labor with fetal distress or before labor with a fetal “insult”. hypoxic event = fetal distress -> asphyxia
Yellow Meconium = thin mec stain
Green Meconium = thick meconium stain
Asphyxiated newborn has prolonged hypoxia; acidosis (metabolic & respiratory); hypothermia; hypoglycemia
Manifestations Meconium Stain – will aspirate into lungs --à course rales, tachypnea, barrel chest, nasal flaring, retractions…Notify RT.. PCP or R.T. will DeLee suction before newborn takes 1st breath
If mec aspirated, ^ risk for pneumonia/infection or “meconium aspiration syndrome” or PPHN, “persistent pulmonary hypertension” d/t low O2 sats and persistent fetal circulation (reverts to inutero circulation (ductus arterous)
Anticipate full resuscitation for severely asphyxiated newborn…. Be prepared to treat hypoxia, hypothermia, hypoglycemia and hypoperfusion (volume); Allow for multisystem insults; Anticipate drugs will be ordered to improve myocardial function and improve renal perfusion. Example dopamine.
Pitocin, “pit” = oxytocin, a synthetic hormone normally produced by ant. pituitary gland, stimulates labor contractions.
Pitocin use in labor begin or augment labor; IUGR or demise; PROM (no labor); Postmature > 42 weeks; Maternal medical problem i.e. DM, hypertension; Multip w/ hx precipitous labor who lives far away from hospital
Other commonly used agents to induce or ripen cervix Prostaglandins –Cervidil, Prepidil, Cytotec; AROM; Laminaria – Foley, seaweed; Enemas, sex, nipple stimulation, stripping membranes
What to Assess when inducing labor Fetal position – longitudinal lie; Fetal age; Lung Maturity; Ripe cervix: Bishop’s Score >7 ripe; Engaged; No contraindications: +HSV, CPD, previous c/s, previa, ominous FHR pattern
Increased RISK for the need to be induced Multiple gestation; Polyhydramnios; Grand parity; Maternal age >35
Essential Knowledge about Pitocin Measured in mu = mili units; MD orders: start with 0.5 mu/min to 3 mu/min; ½ Life 10-12 minutes (IV) (we used to believe 3 min)
Pitocin Assessment Ideal Contx=q 2-3 min; strength not > 50 mm Hg (40-90 mmHg); Duration not > 70 sec (40-90 sec); No tachsystole & good resting tone; Complication: rupture& H2O intox, Hypo TN; Monitor FHT& contx, q 15 min..
Facts about the nature of pitocin….Pit is an antidiuretic: effects on the mom ( Check for H20 intoxication; s/s H/A, vomiting, seizures; Check for I & O; Limit IV fluids to < than 150 cc/hour total) effects on baby (hyperbilirubinemia/ jaundice d/t change in fluid status); effects on the post p. mom: (Post partum hemorrhage; < Breastmilk d/t change in fluid status; Pit causes hypotension. Check BP q hr & every ^ in Pit
Nonreassuring FHR Patterns: Fetal heart rate pattern that indicates the fetus is not well oxygenated & requires intervention.
Normal reassuring FHR Patterns Baseline FHR in normal range 110-160 BPM w/variability (controlled by autonomic CNS); Accelerations w/ fetal movement; Early decelerations
variable decelerations – d/t cord compression, can occur with or without contx. Vary in duration (< 60 seconds), depth and timing. May be due to baby on cord and a postion change may help.
Abnormal Nonreassuring FHR Patterns Decreased variability, late decels, Severe variables, Bradycardia - < 110 bpm for > 10 mins; Tachycardia – baseline >160 bpm for at least 10 min.
LATE decels – a gradual V & return to FHR baseline associated w/ uterine contx. Gradual in onset (>30 secs from onset to nadir. nadir occurs after peak of contx.) Commonly decreases by not more than 10 – 20 bpm & rarely to 30 – 40 bpm below baseline. Fetal tolerance is assessed by eval. of baseline rate, variability & presence of accels.
Utereoplacental insufficiency - Examples: Hypotension, diabetes, LUPUS, HTN, Smoking, placenta problems , poor maternal nutrition, Hyper or hypoventilation, anemia, Uterine hyperstimulation , multiple gestation
Treatment of Late Decels (reflects uteroplacental insufficiency) stop or < oxytocin; put in Left lateral position, give O2, start IV fluids, report to MD, - prepare for cesarean if not corrected.
