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134 Cards in this Set
- Front
- Back
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Types of Spontaneous Abortions:
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Threatened Ab: vaginal bleeding
Inevitable Ab: rupture of membranes, cervix dilates Incomplete Ab: not all products of conception are expelled Complete Ab: all contents of conception are expelled Missed Ab: fetus dies and remains in uterus Habitual Spontaneous Ab: 3 or more consecutive abs |
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Threatened Abortion
Manifestations |
Vaginal bleeding
Uterine cramping Persistent backache Pelvic pressure Cervix remains closed and amniotic membranes are intact B-hCG levels continue to rise, fetus continues to grow Vaginal bleeding: may be brief or last for weeks |
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Threatened Abortion
Therapeutic Management |
H & P: uterine tenderness & fever may indicate what?______infection______
Ultrasound B-hCG level Reduced activity level No sexual activity Perineal pad (peripad) counts: note quantity and color of blood Instruct client to look for passage of tissue i.e. contents of conception Emotional support for anxiety, fear, guilt B-hCG: determine if it’s appropriate for gestational level; see if it’s rising as the fetus grows |
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Inevitable Abortion
manifestations: |
ROM
Cervical dilation Active, heavy vaginal bleeding Therapeutic Management: If natural delivery of fetus occurs, no further treatment is needed. If tissue remains in the uterus: D&C Dilation and vacuum curettage under anesthesia |
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Incomplete Abortion
Manifestations: |
Active uterine/vaginal bleeding
Severe abdominal cramping Cervix is open/dilated Products of conception have been expelled from the uterus but remain in the vagina because of their small size |
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Incomplete Abortion
Therapeutic Management |
CV stabilization (bleeding)
Type and crossmatch IV line (fluids, meds) Curettage: remove remaining tissue IV oxytocin (Pitocin) IM methylergonovine (Methergine) If beyond 14 weeks: curettage may not be performed because of the danger of excessive bleeding…in this case, pitocin or prostaglandins are administered to stimulate uterine contractions until all products of conceptions are expelled |
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Complete Abortion
Manifestations: |
All products of conception are expelled from the uterus
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Complete Abortion
Therapeutic Management |
None unless excessive bleeding or uterine infection occurs
Watch for bleeding, pain, fever Abstain from sex until f/u w/MD |
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Missed Abortion: 2 Major Complications
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Infection: fever, vaginal discharge w/foul odor, abdominal pain/tenderness; tx?
Disseminated Intravascular Coagulation (DIC): Defect in coagulation if fetus is retained for a prolonged period (usually occurs after 1st trim) Anticoagulation and procoagulation factors are activated at the same time (Actively bleeding and clotting at the same time) |
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Missed Abortion
Manifestations |
Fetus dies but is retained in the uterus
Uterus stops growing |
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Missed Abortion
Therapeutic Management |
Fetal death confirmation via _ultrasound_______
D&C: 1st trimester Induction of uterine contractions: 2nd trimester Nausea, breast tenderness disappear when fetus dies Fetal death confirmation via ultrasound |
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Nursing Considerations
All Types of Abortion/Bleeding |
FIRST prevent, identification, treatment of
Hypovalemic Shock |
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Assessment-
Signs of Bleeding |
Tachycardia (often earliest sign)
Decreased BP Pale skin & mucous membranes Confusion/Restlessness Cool, clammy skin |
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Interventions
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Fluid replacement (blood not getting to uterus!), meds, emotional support, pitocin, support resources re: miscarriages
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Ectopic Pregnancy
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Implantation of fertilized ovum in an area outside of the uterus-mostly occurs in fallopian tubes
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Ectopic Pregnancy
Risk Factors |
Scarring of tubes by infection, inflammation, surgery
PID IUD Anatomic Defect Common in multiple induced abortions |
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Nursing Considerations
All Types of Abortion/Bleeding |
FIRST prevent, identification, treatment of
Hypovalemic Shock |
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Assessment-
Signs of Bleeding |
Tachycardia (often earliest sign)
Decreased BP Pale skin & mucous membranes Confusion/Restlessness Cool, clammy skin |
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Interventions
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Fluid replacement (blood not getting to uterus!), meds, emotional support, pitocin, support resources re: miscarriages
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Ectopic Pregnancy
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Implantation of fertilized ovum in an area outside of the uterus-mostly occurs in fallopian tubes
