Final study guide for OB PDF

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Final study guide for OB...

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Chapter 25: Complications of Pregnancy Causes, maternal/fetal risk factors, signs and symptoms, nursing interventions and rx’s associated with: Abortion  Loss of pregnancy before the fetus is viable, or capable of living outside the uterus.  Fetus 35 years; assisted reproductive techniques such as gamete intrafallopian transfer (GIFT)  Clinical manifestations: classic signs—missed menstrual period, + pregnancy test, abdominal pain, and vaginal “spotting.”  Implantation in the distal end of the fallopian tube—woman may first exhibit usual early signs of pregnancy. Several wks into pregnancy, intermittent abdominal pain and small amounts of vaginal bleeding occur that initially could be mistaken for threatened abortion.  Proximal end of the fallopian tube, rupture of the tube may occur w/in 2-3 weeks of missed period b/c the tube is narrow in this area. S&S: sudden, severe pain in one of the lower quadrants of the abdomen as the tube tears open and the embryo is expelled into the pelvic cavity, often with profuse abdominal hemorrhage; radiating pain under scapula may indicated bleeding into the abdomen—at risk for hypovolemic shock.  Diagnosis: transvaginal US exam; determination of beta subunit of human chorionic gonadotropin (beta-HCG)—if present but at lower levels than expected. A characteristic bluish swelling w/in the tube is the most common finding.  Therapeutic management: depends on whether the tube is intact or ruptured  Methotrexate (a folic acid antagonist)—used to inhibit cell division in the developing embryo.  Linear salpingostomy to salvage the tube  Ectopic pregnancy results in rupture of the fallopian tube—goal is to control bleeding and prevent hypovolemic shock. When women’s CV status is stable, remove tube (salpingectomy) w/ligation of bleeding vessels may be required.  Rh immune globulin to appropriate Rh negative women.  Nursing considerations:  Methotrexate –nurse must explain AE like N/V and transient abdominal pain.  The woman must be instructed to refrain from alcoholic drinks—decreases methotrexate’s effectiveness—ingesting vitamins with folic acid, and having sex until beta-HCG is not detected.  Continued presence of HCG in serum—requires follow up to see if pregnancy is still present. Placenta Previa  Implantation of the placenta in the lower uterus.  3 classifications: 1.) Marginal (low-lying): placenta implanted in lower uterus, but its lower border is more than 3 cm from the internal cervical os. 2.) Partial: lower border of the placenta is w/in 3 cm of the internal cervical os, but does not completely cover the os. 3.) Total: placenta completely covers internal cervical os.  Incidence and etiology: more common in older women, multipara, women who have had c-section, and women who had suction curettage for induced/spontaneous abortion; African American and Asians have increased risk; cigarette smoking and cocaine use are risk factors; fetus is male.  Clinical manifestations:  Classic sign—sudden onset of painless uterine bleeding in the last half of pregnancy.  Bleeding is painless b/c it does not occur in a closed cavity and does not cause pressure on adjacent tissue.  Bleeding may not occur until labor starts, when cervical changes disrupt placental attachment.

