WH Prenatal Comps Flashcards
Any onset of glucose intolerance after 20 weeks gestation. Usually diagnosed at 28 weeks with glucose screening. Glucose intolerance prior to 20 weeks is preexisting DM. Management is with diet modification first: DGMA1. If diet fails, usually insulin is prescribed (sometimes metformin): GDMA2. GDM patients need to meet with nutritionist, diabetic educator and if on insulin, na endocrinologist to manage insulin therapy. GDM pts will monitor blood sugar QID. Educate regarding following diet plan and strict BS monitoring, encourage exercise. GDMA2 (on insulin) is higher risk for complications and these patients will usually have frequent monitoring for fetal wellbeing at term and have their labor induced at 39 weeks. Complications include macrosomia, polyhydramnios, fetal demise.
Gestational Diabetes
HTN (140/90 or higher) at or after 20 weeks gestation. Diagnosis must have 2 elevated Bp readings at least 4 hours apart (unless severe HTN 160/110 or higher- that is an immediate diagnosis). Increased risk in extremes of age, multiples, prior hypertensive episodes, obesity. Half of gHTN mother progress to preeclampsia. Increased frequency of visits for BP checks, ruling out preeclampsia and fetal well being assessments (BPP, NSTs). Increased incidence of premature delivery, small-for-age newborns, placental abruption. Some women return to normal BP after delivery, some stay hypertensive for weeks. If HTN persists beyond 12 weeks, it is now chronic HTN.
Gestational hypertension
HTN and proteinuria:
300mg protein or greater in 24 hour urine collection sample
protein: creatinine ratio 0.3 or higher
urine dipstick reading of +2 protein (if other testing not available)
Diagnosis of mild preeclampsia
HTN and abnormal lab finding indicating end-organ dysfunction:
platelets less than 100,000
serum creatinine over 1.1 mg/dl
doubled liver transaminases
pulmonary edema
new onset visual or cerebral syndromes (blurred vision, severe headaches, flashing lights)
severe HTN 160/110
Diagnosis of Severe Preeclampsia
Seen in 3-5% of pregnancies.
Risk factors: 1st pregnancy, multiple pregnancy, history of this disease, chronic HTN, DM or GDM, lupus, BMI over 30, age over 35, assisted reproductive pregnancy, sleep apnea, antiphospholipid antibody syndrome.
Cause is thought to be abnormal placentation signaling maternal vasoconstriction, although this is poorly understood. Fetal risks include oligohydramnios, placental abruption, IUGR.
Maternal risks include renal damage or failure, pulmonary edema, liver damage, thrombocytopenia, edema, visual changes, cerebral edema & headaches, hyperreflexia, clonus, and eclampsia (seizures)
Preeclampsia
Malaise, headache, visual changes, rapid weight gain associated with edema can be a clue to evaluate for this disorder, although edema is not part of diagnosis. Oliguria could be related to edema. RUQ abdominal or epigastric pain can be a sign of severe (liver pain).
S/s of Preeclampsia
Tonic-clonic seizure or coma (Treated with magnesium sulfate IV bolus and maintenance infusion and oxygen therapy)
Eclampsia
Assess for magnesium toxicity: Resp depression (resp less than 12/min, SOB), lethargy, oliguria (less than 30 mL/hr), treat with calcium gluconate 1g IV
Common side effects: sweating, flushing, drowsiness, lethargy, headache
Nursing Considerations of Magnesium Sulfate Therapy
Hypertensive complication of pregnancy, may be a more severe form of preeclampsia, increased mortality and morbidity. Hemolysis, Elevated, Liver, Enzymes, Low, Platelet count.
Maternal risks: Disseminated intravascular coagulation (DIC), abruption, renal failure, pulmonary edema, retinal detachment, liver hematoma, often require blood transfusions
Fetal risks: prematurity, IUGR, perinatal death
Diagnosis based on lab values: LDH 600 IU/I or more, AST & ALT twice the upper limit or normal, and platelets less than 100,000.
Treatment is delivery, however 30% of cases are diagnosed postpartum. Primary presenting symptom is RUQ pain, malaise, nausea, and vomiting.
HELLP syndrome
Infection of the membranes and amniotic fluid. Often occurs after prolonged rupture of membranes. Can stimulate labor, preterm labor, PROM, or PPROM. Adverse maternal outcomes include postpartum infections and sepsis. Adverse infant outcomes include stillbirth, premature birth, neonatal sepsis, chronic lung disease and brain injury leading to cerebral palsy and other neurodevelopmental disabilities.
S/s: Maternal fever, uterine tenderness, maternal and/or fetal tachycardia, purulent or foul amniotic fluid.
Treatment is with maternal IV antibiotics and neonatal antibiotics post delivery
Chorioamnionitis/ Intraamniotic infection
Treatment at term is induction of labor. Treatment preterm depends on gestational age. Before 34 weeks, corticosteroids are given to promote lung maturity. Antibiotics typically given in PPROM if labor is delayed. Magnesium sulfate IV may be given before 32 weeks if delivery is anticipated within 24 hours as it provides neuroprotection for the preterm infant.
Treatment of PROM/PPROM
Rupture of membranes prior to the onset of labor. PROM= 8-10% of pregnancies. PPROM= 3% of pregnancies. Can be caused by infection, usually no identified cause. Evaluation is by visualization of amniotic fluid or evidence of fluid on ph paper, microscopic visualization of “ferning”, or specialized commercial testing swab (ROMplus). Examinations must be done with sterile gloves and equipment to minimize bacterial spread. Fluid collection is usually performed using a speculum and sterile swabs
PROM/PPROM
Onset of labor prior to 37 weeks gestation. Major risk factors include multiple pregnancy, co-morbidity with HTN or diabetes, uterine malformation, substance abuse (cocaine), infection, history of preterm birth, maternal stress. Half of the women experiencing preterm birth have no risk factors. Preterm birth is the leading cause of death in children under age 5 worldwide. Signs and symptoms are the same as for term labor. Testing may include fetal fibronectin (ffN) vaginal swab - a negative result is reassuring. Transvaginal ultrasound can be used to visualize the cervical length and effacement.
Preterm labor
Corticosteroids are given to mother to promote fetal lung maturity. Betamethsone IM once, repeat in 12-24 hours once stimulates the release of surfactant. Treat with tocolytic medications to delay delivery, usually effective for only 2-7 days (after 34-36 weeks, labor is usually allowed to proceed)
Treatment of Preterm before 34 weeks
Indomethacin (COX2 inhibitor, NSAID)- 48 hour treatment due to fetal effects of premature closure of ductus arteriosis.
Nifedipine (calcium channel blocker, antihypertensive)
Terbutaline (beta-2 agonist, bronchodilator)- significant maternal side effects.
Magnesium sulfate- less effective at stopping labor than the others, but can offer neuroprotection to babies under 32 weeks gestation, reducing their risk of cerebral palsy. Overdose can cause magnesium toxicity: reversal is with calcium gluconate. S/s of magnesium toxicity: hypotension, SOB, resp less than 12/,im, resp arrest, oliguria
Tocolysis: inhibition of preterm labor