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Ectopic Pregnancy
Risk Factors |
Scarring of tubes by infection, inflammation, surgery
PID IUD Anatomic Defect Common in multiple induced abortions |
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Ectopic Pregnancy
Manifestations |
Triad of Symptoms-
Missed menstrual period Abdominal & pelvic pain Vaginal spotting or light bleeding |
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Ruptured Tube Symptoms
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Sudden, severe pain in one of lower quadrants of abdomen
Intrabdominal hemorrage Irritation of diaphragm-increased shoulder or neck pain s/s of hypovolemic shock |
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Ectopic Pregnancy
Diagnostic Evaluation |
Ultrasound
B-hCG levels lower than normal-indicative of abnormal pregnancy |
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Ectopic Pregnancy
Therapeutic Management |
Unruptured Tube-
-Cytotoxic med (methotrexate) to inhibit cell division (kills fetus) -Surgery to open tube & remove embryo |
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Ectopic Pregnancy
Ruptured Tube |
-Control bleeding
-Prevent hypovolemic shock -Surgery to remove affected tube -if given methotrexate educate about SE nausea, no alcohol, no folic acid |
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Hydatidiform Mole
Gestational Trophoblastic Disease |
Occurs when ovum is fertilized by sperm that duplicates its own chromosomes while chromosomes of ovum are inactivated
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Hydatidiform Mole
Incidence & Etiology |
Placenta but not fetus develops
Cause-unknown Malignant tissue changes follow 15-20% U.S. & Europe: 1 in 1500-2000 pregnancies |
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Hydatidiform Mole
Manifestations |
Vaginal bleeding
Uterus larger than expected for EGA Excessive nausea/vomiting (high B-hCG) Early dev of preeclampsia B/f 24 weeks |
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Hydatidiform Mole
Follow Up |
Cannot get pregnant for at least 1 year after HCG levels drop to normal levels
follow up HCG levels every 2-4 wks until back to normal Then HCG & chest xray for yr |
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Hydatidiform Mole
Diagnostic Evaluation- Ultrasound, B-hCG |
Evacuate mole is the only thing that can be done
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Hemorrhagic Conditions
Late Pregnancy Placenta Previa-Types |
Marginal-low lying placenta-implanted more than 3 cm from cervical os
Partial-w/in 3 cm of cervix Total-completely covers cervix |
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Manifestations
(painless) |
Sudden onset of painless, bright red uterine bleeding
Bleeding may be scant or profuse Bleeding may stop & start Bleeding may not occur until labor starts |
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Diagnosis?
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Ultrasound
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Therapeutic Management
(depends on gestational age of baby) Home Care |
If stable, monitor to get as close to term as possible
Need to have blood available Bed rest, not far from hospital |
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Placenta Previa
Inpatient Care |
-Daily fetal assessments
-Scheduled C/S if fetus is >36 wks & fetal lungs mature -Emerg C/S regardless of EGA if excessive bleeding or alteration in mom's CV status |
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Placenta Previa
Nursing Considerations |
External fetal monitoring
Ultrasound No vaginal exams! Administer oxytocin |
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Abruptio Placenta
Incidence & Etiology |
Separation of normally implanted placenta after 20 wks gestation
occurs when bleeding & formation of hematoma on maternal side of placenta causes separation |
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Abruptio Placenta
unknown cause Risk Factors: |
Abdominal trauma, smoking
Hypertension, previous abruption, coagulopathies, autoimmune disorders, cocaine use |
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Abruptio Placenta-
5 Classic Signs & Symptoms |
Vaginal bleeding (slight)
Abdominal or low back pain Uterine irritability (Board-like) High uterine resting tone (IUPC)-baby can't get oxygen it needs, babys HR drops(non-reassuring FHR) Uterine tenderness |
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Abruptio Placenta
Diagnostic Evaluation |
Ultrasound
Marginal vs. Partial vs. Complete |
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Abruptio Placenta
Nursing Considerations |
Bed rest, left lateral side
CV assessment, maintain IV access, C/S prep as needed, emotional support |
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DIC
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Placental/uterine bleeding-simultaneous decrease in clotting factors and an increase in anticoagulants-circulating blood is unable to clot-allows bleeding from any area
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Kleinhauer-Betke Test
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Determines if any fetal blood cells are in maternal blood-if yes, then placenta has ruptured
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DIC Labs
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-Decreased fibrinogen
-Decreased platelets -Increased prothrombin time & partial prothrombin time |
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DIC
Therapeutic Management |
Delivery is priority!
