Care of Childbearing Women PDF

Care of Childbearing Women 1. Placenta Previa – “Afterbirth” (low lying placenta) – exist when the placenta is inserted wholly or partially into the lower uterine wholly or partly into the lower uterine segment of the uterus, partially or completely covering the internal cervical opening....

Care of Childbearing Women 1. Placenta Previa – “Afterbirth” (low lying placenta) – exist when the placenta is inserted wholly or partially into the lower uterine wholly or partly into the lower uterine segment of the uterus, partially or completely covering the internal cervical opening. Early Detection of Impaired placental implantation o Ultrasound o Colored Doppler Causes: o due to uterine endometrial scarring or damage in the upper segment, which may incite placental growth in the unscarred lower uterine segment. o Uteroplacental under perfusion – may cause placenta to encroach on the lower uterine segment. Therapeutic Management o Depends on the extent of bleeding o Closeness of the placenta to the cervical OS o Weather the fetus is developed enough to survive Risk Factors: o Maternal age > 35 years o Previous C/S o Multiparity o Uterine Insult or injury o Cocaine Use o Previous D&C o Prior placenta previa o O birth which leads to Infertility treatment o Multiple gestations o Smoking o HTN or Diabetes TAKE NOTE: avoid doing vaginal examinations in the woman with placenta previa because they may disrupt the placenta & cause hemorrhage 1  2. Abruptio Placenta – Placental abruption – early separation of a normally implanted placenta after the 20th week of gestation prior to hemorrhage. Bleeding occurs between decidua & placenta. Pathophysiology: maternal vessels tear away from the placenta & bleeding occurs between the uterine lining & the maternal side of the placenta Cause of 2nd & 3rd trimester bleeding with high mortality rate Classic Manifestations: o Painful (knife like abdominal pain), dark red vaginal bleeding, uterine tenderness & contractions & decreased fetal movement Maternal risks are: o Obstetrical Hemorrhage o Blood transfusions o Hysterectomy o DIC o Sheehan syndrome or postpartum gland necrosis Perinatal consequence: o Low birth weight o Preterm birth o Asphyxia o Stillbirth o Perinatal death Therapeutic Management: o Control & restore blood loss o Prevent coagulation disorders – DIC (S/S: decreased brinogen & platelets, Prolonged PT/PTT, Positive D-dimer test & brin ▪ Anticoagulation – LWH ▪ Transfusion of FFP & cryoprecipitate o C/S if fetal distress id imminent 3. Preeclampsia/Eclampsia – new onset HTN accompanied by proteinuria &/or maternal organ dysfunction that targets the heart, hepatic, renal & CNS. 2 fi fi  Pathological Changes are: o Pulmonary edema o Oliguria o Seizures o Thrombocytopenia – number of platelets in your blood is lower than normal (Normal 150,000 - 450,000 platelets/microliter of blood o Abnormal liver functions Two stage events o Vasospasm – endothelial injury (leading to platelet adherence, brin deposition & presence of schistocytes (fragments of erythrocytes) – ***cause elevation of BP & reduce bld. ow to the brain, liver, kidneys, placenta & lungs. o Hypoperfusion – HTN, proteinuria, headache, nausea & vomiting, retinal vascular changes causing blurred vision & hyperre exia due to hypoperfusion Therapeutic Management o Delivery of the placenta o Low dose ASA (75 – 100 mg) from 12 weeks to delivery Risk Factors o Multifetal gestation o Previous pregnancy with preeclampsia o Renal disease o Autoimmune o Diabetes o 1st pregnancy o Periodontal disease o Chronic HTN o Obesity Management o Bed Rest – lateral recumbent position to improve uteroplacental blood ow o Prenatal visit & testing: CBC, clotting studies, liver enzymes & platelet levels o Monitor BP & report any elevation o Report in decrease of fetal movements o Diet: low sodium, encourage to drink 6-8 glasses of water daily, balanced high protein diet, high ber o If BP remains high – admission to hospital is warranted 4. HELLP Syndrome (Hemolysis, elevated Liver enzymes & Low Platelet count) – variant of preeclampsia/eclampsia occurs with up to 20% of pt’s labelled as preeclampsia with severe features: o Increased risks for cerebral hemorrhage o Retinal detachment 3 fi fl fl fi fl  o Hematoma/Liver rupture o DIC o Placental Abruption o Eclampsia o Acute renal failure o Pulmonary edema o Maternal Death Pathophysiology: abnormal vascular tone, vasospasm, coagulation defects Therapeutic Management o Stabilization of BP – use of hydralazine & labetalol o Assessment of Fetal wellbeing – to determine optimal time of birth o Rapid acting hypertensive agents o Prevention of convulsions or further seizures with Magnesium sulfate, use of steroids for fetal lung maturity o Bld. products such as PRBC, FFP, Platelets to address microangiopathic hemolytic anemia. o Birth maybe delayed up to 96 hrs. so that betamethasone or dexamethasone can be given to stimulate lung maturation in pre-term fetus. 