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Digital exam of cervical os or stimulation of contractions when placenta previa is present can cause add’l placental separation or tear the placenta itself—hemorrhage.  Until the location and position of placenta is verified by US, no manual exams should be performed and administration of pit.  Therapeutic management: HOME CARE—must meet general criteria: no evidence of active bleeding, able to maintain bed rest at home, home is located w/in a reasonable distance from the hospital, emergency systems are available for immediate transport to the hospital 24 hrs, and woman can verbalize understanding risks associated with previa and how to manage her care.  Nursing considerations:  Home care—include strict bed rest except for elimination and shower, and presence of another adult to manage the home. Teach: assessing color and amount of vaginal discharge/bleeding, especially after each urination or BM; assessing fetal activity (kick counts) daily; assessing uterine activity; refraining from sex to prevent disruption of placenta.  Inpatient care—a significant change in fetal heart activity, episode of vaginal bleeding, or signs of preterm labor should be reported immediately. Delivery may be schedule if the fetus is older than 36 weeks gestation and lungs are mature.  Delivery may be necessary regardless of fetal immaturity if bleeding is excessive and woman demonstrates signs of hypovolemia or signs of fetal compromise. Abruptio placenta  Separation of a normally implanted placenta before the fetus is born occurs in cases of bleeding and formation of a hematoma (clot) on the maternal side of the placenta. Clot expands = further separation occurs.  The major dangers for the woman are hemorrhage and consequent hypovolemic shock and clotting abnormalities.  Major dangers for fetus—asphyxia, excessive blood loss and prematurity.  Incidence and etiology—maternal cocaine use (causes vasoconstriction in the endometrial arteries) is a strong risk factor and the leading cause of abruptio; other risk factors—maternal HTN, cigarette smoking, multigravida status, short umbilical cord, abdominal trauma and PROM, and hx of previous premature separation of the placenta.  Clinical manifestations  Five classic S&S: bleeding (vaginally or concealed); uterine tenderness that may be localized at the site of abruption; uterine irritability with frequent low-intensity contractions and poor relaxation between contractions; abdominal or low back pain that may be described as aching or dull; high uterine resting tone identified with use of an intrauterine pressure catheter.  Amniotic fluid has a classic “port wine” color.  It may be sudden and severe when bleeding occurs into the myometrium (uterine muscle) or be intermittent and difficult to distinguish from labor contractions.  Uterus may become exceedingly firm (boardlike) and tender, making palpation of the fetus difficult.  Therapeutic management  If condition is mild, fetus is under 34 weeks, and showing no signs of distress, tx involves bed rest and possible administration of tocolytics and steroids to accelerate fetal lung maturity.  Immediate delivery of the fetus is necessary if signs of fetal compromise exist or if the expectant mother exhibits signs of excessive bleeding.  Blood products for replacement should be available, and two large-bore IV lines should be started for replacement of fluid and blood.  Serial Kleihauer-Betke (K-B) tests determine if fetal bleeding is worsening.  Rh (-) given Rhogam to prevent possible sensitization.  Signs of concealed hemorrhage in abruption placenta  Increased fundal height  Hard, board-like abdomen  High uterine baseline tone  Persistent abdominal pain  Systemic signs of early hemorrhage (tachycardia for both, tachypnea, falling BP, falling urine output and restlessness)  Persistent late decels in FHR or decreasing baseline variability.  Slight or vaginal bleeding Hyperemesis Gravidarum (HEG)  Is persistent, uncontrollable vomiting that begins in the first weeks of pregnancy and may continue throughout pregnancy.  Etiology—condition is more common among unmarried white women, during 1st pregnancies, and in multifetal pregnancies. Other possible causes: allergy to fetal proteins; elevated levels of pregnancy-related hormones (HCG and estrogen)  Therapeutic management—lab studies: H&H levels elevated b/c of dehydration, reduced Na+, K+, and Cl- levels; elevated creatinine levels indicate renal dysfxn. Tx: occurs primary at home; pyridoxine (vitamin B6) provide some relief. Other drugs: Phenergan, Benadryl, Zantac, Pepcid, Nexium, Prilosec, Reglag, Zofran.  If drugs are required, a single drug is 1st prescribed in th lowest effective dose to minimize fetal effects.

 IV f&e placement or TPN may be necessary. Nursing considerations  I&O’s  Daily weights—first thing in the morning and in similar clothing each day.  Urine tested for ketones  Wt loss and presence of ketones in the urine suggest that fat stores and protein are being metabolized to meet energy needs.  Signs of dehydration: decreased fluid intake ( or = 140 mm Hg or a diastolic BP of > or = 90 occurring after 20 weeks of pregnancy that is accompanied by significant proteinuria (>0.3 g in 24-hr urine collection; random urine dipstick eval of > or =+1)  Eclampsia—progression of preeclampsia to generalized seizures that cannot be attributed to other causes.  Chronic HTN—elevated BP was known to exist before pregnancy. Preeclampsia  HTN develops during the last half of pregnancy in a woman who previously had normal BP; renal involvement may cause proteinuria; only known cure is birth of fetus.  Incidence and risk factors—major cause of perinatal death and often associated with IUGR. Women who had prior pregnancies w/out HTN are more likely to have preeclampsia if a new partner has previously fathered a pregnancy in another woman that was complicated by the disorder.  Risk factors for pregnancy-related HTN: 1st pregnancy, age >35 years, anemia, family hx of pregnancy-induced HTN, chronic HTN or preexisting vascular disease; chronic renal disease, obesity, DM, antiphospholipid syndrome; multifetal pregnancy, angiotensin gene T235, and mother/sister who had preeclampsia.  Pathophysiology—result of generalized vasospasm; in normal pregnancy, there is an increase in volume and CO, but BP doesn’t normally rise. In preeclampsia, peripheral vascular resistance increases b/c women are sensitive to angiotensin II. TXA2, produced by kidney and trophoblastic tissue, causes vasoconstriction and PLT aggregation (clumping). Vasospasm decreases the diameter of blood vessels, results in endothelial cell damage and decreased EDRF.  Changes that are significant in preeclampsia:  Decreased renal perfusion = increase in BUN, creatinine and uric acid; glomerular damage, allowing protein to leak across the glomerular membrane.  Loss of protein allows fluid to shift to interstitial spaces, may result in edema and a reduction in intravascular volume, which causes increased viscosity of the blood and a rise in HCT level.  Add’l angiotensin II results in further vasospasm and HTN; aldosterone increases fluid retention and edema worsens.  Reduced liver circulation = hepatic edema and subcapsular hemorrhage = elevation of liver enzymes in maternal serum; epigastric pain is a common symptom.  Decreased blood flow to brain = small cerebral hemorrhages  headache, visual disturbances (blurred vision, “spots” before the eyes, and hyperactive DTRs)  Decreased colloid oncotic pressure = results in pulmonary edema. Dyspnea is the primary symptom.  Decreased placental perfusion = increase the risk for abruptio placenta and HELLP syndrome; IUGR and persistent hypoxemia and acidosis when maternal blood flow through the placenta is reduced.  Clinical manifestations of preeclampsia  Classic signs—first indication is HTN (BP should be measured uniformly at each office visit—seated and her arm supported; cuff size should be appropriate for the size of her arm); proteinuria (clean catch specimen to prevent contamination of the specimen by vaginal secretions/blood)  Additional signs—retina (vascular constriction and narrowing of the small arteries); hyperreflexia; liver, renal and hepatic dysfxn; coagulation impaired (decreased in PLTs); generalized edema (noted as rapid wt. gain first)  Symptoms—continuous headache, drowsiness or mental confusion (poor cerebral perfusion and can be precursor for seizures); blurred or double vision or spots before the eyes, indicate arterial spasms and edema in the retina; epigastric pain or “upset stomach,” are particularly ominous b/c they indicate distention of the hepatic capsule and often warn that a seizure is imminent.  Therapeutic management of Mild preeclampsia 