Blood replacement products |
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DIC can occur with other hemorrhagic conditions of pregnancy such as:
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Abruptio Placentae or
Preeclampsia |
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Hemorrhage-Hypovalemic Shock
First Sign Is? |
Fetal tachycardia
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Early Signs of Hemorrhage
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Maternal tachycardia
Normal BP Increased respiratory rate Cool, clammy skin |
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Hemorrhage Assessment
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Why bleeding & where from
Amount & nature of bleeding, vitals, pain, previa, abruption, FHR, contractions, OB history, due date |
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Late Signs of Hemorrhage
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Decreased maternal BP
Decreased urine output Restless Cold & Clammy |
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Hemorrhage-Diagnosis
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Alteration in fluid balance
Hypovalemia |
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Hemorrhage-Planning
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Monitor for hypovalemia
Fluid replacement, left side lying, prep for surgery, 2nd IV line (18 gauge) |
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Hemorrhage-Interventions
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Pad counts, IV access (18 gauge) left side, labs, blood work, surgical prep
Evaluate |
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Hyperemesis Gravidarum
Etiology |
Persistent, uncontrollable vomiting-begins 1st wks of preg & may continue throughout
Unknown cause |
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Hyperemesis Gravidarum
Therapeutic Management |
Rule out other causes (PUD, cholecystitis)
Increased HCT & HGB=dehydration Electrolytes-decreased Na,K,Cl Increased creatinine=kidney dysfunction (not filtering) |
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Hyperemesis Gravidarum
Therapeutic Management cont |
Antiemetics-phenergan, zofran, reglan, methylprednisone
IV fluids-NaCl with K Electrolyte replacement TPN-enteral feeding via NGT |
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HG-Assessment
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I & O (out at least 30 ml/hr)
Record of bowel elimination Skin/mucous membranes (tenting, dry) Daily weights Urine tested for ketones (indicates protein & fat being metabolized to meet energy needs) |
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HG-Nursing Considerations
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Reduce vomiting-small portions more frequently
Eliminate foods w/ strong odors Low fat, easily digested carbs (fruit, bread, cereal, rice, pasta) Soups, liquids-sit up for 1 hr after eating to decrease reflux |
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Pregnancy Induced Hypertension
PIH |
Preeclampsia
Eclampsia Gestational HTN Chronic HTN Preeclampsia Superimposed on Chronic HTN |
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Preeclampsia-3 Signs
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HTN, proteinuria, generalized edema
BP 140/90 after 20 wks Proteinuria >0.3 grams in 24 hr |
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Eclampsia
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Preeclampsia w/ generalized seizures & increased blood pressure
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Gestational HTN
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Increased BP after 20 wks that is not associated w/ preeclampsia (without protein)
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Chronic HTN
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Increased BP existed prior to pregnancy
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Preeclampsia Superimposed on Chronic HTN
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After 20 wks, sudden increase in BP, proteinuria, thrombocytopenia, abnormal liver enzymes
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Preeclampsia Risk Factors
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1st pregnancy, >35 years old, African Amer, chronic htn, renal disease, +family history, overweight, prepregnancy diabetes, multiple gestation, immunologic disorders (lupus)
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Preeclampsia Pathophysiology
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Generalized cyclic arterial vasospasm w/ unknown underlying cause-decreases CO2 which decreases perfusion
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Preeclampsia-Signs & Symptoms
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HTN, proteinuria, brisk DTR's (hyperreflexia), 3+ edema in lower legs, hands, face, pulmonary, rapid weight gain (fluid), headache, visual disturbances, epigastric pain, decreased urine (dark)
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Preeclampsia-Treatment?