5. ABO Incompatibility – blood type or RH factor Incidence: o Mom with bld. Type O becomes pregnant with a fetus with a different blood type (Type A, B, or AB); with anti-A & anti-B antibodies o Mom serum contains naturally occurring anti-A & anti-B which can cross the placenta & hemolyze fetal RBC. Nursing Assessment: o Prenatal visit – Determine Mom’s bld. Type & Rh status o Obtain if any history of hemorrhage o If Mom is Rh negative who maybe pregnant with Rh positive fetus, prepare client for antibody screen (indirect Coombs test) to determine whether she has developed isoimmunity to Rh antigen. This test detects unexpected circulating antibodies in a woman’s serum that could be harmful to the fetus. o If the indirect Coombs test is negative ( meaning no antibodies are present, then the mom is a candidate for RhoGAM. o If the test is positive, RhoGAM is of no value because isoimmunization has occurred. In this case the fetus is observed for hemolytic disease. o Standard dose: 300 mcg, which is effective for 15 ml of fetal bld. Cells 4  o Rh immunoglobulin – help destroy any fetal cells in the maternal circulation before sensitization occurs, thus inhibiting maternal antibody production. o Time to receive it: between 28 – 32 weeks gestation & again within 72 hrs. after giving birth. o RhoGAM indicated: 1. Ectopic pregnancy 2. Chorionic villus sampling 3. Amniocentesis 4. Prenatal Hemorrhage 5. Molar Pregnancy 6. Percutaneous Umbilical Sampling 7. Therapeutic or Spontaneous Abortion 8. Fetal Death 9. Fetal Surgery 6. Polyhydramnios – too much amniotic uid (> 2000 mL) surrounding the fetus between 32 – 36 weeks Risks: o Maternal diabetes o Fetal abnormalities – 1. upper GI obstruction or atresia 2. Neural defects 3. Interior abd. wall defects 4. Impaired swallowing in fetus with chromosomal abnormalities such as trisomies 13 & 18 Therapeutic Management: o Close monitoring & frequent prenatal visits o Removal of uid by amniocentesis o If with pain & SOB, amniocentesis or arti cial rupture to reduce uid & pressure o Med: Use of prostaglandin synthesis inhibitor (indomethacin) to decrease amniotic uid by decreasing fetal urinary output 7. Oligohydramnios – decrease amount of amniotic uid (< 500 mL) between 32 – 36 weeks; prevents the fetus from making urine or blocks it from going into the amniotic sac. Puts the fetus at an increased risk of perinatal morbidity & mortality. Reduction in amniotic uid reduce the ability of the fetus to move freely without risk of cord compression, which increases the risk for fetal death & intrapartal hypoxia. Therapeutic Management – o Serial ultrasounds & fetal surveillance through nonstress testing & biophysical pro les 5 fl fl fi fl fl fl fi fl  o Amnioinfusion – improve fetal heartrate patterns, decrease C/S births possibly minimize the risk of neonatal meconium aspiration syndrome 8. Diabetes Pathophysiology: characterized by a series of metabolic changes that promote accumulation of adipose tissue in early pregnancy followed by insulin resistance later in gestation. This is due to existence of pancreatic beta cells dysfunction prior to pregnancy & the unmasking of this problem by the development of the insulin resistance during pregnancy, which requires enhanced insulin production to maintain normal blood sugar ranges. Types o Gestational Diabetes – glucose intolerance with its onset during pregnancy usually diagnosed second & third trimester of pregnancy that is not clearly overt prior to gestation. o Pregestational Diabetes – alteration in carbohydrate metabolism identi ed before conception – type I & type II Neonatal Complications: o Macrosomia (big baby) o Hypoglycemia o Birth trauma due to shoulder dystocia o Cord Prolapse o Preterm birth secondary to polyhydramnios Maternal Complications o Preeclampsia o C/S o Risk of developing cardiovascular disease o Hydramnios o Dif cult labor o Still birth Care of Gestational Diabetic Mom o Nutritional management o Exercise o Insulin is required – intermediate & short acting insulin Diagnostic Testing o Urine check for protein o Urine test for ketones – need to be evaluated for eating habits o Kidney function evaluation o Eye exam o HgA1C – 4-6 weeks to monitor trends o Hypertension o Obesity o Recurrent monilia infection o S/S of glucose intolerance – polyuria, polydipsia, polyphagia, fatigue 6 fi fi  o Presence of glycosuria or proteinuria Preventing complication: o Keep appointments o Blood glucose self-monitoring o Perform fetal kick counts. Document & report any decrease in activity o Drink 8-10 glasses of water each day to prevent bladder infections & maintain hydration 9. Ectopic Pregnancy -pregnancy in which the fertilized ovum implants outside the uterine cavity. As the embryo enlarges, it creates a potential for organ rupture because only uterine cavity is designed to expand & accommodate fetal development. Rupture & hemorrhage may occur due to the growth of the embryo. Medical emergency Implantation – fallopian tube, some in the ovary, intestine, cervix, or abdominal cavity. Causes of blockage: o Failure of the tubal epithelium to move the zygote (cell formed after the egg is fertilized) down the tube to the uterus due to tubal scarring secondary to Pelvic in ammatory disease. Organisms such as Neisseria gonorrhea & Chlamydia trachomatis attack the fallopian tubes, producing silent infections. o Tubal surgery o Infertility o Intrauterine contraceptive system o Previous ectopic pregnancy o Uterine broids sterilization o Smoking Therapeutic Management o Non-ruptured 1. Laparoscopic 2. Surgery 3. IM – Methotrexate S/S o Abdominal Pain – hallmark with spotting at 6-8 weeks after missed menstrual period o Amenorrhea o Vaginal bleeding Medical Intervention o IM Methotrexate o Monitor beta-hCG level – low level - Surgical Intervention – laparotomy & removal of tube – goal of preventing hemorrhage 7 fi fl 8