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Only cure for preeclampsia is delivery of the baby. If the fetus is or =110  Delivery is usual, even if the gestation is 140/90 can indicate preeclampsia; decrease is dehydration/hypovolemia.  Pulse—bradycardia can occur—reflect the large amount of blood that returns to the central circulation after delivery of the placenta  RR—breath sounds if mom was C-section, receiving mag sulfate, smoker, recent/recurrent respiratory infection.  Temperature—100.4 F common during the first 24 hours; if the elevated temp persists longer than this, think infection; be alert to sings of afterpains, perineal discomfort, and breast tenderness  Fundus  Firmly contracted and at or near the level of umbilicus  Above level or shifted from middle of abdomen to the right—bladder may be distended.  Fundus is difficult to locate or soft “boggy” nurse stimulates the uterine muscle to contract by gently massaging the uterus.  To expel clots, nurse should massage fundus until firm and then support the lower uterine segment— prevents inversion of uterus when the nurse applies firm pressure downward toward the vagina to express clots that have collected in the uterus.  Drugs to maintain contraction—oxytocin, methergine, and hemabate  Lochia  Constant trickle, dribble, or oozing of lochia indicates excessive bleeding and requires immediate attention.  Excessive lochia in the presence of a contracted uterus suggests laceration of the birth canal.  Signs of infection—foul odor (should be fleshy, earthy, musty smell); maternal fever, tachycardia and uterine tenderness and pain; absence of lochia  Perineum  REEDA—redness, erythema, ecchymosis, discharge and lack of approximation.  Bladder elimination  Frequent voidings of less than 150 ml suggest urinary retention with overflow.  When the mother can void at least 300-400 ml, bladder is usually empty.  Breasts  1st-2nd day—soft and nontender.  Engorgement may occur despite preventive measures—inspect for dimpling; thickening.  Breasts should be palpated for firmness and tenderness  Lower extremities  Homan’s sign  DTR—1+ and 2+, higher suggest preeclampsia. Nursing care  Providing comfort measures  Ice packs—alleviate perineal pain; causes vasoconstriction and most effective applied after birth to prevent edema and numb area; remove 10 minutes before a fresh pack is applied  Perineal care—squirting warm water over the perineum after each voiding or bowel movement; gently patted rather than wiped dry.  Topical meds—anesthetic sprays—hold the nozzle of the spray 6-12 incres from her body and direct towards perineum  Sitting measures—squeeze her buttocks together before sitting and lower her weight slowly; sitting slightly on the side  Sitz baths—provide continuous circulation of water, cleansing and comforting; cool water reduces pain caused by edema and effective first 24 hours; warm water increases circulation, promotes healing, and effective after 24 hours.  Analgesics—no more than 4 g of acetaminophen in 24 hours.  Promote bladder elimination  Medicate  Running water in sink/shower, placing mother’s hands in warm water, and pouring water over vulva  Providing hot tea/fluids of choice  Asking mother to blow bubbles through a straw.  Proving fluids and food  2500 mL/day  Ice chips after c-section, then regular diet as tolerated.  Preventing thrombophlebitis  Ambulate

