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PREGNANCY INDUCED HYPERTENSION (PIH):


Most commonafter 20 weeks; lower socioeconomic group
High risk for: IGR, fetal distress, increased uterine contractility, and abruption placenta
Reynolds Risk Score (RRS)measures risk factors for CVD
Gestational hypertension (GH):
1. After 20 weeks
2. Without proteinuria or edema
3. Resolves within 6 weeks after birth
Mild Preeclampsia
1. Nonconvulsive form
2. >140/90 after 20 weeks gestation
3. Proteinuria 1-2+
4. Weight gain: 4.4 lbs per week in last 2 trimesters
5. Slight edema of face or upper extremities
6. Associated with vasospasm and decreased renal perfusion
7. More common in young primigravidas, women over 35, multiple gestations, DM,
and molar pregnancy
8. At risk for stroke, DIC, renal failure, and hepatic rupture
9. Resolves after delivery
Severe preeclampsia
1. Non-Convulsive
2. BP reaches or exceeds 160/100
3. Proteinuria 3-4+
4. Oliguria, cerebral or visual disturbances such as HA or blurred vision, hyperflexia, pulmonary
or cardiac problems, thrombocytopenia, hepatic dysfunction, right upper quadrant and
epigastric pain
5. Severe peripheral edema
6. Serum creatinine > 1.2
Eclampsia
1. Same as severe preeclampsia, but Convulsive form with seizures and/or coma
2. >180/110 (on two occasions 6 hours apart-while on bedrest) after 20 weeks
3. HELLP syndrome
4. At risk for hemorrhage, stroke, pulmonary edema and hepatic rupture
Complications:
1. abrupto placenta
2. HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelet count)
3. Coagulopathy
4. Stillbirth
5. Seizures
6. Coma
7. premature labor
8. renal failure
9. maternal hepatic damage.
Contributing factors:
1. Preexisting vascular diseasehyperlipidemia, HTN, PAD, CHF, stroke
2. Maternal age (>40)
3. Chronic renal disease

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4. Pyelonephritis
5. DM
6. Multiple fetuses
7. 1st pregnancy
8. Morbid obesity
9. Rh incompatibility
10. Molar pregnancy
11. Diets high in saturated fat, trans fat, cholesterol, calories, alcohol, and salt
12. Diets low in fiber, fruits, and vegetables
13. Smoker
Signs & Symptoms:
1. Sudden weight gain
2. Irritability
3. Severe frontal headache
4. Emotional tension
5. Blurred vision
6. Epigastric pain or heartburn
7. Preeclampsia: 160/110 or >
8. Eclampsia: SBP > 180 with seizures
9. Generalized edema, especially of face
10. Pitting edema of legs and feet
11. Oliguria
12. Hyperreflexia
13. Vascular spasm, papilledema, retinal detachment or edema, arteriovenous nicking
or hemorrhage (seen on ophthalmoscopy)
PRIORITY Nursing DX:
1. Deficient Fluid Volume
2. Risk for Injury
3. Anxiety
4. Deficient Knowledge
IMPLEMENTATION & COLLABORATIVE CARE:
1. Only cure delivery
2. TX: Mag Sulfate before or after PIH onset to depress vascular and neurologic
activity, lower BP, and prevent or stop seizures
3. Goal of care deliver healthy, viable infant while safeguarding mothers health
4. Enforce bedrest in side-lying position
5. Quiet, calm environment
6. Lifestyle changes: weight control, increase physical activity, stop alcohol intake,
sodium restriction, increase fresh fruits, vegetables, and low-fat dairy products,
reduce intake of saturated fats
7. Stop smoking
8. Consume oily fish twice weekly
9. If high risk for CVD325mg ASA daily
10. Limit caffeine
11. Assess fetal maturity and betamethasone treatment to assist maturation of lungs
before delivery if indicated
12. Frequent maternal assessments: BP, HR, RR, edema, deep-tendon reflexes
13. Assess for: HA, visual changes, epigastric pain

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14. Frequent fetal assessments: FHR, fetal compromise, and/or signs of labor
15. Foley monitor renal output; strict I&O; evaluate urine for protein; assess daily
weight
16. Administering anti-hypertensives, magnesium sulfate, and/or oxygen
17. Administer magnesium sulfate
a. Seizure prevention
b. Serum level 5-8mg/dl
c. > 8mg/dl toxic
d. Decreased urine output can increase risk of toxicity
e. Depressed reflexes and respirations < 12-14 may indicate toxicity
f. Calcium gluconate emergency administration to counteract toxicity
18. Induction or C-section when fetus mature or if maternal condition worsens
19. Teaching and support
20. Evaluate NB for signs of depression related to mag/sulfate

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DIABETES: p. 333
TYPE 1: absolute insulin insufficiency
TYPE 2: insulin resistance or deficiency
GESTATIONAL DIABETES: glucose intolerance due to pregnancypancreas unable to meet
increased demands for insulin production during pregnancyusually resolves within weeks of
delivery
Effects of pregnancy on glucose metabolism:
1. 1st trimester insulin needs decreased
2. Late 1st trimester insulin requirements rise as glucose use and glycogen storage by
mother and fetus increase
3. Human placental lactogen (hPL) from placenta causes resistance to action of
maternal insulin increases circulating glucose for fetal use and increases demand
on moms pancreas to produce more insulin
4. Fetus produces own insulin but gets glucose from mom across placenta; amount
of glucose a/v in moms circulation stimulates fetal pancreas to produce insulin