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Only treatment is delivery!
If <34 wks, maternal steroids to accelerate fetal lung maturity and try to delay delivery x48 hrs |
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Preeclampsia Home Care Candidate
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BP systolic greater than or equal to 140 but less than 160
diastolic greater than or equal to 90 but less than 110 1+ protein |
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Preeclampsia Home Care Treatment
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MD every 3-4 days, education-worsening s/s, fetal movement, s/s of labor; restricted activity, daily weight, urine dipped for protein, regular diet no added salt, fetal kick counts
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Preeclampsia Treatment Inpatient
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BP greater than 160 over 110
3+ protein, visual disturbances, increased creatinine, liver function tests, decreased urinary output, edema worsening, multisystem involvement, give mag sulfate |
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Medical Alert-
Magnesium Sulfate (anticonvuslant) Always give IV piggyback |
CNS depressant
NOT an antihypertensive prevents uterine contractions Antidote-Calcium gluconate (have to have by bedside) |
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Magnesium Sulfate toxicity
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Asses FHR variability
Therapeutic Maternal Blood Level 4-8 mg/dl >8 is toxic Serum >8 is toxic, lethargy, resp rate <12 min., DTR's 0 or +1 |
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Antihypertensives (in addition to mag sulfate if necessary)
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Hydralazine (apresoline)
Nifedipine (calcium channel blocker) Labetalol (beta adrenergic blocker) |
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Preeclampsia Postpartum Management
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Continue assessment x48 hrs
Usually remains on mag sulfate for 24 hrs after delivery Recovery-urine output increases, reduced edema w/ weight loss, no urine protein, normal BP in 2 wks |
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Eclampsia
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Patient has had seizures, usually tonic clonic, breathing stops
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Eclampsia Process
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Facial twitching followed by rigidity of body-tonic clonic movements, breathing stops then resumes w/ a long, noisy inhalation-slow to regain conciousness
Fetal bradycardia, loss of variability, late decels Give mag sulfate! |
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PIH HELLP Syndrome
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Hemolysis
Elevated Liver Enzymes Low Platelets |
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HELLP Symptoms
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RUQ, lower chest, or epigastric pain
liver has edema, tenderness, n/v |
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Chronic HTN
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HTN preceded pregnancy or woman is hypertensive prior to 20 wks
BP 140/90 without proteinuria |
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Chronic HTN Risk Factors
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Advanced age, obese, heredity, African American, preeclampsia risk is greater with HTN
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Chronic HTN Antihypertensives
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Careful choices-may reduce placental blood flow
Used if diastolic is >100 Aldomet, Hydralazine (apresoline) Avoid diuretics-can shrink blood volume |
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Rh Incompatibility
2 Circumstances |
Mom is Rh negative
Fetus is Rh positive (dad must be Rh positive) problem for fetus not mom |
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Rh Pathophysiology
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maternal & fetal blood should not mix
reality-drop or two of fetal blood may enter maternal circulation-initiating antibody production to destroy Rh positive blood (isoimmunization or sensitization) |
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Rh Incompatibility Treatment
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Give mom Rhogam
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Rh Sensitization Can Also Occur w/ what other pregnancy related occurences?
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Abruption, miscarriage, spontaneous abortion
placental delivery |
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First Child not Affect by Incompatibiliy Because...
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Baby has not built up antibodies yet
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Rh Fetal & Neonatal Implications
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Fetal RBC's destroyed which decreases O2 carrying capacity
Bilirubin levels increase Destructionof RBC's causes production of immature RBC's (erythroblastosis fetalis) |
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Hydrops Fetalis
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Generalized fetal edema due to anemia which can end in fetal congestive heart failure
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Rh Prenatal Assessment
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1st visit-maternal blood type
If Rh neg-needs antibody titer if indirect coombs=neg, mom unsensitized, fetus not at risk if unsensitized, rhogam given at 28 weeks if sensitized (positive indirect Coombs), test is repeated to watch for increases. increases indicate fetus may be in danger from RBC destruction |
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How does Rhogam work?