 Compression stockings; ted hoses Nursing care for c-section assessment  Pain relief  Respirations—checked every 15 minutes for the 1st hour, every 30 for 3-6 hours; 30-60 minutes for the remainder of 24 hours; auscultate breath sounds; IS; cough, deep breathe  Abdomen—auscultate bowel sounds; surgical dressing assessment  First 24 hours—provide pain relief, overcome effects of immobility, provide comfort  After 24 hours—resume normal activities; assist mom with infant feeding (sitting w/pillow on lap to protect incision; side-lying position) prevent abdominal distention (early ambulation, exercises to tighten muscles; avoid carbonated beverages; pelvic lifts; simethicone; rectal suppositories)  Counseling about sexual activity—when perineal discomfort and bleeding subside/ended—2-4 weeks after giving birth; breastfeeding women have low estrogen, may need lubrication; 3rd-4th degree lacerations may need more time to heal.  Risks & complications associated during the postpartum period *(1 slide)  Common complications of the postpartal period include: Postpartum Hemorrhage:  Early-1st 24 hrs  Late-24 hrs-6wks  EBL > 500ml NSVD  >1500ml C/S  HCT ↓ 10% from admission  PPH is significant cause of maternal morbidity & mortality Predisposing factors:  Overdistention  Multiparity  Rapid or prolonged labor  Oxytocin induction of labor  Precipitous induction of labor  Precipitous delivery  Cesarean section  Rupture of membranes(> 24 hours) Chapter 14: Intrapartum fetal surveillance  Fetal heart rate assessments  Purpose of intrapartum fetal assessment is to evaluate how the fetus tolerates labor and to identify hypoxic insult to the fetus during labor.  Low technology approach uses intermittent auscultation (IA) of the FHR and palpation of uterine cavity; EFM (electronic fetal monitoring) is the high-technology approach to intrapartum fetal surveillance. Fetal oxygenation—needs five related factors: 1.) Normal maternal blood flow and volume to the placenta 2.) Normal oxygen saturation in maternal blood 3.) Adequate exchange of oxygen and CO2 in the placenta 4.) An open circulatory path between the placenta and fetus through vessels in the umbilical cord 5.) Normal fetal circulatory and oxygen-carrying functions.  Uteroplacental exchange  Oxygen and nutrient rich blood from mom enters intervillous spaces of the placenta via spiral arteries  Oxygen and nutrients from mom pass into fetal blood that circulates w/in capillaries inside the chorionic villi in the intervillous spaces.  Maternal blood carrying fetal waste products drains from the intervillous spaces through endometrial veins and returns to mother’s circulation for elimination in her body.  During labor, contractions compress spiral arteries (as mentioned above is the passage of oxygen and nutrient rich blood from mom to the placenta) stopping blood flow into intervillous spaces at the peak of strong contractions.  Since compression of the spiral arteries stop blood flow to placenta, hence to the fetus, oxygen supply depends on fetal erythrocytes and in the intervillous spaces—enough for 1-2 minutes.  Fetal circulation—umbilical vein carries oxygenated blood to the fetus, and two umbilical arteries carry deoxygenated blood from the fetus to the placenta.  Regulation of fetal heart rate: 1.) Autonomic nervous system  Sympathetic—increases the HR and strengthens myocardial contractions through release of epi and norepinephrine. 

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Parasympathetic—stimulation of vagus nerve—reduce FHR and maintain variability—gradually exerts greater influence as fetus matures at 28-32 weeks that’s why average FHR in term fetus is lower than in preterm. 2.) Baroreceptors—stimulate vagus nerve to slow FHR and decrease BP and lowering CO. 3.) Chemoreceptors—respond to changes in low O2, high CO2, low pH  stimulate increase in HR. 4.) Adrenal gland—medulla secretes epi and norepinephrine in response to stress  accelerates HR; cortex: fall in BP, secretes aldosterone. 5.) Central nervous system—causes the HR to increase during fetal movement and decrease when the fetus is quiet.  Pathological influences on fetal oxygenation  Maternal cardiopulmonary alterations—epidural block can cause vasodilation, which increases capacity of maternal vascular bed. The amount of blood available to fill her vessels is unchanged; aortocaval compression—pregnant woman in supine; maternal hypertension  Uterine activity—placental disruptions (abruption placenta—partial separation before birth; infarcts reduce placental SA available for exchange); interruptions in umbilical flow (usual cause is umbilical cord compression d/t oligohydramnios or inadequate Wharton’s jelly for cushioning; what happens: thin walled umbilical vein gets compressed first as a result you would have hypotension, baroreceptors/chemoreceptors respond to increa...