Severe variables etiology – cord compression…Vein compresses –> stim. of baroreceptors causes ^ in HR d/t V in BP… the stiffer arteries compress & baroreceptors detect ^ in vascular resistance As contx strenthens, vagal response is triggered & HR falls; Depth of variable is reflex mediated & NOT related to hypoxia; >60 sec long, prolonged return to baseline, V variabililty, & >60 bpm in depth
Severe variables interventions check for cord prolapse, stop or < oxytocin, change position of mom (hands and knees), give O2, start IV fluids in prep for surgery, report to MD, perhaps amnioinfusion, prepare for cesarean if not corrected.
Bradycardia - < 110 bpm for > 10 mins.; If associated with decreased variability and late decels – impending doom – is a sign of severe hypoxia -associated with fetal heart block & Down’s in fetus
Tachycardia – baseline >160 bpm for at least 10 min.; sympathetic nervous system is stimulated, usually with accompanying decreased variability Maternal causes– fever, infection, meds., endogenous adrenaline, hypoxemia, anemia; Fetal causes- infection, compensating for hypoxia, prematurity, congenital anomalies
Abortion –medical or surgical termination of pregnancy before the fetus is viable & capable of extrauterine existence, usually less than 21-22 weeds gestation OR when fetus weighs less than 500-600 grams.
Miscarriage (spotaneous abortion) – loss of pregnancy that occurs naturally without interference or known cause; occurs in 15-20% of pregnancies, usually in the first trimester.
SAB: initials indicating spontaneous abortion.
Fetal demise (fetal death) death of developing fetus after 20th week of gestation
Stillborn – a fetus that is born dead
Neonatal death – death of infant between birth & 1st 28 days of life
Causes of Miscarriage are Unforeseen, Unpreventable…genetic errors = major cause 1st 12 weeks of pregnancy; Low progesterone (maintains pregnancy); uterine structure so egg cannot implant properly “Incompetent cervix” opens prematurely 2nd or early 3rd trimester – treatment is “cerclage” with next pregnancy; “Blighted ovum” abnormal development of egg d/t chromosome or genetic problem ; Infections – STIs, UTI
D&C if miscarriage “incomplete” or “inevitable” to prevent Prolonged bleeding or Infection; Misoprostol – Cytotec for “missed” AB and client prefers not to wait for SAB or have D&C; Wait for spont. expulsion, while monitoring closely for s&sx of infection and hemorrhage
Ectopic Pregnancy – out of place’ Implantation in fallopian tube (95%) or on ovary, on cervix, or on broad ligament of abdomen; Rapidly growing embryo & placenta place pressure on structure & rupture may occur (10-12 wks)
Causes of ectopic pregnancy Adhesions on fallopian tubes after infection (STIs –Chlamydia); surgery adhesions; Fibroid tumors; IUD – Mirena, Paragard – DO NOT CAUSE Ectopic if you get pregnant w/ one in place, more likely to be ectopic
Signs/Symptomsof ectopic pregnancy Pain (pelvic), sometimes referred shoulder pain; Hypotension & syncope; Vaginal spotting or bleeding into cul-de-sac (peritoneal cavity behind the vagina, anterior to rectum).
Tests of ectopic pregnancy May have Neg. Urine Preg. Test d/t low levels of HCG. Need to do serum PT – not urine; REMEMBER – every woman with a uterus & pelvic pain & bleeding, is pregnant & R/O ectopic.rwise.
Clinical Management ectopic pregnancy Remove- either surgical or medical (methotrexate) if early enough; When possible, repair fallopian tube (scar tissue predisposes to future ectopic pregnancy); Psychological support –
Causes of Fetal Death: Abruption; Prematurity; Cord accident; Genetic anomalies; Exsanguination; infection; hypoxia; isoimmunization
Clinical Management of Fetal Death: signs are changes in fetal movement patterns; Once dx is made, tx involves artifical induction (misoprostol, Cytotec, Prostaglandins -E2 or F2 alpha, Pitocin if in 3rd tri) – monitor coagulation labs
Premature Newborn Definition: Gestational age of less than 37 weeks regardless of weight
Assessment of gestational age – Ballard, Dubowitz form page 525
Implications for nursing in premature birth at least one person at the birth skilled in neonatal rescusitation (R.T., Peds, MedStar); prepare for possible transport; limitations of Level II and III hospitals
1st breath initiated by combination of - cold receptors- chemoreceptors that detect lowered PO2 & increase in PCO2, -stimulation – light, noise & -pressure changes
Aveoli expansion occurs d/t fetal lungs are full of fluid. pulmonary blood vessels & constricted in utero & blood is shunted from from the pulm. Artery through ductus arteriosis into the aorta.. at birth, fluid absorbed into lungs & replaced by air; umbilical arteries & vein constrict & ^ systemic BP leads to closure of foramen ovale; ^ in O2 allows pulm. vessels to relax & ductus arteriosis constrict.