Effects of DM on pregnancy and fetus relate to degree of control of blood glucose (BG levels
between 70-110 and degree of vascular involvement; complications more common with DMI
and include the following:
1. Maternal hydraminosincreased volume of amniotic fluid
2. Preeclampsia, eclampsia, ketoacidosis, and worsening retinopathy
3. Dystocia (abnormal labor or childbirth), shoulder dystocia, and stillbirth
4. Neonatal macrosomnia (large body), hypoglycemia, hyperbiliruinemia, increased incidence
of congenital anomalies, and delayed fetal lung maturity fetal RDS
ASSESSMENT:
1. Risk factors:
a. FH of DM
b. Maternal obesity
c. Maternal age > 30
d. Previous LGA infant
e. Previous unexplained stillbirth
2. Classic DM symptoms:
a. Polyuriaexcess urine output
b. Polydipsiaexcessive thirst
c. Polyphagiaexcessive hunger
d. Hyperglycemia
e. Blurred vision
f. Excess weight gain
g. Increased candida infections
3. Urine assessment for glycosuria and ketones
4. DM screening: 28 weeks (or earlier if risk factors)
a. 50-gram oral GTT
b. If BG > 140 at one hour 3-hour 100-gram oral GTT completed
PRIORITY Nursing DX:
1. Risk for Imbalanced Nutrition, Maternal & Fetal: More Than Body Requirements
2. Risk for Injury: Maternal and Fetal
3. Anxiety
4. Deficient Knowledge

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IMPLEMENTATION & COLLABORATIVE CARE:


1. Educate on ADA diet with no concentrated sweets; diet may control DGD; avoid excessive
weight gain; caloric needs will increase with pregnancy
2. Medications: glyburideusually AVOID oral meds d/t birth defects; human insulin more
commonly used
3. Educate need for frequent monitoring of BG, urine glucose and ketones; diary of test results
and activity; fetal kick counts
4. Regular nonstrenuous exercise (walking) for weight control
5. HbA1c q 3 months
6. Monitor fetal well-being:
a. Quadruple screen
b. US for abnormalities, amniotic fluid volume, and fetal size
c. Fetal movement counts
d. Weekly non-stress test (NST) from 28-32 weeks
e. Bio-physical profile (BPP)
f. Amniocentesis for lung maturity to assess LS ratio (normal 1:2, needs to be 1:3)
7. Monitor mom for possible complications:
a. Infection
b. Preeclampsia
c. Diabetic ketoacidosis
8. Possible induction of labor at 38-39 weeks to reduce risk of stillbirth
9. Prepare for possible shoulder dystocia
10. Insulin requirements drop dramatically after delivery of placenta and removal of hormonal
influences; mom may need no insulin or decreased dose
11. Educate mom on following signs of:
a. Hypoglycemia: weakness, headache, nervousness, hunger, blurred vision; pale, moist
skin; shallow respirations, rapid pulse, tingling extremities
b. Hyperglycemia: thirst, increased urination, abdominal pain, nausea and vomiting,
flushed skin, fruity (acetone) breath

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HYPERTHYROIDISM: Treat with PTU
S&S:
1. Heat intolerance
2. Diaphoresis
3. Fatigue
4. Anxiety
5. Emotional lability
6. Tachycardia
7. Weight loss d/t nausea, vomiting, diarrhea
8. Low TSH
9. Elevated T3 & T4
HYPOTHYROIDISM: Treat with levothyroxine or Synthroid
S&S:
1. Weight gain
2. Hair loss
3. Constipation
4. Cold intolerance
5. Dry skin
6. Brittle nails
7. Elevated TSH
8. Low T3 & T4

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PLACENTA PREVIA (3 types): (key words: PAINLESS; BRIGHT RED BLOOD)


Placenta implants in lower uterine segmentthree types:
1. Marginalcovers portion of cervical os
2. Partialplacenta caps larger part of internal os
3. Totalplacenta covers all of internal osgreater blood loss
Common cause of bleeding during 2nd half of pregnancy
More common after age 35; multigravida
CRITICAL COMPONENT: sterile vaginal exam is CONTRAINDICATED in all pregnant women with
extensive vaginal bleeding until source of bleeding is identified. IF performed with placenta
previa increased maternal bleeding and can dislodge more of the placenta
Fetal prognosis dependent on GSA and amount of blood loss
Risk factors:
1. Endometrial scarring:
a. Previous placenta previa
b. Prior c-section abortion
c. Mutiparity
2. Impeded endometrial vascularization
a. Advanced maternal age
b. DM or HTN
c. Cigarette smoking
d. Uterine abnormalities/fibroids/endometritis
3. Increased placental mass
a. Large placenta
b. Multiple gestation
SIGNS & SYMPTOMS:
1. PAINLESS, bright red, vaginal bleeding after 20 weeks
2. Vaginal bleeding before labor onsetepisodic and stops spontaneously
3. May be asymptomatic
4. Soft, nontender uterus
5. Fetal malpresentation
6. Minimal descent of fetal presenting part
7. Good fetal heart sounds or may be bradycardic or variable deceleration.
INTERVENTIONS & COLLABORATIVE CARE:
1. NO VAGINAL EXAM
2. Control blood loss & provide blood replacement
3. Oxygen(blood loss decreases oxygen to fetus)
4. Monitor vaginal bleeding and uterine activity
5. Enforce bedrest with bathroom privileges
6. FHR & uterine contractions
7. Monitor labs: CBC, platelets, PT/INR
8. Continuous monitoring: BP, HR, RR, I&O, FHR
9. Prepare for c-section
NOTIFY PHYSICIAN for any of following:
1. Increase in vaginal bleeding
2. BP < 90/60; HR < 60 or > 120; RR < 14 or > 26
3. Temperature > 100.4F (38C)
4. Urine output < 30 ml/hr