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Passive antibodies against Rh factor
Prevents formation of active antibodies |
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Rh Prenatal Management cont.
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Amniocentesis-looks for presenc of bilirubin (baby has erythroblastosis fetalis)
Ultrasound-evaluates fetal condition (hydrops) Intrauterine transfusion-direct infusion of O Negative erythrocytes into umbilical cord by percutaneous umbilical blood transfusion |
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Rh Postpartum
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Unsensitized mom-give Rhogam within 72 hrs of delivery
Rh negative infant-don't have to do anything also rhogam 72 hrs after amnio, abortion, CVS, trauma |
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ABO Incompatibility is when...
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Mom is O
Fetus is A, B, or AB Blood types A, B,AB contain antigen not present in type O People with O develop anti-A or anti-B antibodies naturally as a result of exposure to antigens in foods or to infection by gram negative bacteria JAUNDICE-side effect |
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ABO Incompatibility
Antibodies |
IgG-crosses placenta-hemolysis of fetal RBC's
IgM does not cross placenta Much less severe than Rh incompatibility b/c primary ABO antibodies, IgM do not cross placenta Screen newborn for hyperbilirubinemia (jaundice) |
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Diabetes Mellitus (DM)
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Disorder of carbohydrate metabolism caused by partial or complete lack of insulin secretion by beta cells of pancreas
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DM Etiology
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Without insulin glucose accumulates in the body (blood) resulting in hyperglycemia
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Body tries to dilute glucose by...
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-Polydipsia
-Polyuria -Glycosuria |
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DM Metabolic Processes
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Since body can't metabolize glucose, starts to break down protein & fat to meet energy needs
Protein metabolism-negative nitrogen balance Fat metabolism-buildup of ketones |
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DM-Early Pregnancy (1-20) wks
Metabolism |
Maternal Insulin requirements drop, metabolism doesn't change
However, there is increased insulin released resulting in HYPOGLYCEMIA |
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DM-Late Pregnancy (21 wks-birth) Metabolism
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Maternal insulin needs increase-fetal growth accelerates-placental hormones are antagonistic to maternal insulin-makes more glucose available to fetus and at same time may make mom HYPERGLYCEMIC
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DM-Type I (insulin dependent)
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Insulin dependent
pancreatic beta cells that produce insulin are destroyed by body's immune cells any age, sub-q injection for life |
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DM-Type II (non-insulin dependent)
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Insulin resistance
Pancreas don't produce enough insulin to metabolize glucose Advanced age, obesity Controlled w/ diet, exercise, oral meds |
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Gestational DM
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Onset of glucose intolerance during pregnancy
More likely to recur in subsequent pregnancie May or may not require insulin |
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Gestational DM
Risk Factors |
African Amer, Hispanic, Amer Indian
Family hx, advanced age, obesity, multiple gestation, unexplained loss, previous LGA baby, congenital anomaly |
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Preexisting DM
Maternal Effects |
Preeclampsia
Ketoacidosis UTI's Hydramnios, PROM, shoulder dystocia, injury to birth canal, c-section more likely, postpartum hemorrhage |
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Preexisting DM
Fetal Effects |
Congenital malformations-neural tube defects, cardiac defects, macrosomia, IUGR
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Preexisting DM
Neonatal Effects |
Cardiac dysfunction, hypoglycemia, hyperbilirubinemia, respiratory distress syndrome
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Preexisting DM
Fetal Surveillance |
Testing for anomalies-triple marker screening (1st tri) neural tube defects, chromosomal abnormalities
Ultrasound, fetal echo 20-22 wks structural or cardiac probs 3rd tri-kick counts, BPP, NST:reactive CNS, ultrasound |
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Insulin Therapy
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Combo of short & long acting
Regular/NPH combo b/f breakfast Regular-before dinner NPH-bedtime (intermediate acting) |
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Insulin Therapy
1st Trimester |
decrased Insulin necessary due to antagonistic action of placental hormones, n/v, fetus taking mom's glucose
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IT-2nd & 3rd Trimester