At term, may take up to 10 mins. for 02 saturation to reach > 90%
Premature Newborn Lung expansion limited by neonate’s heart proportionally taking up ^ space; V number& functioning of alveoli – V surfactant; immature brain and decreased resp. drive & weak muscles make spontaneous respirations difficult & harder to clear birth fluid
Limited lung expansion in the premature compromises cardiac system Closure of ductus arteriosus depends on free blood flow through the pulmonary artery & good oxygenation of the blood; O2 sats > 95% may be too high for babes <32 wks d/t fragile capillaries
Assessment of neonate who has difficulty establishing respirations at birth: . Observe closely for cardiac murmur & PDA
Preemies are @ risk for Respiratory Distress Syndrome d/t lack of surfactant leads to atelectasis, loss of function of residual capacity, and ventilation perfusion problems.
If develop RDS nurse will see Retractions –sub, inter and suprasternal; Nasal flaring; Expiratory grunt – cyanosis, crackles; Tachypnea, apnea; “ground glass” in x-ray..Monitor - HR, color, BP, P, O2 sat, acid/base balance
RDS Treatment- Oxygenation – NC, hood, CPAP; May need mechanical ventilation; Surfactant; Umbilical cath – for meds and blood draws
Preemies are @ risk for Circulatory Issues Patent ductus arteriosus (PDA) is common (Tx indomethacin, ibuprofen (NSAID); Fragile vessels: Retinal vessel damage –ROP & Intraventricular hemorrhage -IVH
NEC = necrotizing enterocolitis – 2- 5% NICU patients Acute inflammation of GI mucosa leading to perforation and peritonitis
Associated Factors in NEC in the premature infant Some hypoxic event – intestinal eschemia or Substrate in lumen – formula, meconium or Bacterial Infection or Prematurity
NEC in Premature Newborn: GI assessment Increasing abd. distention (measure abd girth); - Zero bowel tones; - Bloody stools - guiac +; Emesis w/ feeding; ^ residuals after each feeding; - x-ray shows bowel loop distention - air in intestinal wall, abd cavity
NEC in Premature Newborn: Management Stop feedings; GI rest – baby Salem sump tube; Guiacs; assess bowel tones, vs, abd girth q 4 hr; Antibiotic therapy; Surgery if needed . . .colostomy. Greatly > mortality
Normal glucose level for infant greater than 40
Hypoglycemia in Premature Newborn (Preemies are @ risk for Hypoglycemia) abnormal chemstrip < 40; . Sx - jittery, hi-pitched cry, cyanotic lips
Nursing Interventions for hypoglycemia in the premature newborn provide calories – breastmilk, D10W, formula, depending on developmental status, respiratory status and provider orders & monitor glucose levels
Hypothermia Etiology in Premature Newborn V in temp causes ^ metabolic rate which ^ 2 demand; Cells become hypoxic causing acidosis; Acidosis & hypoxia mimic fetal circulation & baby may revert to fetal patterns of oxygenation.
Hypothermia in Premature Newborn Principles Immature Temp center in brain; Can’t shiver; Preemies have: < muscle mass; < brown fat; < heat-preserving subcutaneous fat; large body surface area; immature liver – low glycogen stores
Hypothermia in Premature Newborn Interventions Keep babe warm (isolette or warmer); Monitor temp ^ warmers by 2 degrees @ a time
Preemies are at risk for -physical and emotional abuse d/t stress out good for nuthin’ parents.
Preemies are at risk for these complications Hypothermia; Hypocalcemia; Hypoglycemia; Hyperbilirubinemia; Birth trauma; Infection, Sepsis; Intracranial hemorrhage; Apnea, SIDS
Transient Tachypnea of the Newborn Self limited disorder of newborns, usually near term, that develops w/in 6 hrs of life. Due to transient pulmonary edema d/t delayed clearing of lung fluid..Rsk factors: precip, preemie, c/s without labor
If develop TTNB will see- Tachypnea (80 – 120) vs normal_30-50; mild subcostal retractions, grunting; Fluid in chest x-ray; Mild cyanosis
If develop TTNB will need Supportive therapy for 12 – 72 hours; Keep warm; Pulse ox, monitor for acute R distress; Closely evaluate RR. Ability to feed will depend upon RR. May need IV or NG feeds until RR <80
Normal is “AGA” (Appropriate for Gestation Age) Wt falls btw 10th & 90th percentile for age -
SGA (Small for Gestation Age) weight falls below 10th percentile for age (used to say <2500gms) constitutionally small or IUGR d/t pathology
Factors associated with SGA genetic predisposition; malnutrion; infections –TORCH; maternal dz; teratogens; postmature; chromosomal abnormalities; abruption, previa; age, race, SES (socio economic status); velamentous cord
IUGR (Intrauterine Growth Restriction) (Rate of growth does not meet expected growth pattern)
Symmetrical IUGR – usually insult is early in pregnancy and persists. Baby is proportionately low in wt., length and head circumference
Asymmetrical IUGR – occurs later in pregnancy and is “brain sparing”. Head is much bigger in proportion to wt. and to a lesser degree, ht.