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5.
6.
7.
8.

O2 sat < 95%


Decreased LOC
Onset or increase in uterine activity
Non-reassuring fetal status

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ABRUPTIO PLACENTAE: (key words: PAINFUL; DARK RED BLOOD; SUDDEN onset)
Premature separation of placenta from uterine wall
Usually occurs after 20 weeks; most commonly 3rd trimester
Three classifications:
1. Mid-grade or mild separation (marginal):
a. mild separation with internal bleeding between placenta and uterine wall
b. mild to moderate vaginal bleeding
c. vague lower abdominal wall discomfort
d. fetal monitoring indicating possible uterine irritability
e. strong and regular FH tones
2. Moderate grade 2 or moderate separation (central):
a. Continuous abdominal pain
b. Moderate DARK RED vaginal bleeding
c. Severe or abrupt onset of symptoms
d. VS may indicate impending shock
e. Tender uterus, remaining firm between contractions
f. Barely audible or irregular and bradycardic FH tones
g. Labor starts w/I two hours and proceeds rapidly
3. Severe grade 3 or severe separation (complete):
a. ABRUPT onset of agonizing, unremitting uterine pain
b. Moderate vaginal bleeding
c. VS indicate rapidly progressive shock
d. Absence of FH tones
e. Tender uterus with border-like rigidity
f. Possible increase in uterine size if abruption severe & concealed
RISK FACTORS:
1. Previous abruption
2. Chronic HTN or HTN of pregnancy
3. Abdominal trauma
4. Multi-parity
5. PROM
6. Smoking or cocaine or methamphetamine use
7. Uterine anomalies/fibroids
8. Advanced maternal age
9. DM
Risks for Mom:
1. Hemorrhagic shock
2. Disseminated intravascular coagulation (DIC)
3. Hypoxic damage to organs (such as kidneys, liver, brain)
4. Postpartum hemorrhage
Risks for NB:
1. Preterm birth
2. Hypoxia, anoxia, neurological injury, and fetal death r/t hemorrhage
3. IGR
MATERNAL ASSESSMENT FINDINGS:
1. Hypovolemic shock, hypotension, oliguria, thread pulse, shallow/irregular respirations,
pallor, anxiety

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2. Vaginal bleeding (but may be concealed hemorrhage)


3. Severe abdominal pain
4. Uterine contractions/tenderness/increasing uterine distension
5. Uterus enlarged or irregular shape
6. N/V
7. Decreased renal output
FETAL ASSESSMENT FINDINGS:
1. Tachycardia
2. Bradycardia
3. Loss or variability of FHR, late decelerations, decreasing baseline FHR
4. Distress evident
5. Engagement may be noted
INTERVENTIONS & COLLABORATIVE CARE
1. 911 medical management: unstable mom or fetus:
a. C-section delivery indicated
b. Monitor maternal volume status
c. Restore blood loss
d. Monitor coagulation state
2. IF mom & fetus are stable:
a. Hospitalization
b. monitor FHR
c. monitor maternal bleeding
d. Monitor uterine activity
e. Monitor abdominal pain
f. Monitor vaginal bleeding
g. Monitor maternal CBC, PT/INR
h. Corticosteroids may be given to accelerate fetal lung maturity
i. Strict I&O

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PROM: Premature Rupture of Membranes