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Increased insulin required due to decrease in placental hormones, decreased n/v
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IT-During Labor
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Tight control 80-110 mg/dl
Type 1-hourly glucose checks w/ either subq or IV reg insulin Type II-variable glucose checks (Every 2-4 hrs) usually don't need insulin |
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IT-Postpartum
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Decreased insulin needs after delivery of placenta (no more antagonistic hormones)
Monitor glucose closely |
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Insulin Therapy
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Combo of short & long acting
Regular/NPH combo b/f breakfast Regular-before dinner NPH-bedtime (intermediate acting) |
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Insulin Therapy
1st Trimester |
Insulin necessary due to antagonistic action of placental hormones, n/v, fetus taking mom's glucose
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IT-2nd & 3rd Trimester
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Increased insulin required due to decrease in placental hormones, decreased n/v
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IT-During Labor
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Tight control 80-110 mg/dl
Type 1-hourly glucose checks w/ either subq or IV reg insulin Type II-variable glucose checks (Every 2-4 hrs) usually don't need insulin |
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IT-Postpartum
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Decreased insulin needs after delivery of placenta (no more antagonistic hormones)
Monitor glucose closely |
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Identifying GDM
1 Hr Glucose Challenge Test |
1 Hour glucose challenge test
24-28 wks, no fasting necessary, 50g oral glucose solution 1 hr prior to blood glucose Glucose >or = 140mg/dl requires additional testing with 3 hr GTT |
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Identifying GDM
3 Hr Oral Glucose Tolerance Test |
Gold standard for dx
High carb diet 3 days prior Fast from midnight day prior Fasting glucose obtained 100 g of oral glucose solution Blood glucose drawn @ 1,2,3 hrs after ingestion of glucose GDM diagnosed if fasting glucose is abnormal, 2 or more other values are abnormal |
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Maternal Hypoglycemia
Signs and Symptoms |
Dizziness, confusion, shakiness, hunger, nausea, sweating, cool and clammy skin
give orange juice! |
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Maternal Cardiac Disease
CV Alterations During Pregnancy |
Increased plasma volume
Increased cardiac output (d/t increased HR & increased stroke volume) Normal heart adapts to these changes |
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Rheumatic Heart Disease
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Follows strep throat infection
Can cause scarring of heart & valve stenosis |
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Mitral valve stenosis
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Obstructs blood flow from left atrium to left ventricle
Left atrium dilates Pressure in pulmonary veins elevated Pulmonary HTN, edema, CHF |
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First s/s of heart failure
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Dypsea, SOB, heart speeds up, rails, progressive edema
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Left Sided Heart Failure-
Left side has to pump harder |
Normal tachycardia of pregnancy shortens diastole and decreases time available to cross valves-back pressure on pulmonary trunk, decreased BP, pulmonary hypertension increases, fluid leaks into interstitial spaces, pulmonary edema
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Right Sided Heart Failure-blood backs up
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Output of right ventricle is less than what right atria receives causing back pressure-congestion of systemic venous circulation w/ decreased cardiac output to lungs, BP decreases, vein distention, abd fluid, ascites, generalized edema, fatigue
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Class I Heart Disease
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Ex. mitral valve prolapse
uncompromised no limits on physical activity asymptomatic with ordinary activity |
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Class II Heart Disease
small risk |
Slightly compromised
Slight limitation on physical activity Comfortable at rest, ordinary activity causes fatigue, dyspnea, palpitations or anginal pain |
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Class III Heart Disease
great risk |
Marked limitation of physical activity-no housework
Comf @ rest but less that ordinary activity causes excessive fatigue, papitations etc. Markedly compromised. |
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Class IV Heart Disease
great risk |
Inability to perform any physical activity without discomfort
Symtoms of cardiac insufficiency even at rest |
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Cardiac Disease Meds
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Anticoagulants-Heparin & Lovenox-given subq
DO NOT GIVE COUMADIN |