Asymmetrical IUGR Newborn Physical characteristics Normal sized skull; Smaller body; Loose/dry skin; Diminished muscle mass; Sunken abdomen; Thin/dry/dull umbilical cord; Sparse scalp hair;
IUGR Newborn Physiologic complications & nursing assessments respiratory ; Hypocalcemia; Nutritional deficit; Mec aspiration; Body temperature regulation; Infection potential; Musculoskeletal; Hypoglycemic; polycythemia
IUGR Newborn: Interventions Correct the problem, if possible; Glucocorticoids if lungs not mature; Deliver early, if needed, if risk of waiting is < risk of delivery ; Follow closely1st yr – mortality risk < for IUGR babies over AGA babies
LGA Newborn: weight @ or above 90th percentile for age (Macrosomic) complications birth trauma, prolonged vaginal delivery time; difficult birth; increase in cesarean delivery; hypoglycemia; increased incidence of birth defects; respiratory distress; hyperbilirubinemia
LGA Complications/Interventions: assess for trauma; assess for blood glucose; polycuthemia; treat as a premiee in a big body
jaundice in High Risk Newborn Definition – yellow discoloration skin & eyes d/t accumulation yellow bile pigments (bilirubin) in the blood
Jaundice Etiology – immaturity in the liver. Liver conjugates unconjugated bili into water soluable or conjugated bili that is excreted through urine and feces
Physiologic jaundice occurs btw. 1 -7 days of life; ½ babies born who are full term & ¾ all preemies; mild, lasts a few days & then goes away.
Pathologic jaundice if occurs within 24 hours of birth
Other factors which can cause jaundice Prematurity – delay in ability to process/excrete bilirubin; Rh or ABO incompatibilities – hemolysis or premature destruction of infant’s RBC’s; . Drugs used during pregnancy or birth, Trauma – caput, bruising, infection
Serious consequences of jaundice prevented if Rhogam given after abortions, invasive procedures, during and after pregnancy
Breastmilk jaundice – Rare 1:200; Substance in milk inhibits enzyme activity in liver, resulting in slow conjugation & excretion of bilirubin; MD may recommend stop breastfeeding & feed the baby formula x 24 hrs to see if becomes < jaundiced
Jaundice in High Risk Newborn: danger of Kenicterus ^ amount unconjugated unbound bilirubin ...Bili doesn’t stay w/in blood stream..diffuses out & binds w/ tissues w/ High fat content (brain and CNS)…Bilirubin in these tissues – toxic (cerebral palsy, seizure disorder, encephalopathy or death to infant).
Brain damage can occur in elevated Bilirubin@ > 24 mg/100ml
Jaundice in High Risk Newborn Nursing Interventions Breastfeed early –colostrum is a natural laxative; Increase fluids; Phototherapy (ultraviolet light) Sometimes formula is recommended instead of breastmilk x 24 hours to see if enzyme in milk is < bilirubin excretion
Jaundice in High Risk Newborn: Exchange transfusion if severe – seldom necessaryLevels requiring transfusion: > 5 mg at birth; > 10 mg at 8 hours old; > 12 mg at 16 hours old; > 15 mg at 24 hours old
Jaundice in High Risk Newborn Nursing Interventions for phototherapy… Monitor VS – it’s HOT under there! Assess hydration/nutrition – I & Os, daily wt.; Assess & continue to observe lethargy/seizures; Assess & continue to observe for jaundice –Assess bili light function with bili meter; Monitor bili levels; Monitor that eyes & genitalia are covered;
3 parts of stage 1 of labor LATENT, ACTIVE, TRANSITIONAL
conversion for C to F F= 9/5 (C+32)
conversion for F to C C= 5/9x (F-32)
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