PPROM: preterm (before 36 weeks) premature rupture of membranes before onset of labor
SROM: spontaneous break or tear in amniotic sac before onset of regular contractions, resulting
in progressive cervical dilation
Increased risk for the following:
1. Fetal infection
2. Sepsis
3. Perinatal mortality
4. Risks increase with every hour of ruptured membranes, every hour of labor, and every
vaginal examination or other invasive procedure
Predisposing factors:
1. Poor nutrition and hygiene
2. Lace of prenatal care
3. Incompetent cervix
4. Increased intrauterine tension d/t hydramnios or multiple pregnancies
5. Defects in amniotic membrane
6. Uterine, vaginal, and cervical infections (most commonly group B Strept, gonorrhea, and
chlamydia)
Signs & Symptoms:
1. Infection indicated by the following:
a. Maternal fever
b. Fetal tachycardia
c. Foul-smelling vaginal discharge
2. ALERT: mom at risk for chorioamnionitis if period between ROM and onset of labor > 24
hours
ASSESSMENT:
1. Gush of watery, clear, or meconium-stained fluid from vagina with continuous leakage
2. Amniotic fluid turns nitrazine paper blue alkaline pH; urine is almost always acidic and
does not change the yellow nitrazine paper
3. Amniotic fluid shows ferning pattern on microscopic exam
4. Unengaged fetus is at risk for a prolapsed cord
Management:
a. TERM: If spontaneous labor and vaginal delivery dont result w/i 24 hours
1. Assist with induction of labor
2. Assist with c-section if induction fails
b. PRETERM (28-34 weeks):
1. Hospitalize mom
2. Observe for S&S of infection
3. Obtain baseline cultures
4. Assist with induction of labor, administer IV antibiotic if test results are positive for
infection
5. Administer prophylactic antibiotic if patient has group B strep
6. Monitor for signs of maternal infection:
a. Fever
b. Abdominal tenderness
c. Changes in amniotic fluid (purulence or foul odor)
d. Fetal tachycardia (may precede maternal fever)

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e. Report signs immediately to PCP


PRIORITY Nursing DX:
1. Risk for Infection
2. Anxiety
3. Risk for Injury: Maternal or fetal
4. Deficient Knowledge

ALERT: ALWAYS assess FHR immediately after ROM whether it is spontaneous or by amniotomy!!

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PROLAPSED UMBILICAL CORD:
Descent of umbilical cord into vagina before presenting part
CAUSES:
1. PROM
2. Fetal position other than cephalic
3. Placenta previa
4. IU tumors preventing presenting part from engaging
5. Small fetus
6. Hydramnios
7. Multiple gestation
8. Factors interfering with fetal descent
SIGNS & SYMPTOMS:
1. Cord palpable at perineum during vaginal exam or may be visible
2. FHR pattern with variable decelerations
3. US confirms prolapse
MANAGEMENT:
1. ALERT: immediate measures to relieve pressure on cord are initiated
a. Place mom in trendelenburg or knee-chest position
b. Sterile-gloved hand may be inserted into vagina to elevate fetal head up and off cord
2. Administer oxygen
3. Monitor FHR
4. If cord exposed, apply saline-soaked sterile dressings over any portion of cord
5. Prepare to assist in vaginal birth if cervix fully dilated; c-section if cervical dilation
incomplete
ALERT: ALWAYS assess FHR immediately after ROM whether it is spontaneous or by amniotomy!!

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HYPEREMESIS GRAVIDARUM:
Nausea & vomiting secondary to elevated HCG becomes extreme.
Prolonged beyond 12 weeks
Causes weight loss of 5% or more
Dehydration, electrolyte imbalance, ketosis, acetonuria
HISTORY MAY REVEAL:
1. 1st pregnancy
2. < 20 years old
3. Obese
4. Multiple birth pregnancy
5. History of psychiatric disorder
6. Hyperthyroidism
7. Vitamin B deficiencies
8. Elevated stress level
9. GESTATIONAL TROPHOBLASTIC DISEASE: growth and degeneration of cells in placenta to
grape-like clusterscomplete mole with no fetus or partial mole with genetic material
derived from fertilized ovum
SIGNS & SYMPTOMS:
1. Vomiting over prolonged period
2. Dehydration: poor skin turgor, dry mucous membranes
3. Weight loss
4. hypotension
5. tachycardia
TEST RESULTS:
1. UA: ketones, acetones, elevated specific gravity
2. Electrolytes: reduced Na, P, Cl
3. Acidosis due to vomiting
4. Elevated liver enzymes
5. Thyroid test may be elevated
6. Hematocrit may be elevated due to dehydration
TX:
1. IV fluids: lactated ringers
2. Electrolyte replacement as indicated
3. Vitamin B6 and other vitamins as indicated
4. Antiemetic to control nausea and vomiting (promethazine or metoclopramide)
5. NPO for 24-48 hours
6. Advance diet if no vomiting within 24 hours to 6 small meals
7. Enteral nutrition by tube or TPN if vomiting persists
PATIENT SAFETY:
Assess mental status for signs of depression, anxiety, or irritability, which may indicate adverse
reactions to medications.

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Neural tube defects:


Neural tube develops into the brain and spinal cord
Defect is failure of the neural tube to close within 28 days after conception
Cause unknown; link between adequate FOLIC acid prior to pregnancy and in first trimester
Spina bifida occulta:
1. Incomplete closure WITHOUT the spinal cord or meninges protruding
2. Usually no neurologic dysfunction, but may be bladder or bowel disturbances or weakness
in foot
Spina bifida cystica:
1. Incomplete closure WITH the spinal cord or meninges protruding in a sac.
a. Myelomeningocele: sac contains the spinal cord, cerebral spinal fluid, and meninges.
Experiences neurological dysfunction
b. Meningocele: sac contains cerebral spinal fluid and meninges. Rarely experiences
neurologic dysfunction.
Anencephaly:
1. Cerebral hemispheres of the brain and top portion of skull.
2. Brain stem intactwill have cardiopulmonary functions
3. Infant likely to die of respiratory failure within few weeks of birth
Encephalocele:
1. Portions of brain and meninges protrude in the sac.
2. Experiences neurological dysfunction
SIGNS & SYMPTOMS:
1. Spina bifida occulta
a. Tuft of hair in lumbar or sacral area
b. Depression in lumbar or sacral area
c. Hemangioma in lumbar or sacral area
2. Spina bifida cystica meningocele:
a. Presence of sac
3. Spina bifida cystica myelomeningocele:
a. Presence of sac
b. Bowel and bladder incontinence
c. Hydrocephalus
d. Spastic paralysis
e. Club foot
f. Knee contractures
g. Curvature of spine
h. Arnold-Chiari malformation
4. Anencephaly
a. Top portion of skull is missing
5. Encephalocele
a. Mental retardation
b. Paralysis
c. Hydrocephalus
TX:
1. Surgery within 48 hours of birth to close opening and decrease risk of infection and prevent
spinal cord damage
2. Insert shunt to relieve hydrocephalus

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TEST RESULTS:
1. Maternal serum alpha-fetoprotein (MSAFP)high levels
2. Amniocentesis: if MSAFP hightest for alpha-fetoprotein in amniotic fluid (+)
3. US: to assess neural tube defect
4. Transillumination of sac: done after birth. Differentiates between myelomeningocele and
meningocele. Meningocele sac DOES NOT transilluminate.
Nursing Interventions after birth:
1. Infant on side to prevent pressure on sac
2. Keep sac covered with sterile dressing soaked in warm saline
3. Measure head circumference to determine if hydrocephalus develops
4. Monitor for infection around sac
5. Assess for leakage
6. Assess for bladder and bowel function
7. Assess neurologic signs
8. Reposition infant q2h to prevent pressure ulcers and contractures

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GENETIC ABNORMALITIES (condition & common S&S):


TRISOMY 21, 18, 13: Mental retardation, hypotonia; congenital heart disease
TRISOMY 18: Prominent occiput, LOW set ears, ptosis (drooping eyelid), syndactyly (webbed
fingers)
TRISOMY 18, 13: GI tract abnormalities, malformation of other organs, microcephaly
TRISOMY 13: seizures, malformed ears, cleft lip/palate, polydactyly (extra digits)
TURNER (XO) females: No intellectual impairment, perceptual difficulties, low hairline, short
stature, excessive nevi (skin pigmentation/discoloration), wide chest with spaced nipples, no toe
nails, fibrous streaked ovaries, underdeveloped secondary sex characteristics, infertility, renal
abnormalities
KLINEFELTER (XXY) males: mild retardation, gynecomastia, lack of male musculature,
underdeveloped secondary sex characteristics, infertile/sterile

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STIs: Sexually Transmitted Infections:
Infections spread through sexual contact with an infected partner
Increased risks for mom, fetus, or neonate
Possible maternal complications:
1. Preterm labor
2. PROM
CAUSES:
1. Fungi
2. Bacteria
3. Protozoa
4. Parasites
S&S:
1. Typically involve some type of vaginal discharge or lesion
2. Vulvar or vaginal irritation, causing pruritus
MANAGEMENT:
1. Provide antifungal or antimicrobial
2. Teach patient about safer sex practices
3. Explain mode of transmission and how to reduce risk of transmission
4. Urge patient to refrain from intercourse until active infection completely resolve
5. Advise patient partner(s) need to be examined and treated
6. Encourage vulvar hygiene and dryness
7. Avoid soaps, creams, douching, or other ointments
8. Suggest cotton underwear and avoid tight-fitting clothing
Selected STI & pregnancy:
1. Chlamydia
a. May be asymptomatic
b. Dysuria may be in both males and females
c. Heavy, gray-white vaginal discharge
d. Painful urination
e. TX: amoxicillin or azithromycin
f. Most common STI
g. Can be transmitted to neonate during delivery and cause neonatal conjunctivitis and
pneumonia
2. Gonorrhea:
a. May be asymptomatic
b. Yellow-green vaginal discharge
c. Dysuria
d. Urinary frequency
e. Vulval inflammation/cervical swelling
f. Male partner experiencing severe pain on urination and purulent yellow discharge
g. TX: Ceftriaxone or cefexime (and must also give ATB for chlamydiaazithromycin or
amoxicillin)
h. Associated with spontaneous miscarriage, preterm birth, and endometritis in
postpartum
i. Treatment of sexual partner required
j. Severe eye infection leading to blindness in the neonate if infection present at birth
3. Candidiasis:

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4.

5.

6.

7.

8.

9.

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a. Yeast infection
b. May cause oral yeast infection in neonatecalled thrush
c. TX: low-dose Diflucan
Group B Streptococci infection:
a. May be asymptomatic
b. May lead to UTI, intra-amniotic infection leading to preterm birth, and postpartum
endometritis
c. CDC recommends screening at 35-38 weeks in all pregnant women
Trichomoniasis:
a. Yellow-green, frothy, odorous vaginal discharge
b. Vulvar itching, edema, and redness
c. TX: metronidazole (Flagyl)
d. May be associated with preterm labor, PROM, and post-cesarean infection
e. Treatment of partner required, even if asymptomatic
BV: bacterial vaginosis
a. Risk factors:
1. Frequent sexual intercourse without condom
2. Trauma from douching
3. New sexual partner or multiple partners
4. Maternal vitamin D deficiency
b. Thin, watery, white or gray vaginal discharge with FISHY odor
c. clue-cells on wet-mount
d. TX: metronidazole (Flagyl)
Genital Herpes
a. PAINFUL, small vesicles with erythematous base in cervical, vaginal, or anal areas
b. Low-grade fever, flu-like symptoms
c. dysuria
d. Dyspareunia
e. Positive viral culture
f. TX: acyclovir
g. NO cure
h. Abstinence until vesicles completely healed
i. Transmission to neonate possible if active lesions present at birth, which can be fatal
j. C-section if patient has active lesions
Syphilis
a. PAINLESS chancreulcer on vulva or vagina
b. Fever, weight loss, and malaise may be noted
c. Hepatic and/or splenic enlargement, HA, anorexia, maculopapular rash on palms and
soles
d. TX: penicillin G or benzathine
e. Possible transmission across placenta after about 18 weeks gestation spontaneous
miscarriage, preterm labor, stillbirth, or congenital defects
f. Standard screening1st prenatal visit; at 36 weeks if mom has multiple partners
g. Jarisch-Herxheimer RX: sudden hypotension, fever, tachycardia, and muscle aches that
occur within 6-12 hours of treatment, but resolve in 24 hours.
Condyloma acuminate
a. Caused by HPV
b. Genital warts

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c. Soft, grayish pink, cauliflower-like lesions in genital area


d. Can become cancerousmust be biopsied and treated immediately
e. Topical application of TCA (trichloroacetic acid) or BCA (bichloracetic acid)
f. Increased risk of cervical cancer
10. HIV/AIDS:
a. S&S:
1. Lymphadenopathy
2. Fevers
3. Night sweats
4. Weight loss, thrush
5. Thrombocytopenia
6. Diarrhea
7. Severe vaginal yeast infection
8. Abnormal pap
9. Frequent and recurrent BV, trichomonas, and genital herpes infections
10. Sore or lesion on vulva
11. Increased vaginal discharge
12. Pain and bleeding after intercourse
13. Pelvic pain
b. STANDARD precautions
c. Monitor CD4 counts and vial loads
d. Antiviralvaries
e. ALERT: avoid use of internal fetal monitors, scalp blood sampling, forceps, and vacuum
extraction
f. Discourage breast-feeding
11. Pediculosis pubis:
a. crab louse
b. Itching in pubic area
c. TX: permethrin topically to pubic hair for 10-15 minutes, then washed off
d. MAJOR house cleaning
12. Scabies:
a. Burrows under skin
b. Itching that worsens at night or when patient is warm
c. Erythematous, papular lesions; furrows
d. TX: permethrin topically to entire body for 8-14 hours; repeat in 2 weeks if live mites still
exist
e. MAJOR house cleaning
OTHER: (all viral)

HEPATITIS A
1. Fecal-oral
2. Acute infection
3. Immunization available
4. S&S: jaundice, anorexia, nausea, vomiting, malaise, and fever
HEPATITIS B
1. Blood/body fluids
2. CHRONIC infection

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3. Immunization available
4. S&S: Similar to hep A but includes arthralgias, arthritis, and skin eruptions or rash
HEPATITIS C
1. Blood/body fluids
2. CHRONIC
3. No immunization
4. S&S: Similar to hep A but includes arthralgias, arthritis, and skin eruptions or rash
5. People at higher risk:
a. IV drug users
b. Healthcare workers who receive needle stick
c. Multiple sexual partners
HEPATITIS D
1. Blood/body fluids
2. CHRONIC
3. No immunization
4. S&S: Similar to hep A but includes arthralgias, arthritis, and skin eruptions or rash
HEPATITIS E
1. Fecal/oral
2. Acute infection
3. No immunization
4. S&S: jaundice, anorexia, nausea, vomiting, malaise, and fever
5. South Central Asia & Middle East

PELVIC INFLAMMATORY DISEASE (PID):


Normally infection caused by STI: gonorrhea or chlamydia
Other contributing factors:
1. Presence of IUD
2. Douching
3. Menstruation
S&S:
1. Lower abdomen tenderness
2. Fever > 101
3. Cervical discharge and tenderness
4. Urinary tract symptoms
5. Infertility
6. Dyspareunia (painful intercourse)
7. Flu-like symptoms
TEST:
1. Elevated ESR, CRP
2. Cultures positive for chlamydia or gonorrhea
TX:
1. Cefoxitin or ceftriaxone IM and clindamycin
2. All partners need treatment
3. Abstain from sexual intercourse until treatment complete

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HEMOGLOBINOPATHIES OF PREGNANCY: (issues with RBCs)


SICKLE CELL:
Abnormal gene results in production of irregular RBC called hemoglobin Swhich replaces some
of the normal hemoglobin A
RBC collapses in to a crescent shape (sickling)when stresseddehydration, hypoxemia, or
acidosis
Cells sickle, clumpins is noted, obstructs small vessels and blocks blood flow
Short life span Autosomal traite from both parents
Chronic illness with blocked and/or inadequate circulation and tissue/organ damage
Causes pain and over time, organ failure/death
SIGNS & SYMPTOMS:
1. Acute pain d/t blocked vessels & tissue ischemia
2. Extremitiesswelling
3. may have chest pain
4. Livermay have jaundice
5. Kidneyhematuria and/or impaired function
6. Brainstroke, seizures
7. Fatiguesecondary to anemia
8. Fever during sickling episodeinfection
9. Pooling of blood in organs results in enlargement
10. Organ damage d/t vessel blockage:
a. Cardiomegalyweakened heart valves & heart murmur
b. Lungs, kidneys, liver, spleen malfunction & failure
TREATMENTS:
1. Hydration
2. Antibiotic for infection
3. Oxygen
4. Pain medication
5. Electrolyte replacements
6. Bed rest with mild ROM
PT EDUCATION:
1. Adequate hydration
2. Avoid infection
3. Moderate activity & rest as needed
4. Support
THALASSEMIA:
Inherited disorder involving deficiency in production of globin chains in hemoglobin
-thalassemia
Minor
Occurs with trait carrier
Chinese, Thai, African, and Mediterranean descent
Non-symptomatic
-thalassemia(more common)
MAJOR or Cooleys anemia

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Greek, Italian, Syrian descent


Defective hemoglobin and damaged RBCs result in severe anemia
Folic acid deficiency may result
Transfusion dependent
Marked hepatosplenomegaly & bone changes secondary to increased hematopoiesis
Death generally caused by infection or CV complications before 3rd decade of life
Female infants who survive puberty and usually have amenorrhea and severely impaired fertility
Characteristic findings:
1. High RBC
2. Microcytosis
3. Severe anemia
4. Overload of iron so iron may be contraindicated

SIGNS & SYMPTOMS:


1. MAJOR:
a. ANEMIAPallor, fatigue, poor feeding
b. Hypoxia, headache, irritability, bone pain, anorexia
2. MINORasymptomatic
TREATMENT:
1. Maintain adequate Hgb levels
2. Provide blood cells to promote growth and maintain hgb > 9.5

Rh or ABO incompatibility:

If mom Rh (-) and baby Rh (+)


1. FIRST PREGNANCYwill sensitize the mothers system and antibodies will be formed
2. Development of maternal antibodieswill destroy fetus Rh-positive blood
ISOIMMUNIZATION or SENSITIZATION
3. AFTER DELIVERY of Rh (-) infant RHOGAMmom onlywithin 72 hours
INDIRECT COOMBS TEST: to determine if whether mom is sensitized from a previous exposure
o If negative (unsensitized) will receive RhoGAM at 28 weeks as preventive measure to
prevent formation of active antibodies during remainder of pregnancy
o If positive (sensitized)if mom not treated with RhoGAMfetus at risk of having RBCs
destroyed by moms antibodies
DIRECT COOMBS TEST: identifies presence of maternal antibodies in the neonates bloodif
positivenotify PCP

Only MOM GETS RHOGAM

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CV DISEASE: p. 332
CLASS I: ASYMPTOMATICno limitations
CLASS II: asymptomatic at rest, symptomatic with heavy physical activity, slight limitations
CLASS III: asymptomatic at rest, symptomatic with minimal physical activity; considerably limitations
CLASS IV: symptomatic at rest and with any activity; SEVERE limitations
Class I & IIusually do well during pregnancy
Class III & IVsignificantly increased risk of morbidity and mortality with pregnancy

ANTEPARTUM FETAL ASSESSMENTS: 340-343


Chorionic villus sampling (CVS):
Obtained from placenta to detect genetic abnormitiesas soon as 10 week but higher risk of
fetal injury or mortality
Risk for ROM, bleeding, infection
Percutaneous umbilical blood sampling (PUBS): Invasivesample of fetal blood to check for fetal
anemia, isoimmunization, metabolic disorders, and infection. US guided
Biophysical profile (BPP): NON invasive via US visualization of fetus combined with a reactive NST to
note fetal activity and status. Rating of 2passing score
Amniocentesis: invasiveremoval of amniotic fluidto check for fetal abnormalities and fetal lung
maturity
US: used to check well-being of fetusgrowth, number, location, and abnormalities; check position of
placenta
Kick counts: woman lies on her side, counts and records 10 distinct movements in a period of up to 2
hours. Once 10 movements counted, may stop. Or may count fetal movements x 1 hour, 3 times
weekly.
Nonstress tests (NST): use of EFM to measure FHRreactivegood well being; non-reactiveno
accelerationsnon-reassuring
Contraction stress test (CST): used to determine flow of oxygenated blood through the placenta during
a stimulated contraction. If o2 reserves are limited, --fetal hypoxia. POSITIVE testnon-reassuring
Electronic fetal monitoring

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ASSESSING PREGNANCY BY WEEKS:
WEEKS 1-4:
1. Amenorrhea
2. HCG positive 9-10 days after amenorrhea
3. Breasts changes/tenderness
4. Increased fatigue
5. Nausea/vomiting between 4-6 weeks
WEEKS 5-8:
1. Goodells sign (softening of cervix and vagina)
2. Ladins sign (softening of uterine isthmus)
3. Hegars sign (softening of lower uterine segment)
4. Chadwicks sign (purple-blue coloration of vagina, cervix, and vulva)
5. McDonalds sign
6. Cervical mucus plug forms
7. Uterus changes from pear shape to globular
8. Urinary frequency and urgency occur
WEEKS 9-12:
1. FHR detected with US
2. N/V and urinary frequency and urgency decrease
3. By week 12, uterus palpable just above symphysis pubis
WEEKS 13-17:
1. Mom gains 10-12 lbs during 2nd trimester
2. Moms HR increases by about 10 beats/minute
3. Uterine fundus palpable way between symphysis pubis and umbilicus
4. Fetal movements or quickening between 16-20 weeks
WEEKS 18-22:
1. Uterine fundus: just below umbilicus
2. FHR heard with fetoscope at 20 weeks
WEEKS 23-27:
1. Umbilicus level with abdominal skin
2. Striae present
3. Uterine fundus at umbilicus
4. Braxton Hicks start
WEEKS 28-31:
1. Gains 8-10 lbs in 3rd trimester
2. Uterine fundus way between umbilicus and xiphoid process
3. Fetal outline palpable
4. Fetus mobile and found in any position
WEEKS 32-35:
1. May experience heartburn
2. Striae more evident
3. Braxton Hicks increase in frequency and intensity
4. Mom may experience S.O.B.
WEEKS 26-40:
1. Umbilicus protrudes
2. Ankle edema
3. Urinary frequency recurs

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4. Engagement, or lightening, occurs
5. Mucus plug expelled
6. Cervical effacement and dilation begin

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FETAL DEVELOPMENT:
4 WEEKS:
1. C-shaped embryo
2. Head prominent
3. Extremities appear as buds
8 WEEKS:
1. Organ formation complete
2. Heart beating & has separate septum and valves
3. Arms and legs developed
4. Abdomen large
5. Facial features visible
6. Gestational sac visible on US
12 WEEKS:
1. Nail beds beginning to form
2. Heartbeat can be heard using Doppler
3. Kidney function beginning
4. Placenta formation complete with presence of fetal circulation
5. Gender distinguishable
16 WEEKS:
1. FH audible with stethoscope
2. Lanugo present
3. Fetus demonstrates active swallowing of amniotic fluid
4. Skeleton begins ossification
5. Intestines normal position in abdomen
20 WEEKS:
1. Mom can feel fetal movement
2. Hair begins to form eyebrows and scalp hair
3. Fetal sleep and wake patterns
4. Brown fat begins to form
5. Meconium evident in upper portion of intestines
6. Lower extremities are fully formed
7. Vernix covers skin
24 WEEKS:
1. Well-defined eyelashes and eyebrows are visible
2. Eyelids open and pupils react to light
3. Meconium may be present to the rectum
4. Hearing is developing; fetus able to respond to sudden sound
5. Lungs producing surfactant
6. Passive antibody transfer from mother begins
28 WEEKS:
1. Surfactant appears in amniotic fluid
2. Alveoli in lungs begin to mature
3. Male-testes start descend
4. Eyelids can open and close
5. Skin appears red
32 WEEKS:
1. Fetus appears more rounded as more subcutaneous fat is deposited

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2. Moro reflex active


3. Fetus may assume vertex or breech position
4. Iron stores begin to develop
5. Fingernails increase in length
6. Vernix thickens
36 WEEKS:
1. Subcutaneous fat continues to be deposited
2. Soles have a few creases
3. Lanugo begins to decrease
4. Fetus is storing additional glycogen, iron, carbs, and calcium
5. Skin on face and body begins to smooth
40 WEEKS:
1. Fetus begins to kick actively, forcefully, causing discomfort
2. Vernix fully formed
3. Soles with creases over 2/3 of surface
4. Male testes begin to fully descend into scrotal sac

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STAGES OF LABOR:
STAGE 1:
Begins at onset of true labor and has 3 phases
Lasts until complete dilation
Divided into latent, active, and transitional phases
a. Latent phase:
1. Cervical dilation 0-3cm
2. Contractions irregular, short, last 20-40 seconds; frequency every 3-30 minutes
3. Lasts 4.5-8.6 hours
4. Mom calm, laughing, talkative
b. Active phase:
1. Cervix dilation 4-7cm with rapid effacement
2. Progressive fetal descent
3. Contractions regular every 3-5 minutes, lasting 40-70 seconds
4. Mom anxious, and restless as contractions intensify; helplessness
c. Transitional phase:
1. Cervical dilation 8-10cm
2. Contractions regular, strong to very strong, every 1.5-3 minutes, lasting 60-90 seconds
3. Mom tired, irritable, restless, helpless
4. Nausea and vomiting may occur
5. Sensation of needing to have BM
6. Urge to push noted
7. Bloody show increases
STAGE 2:
Complete dilation to birth of baby
2-60 minutes
Occurs in seven cardinal movements:
1. Descent-head enters inlet
2. Flexion-fetal chin flexes downward onto chest
3. Internal rotation-fetal head rotates to fit diameter of pelvic cavity
4. Extension-of fetal head as it passes under symphysis pubis
5. Restitution-the turning of head to one side as neck untwists
6. External rotation-head turned father to one side as shoulders rotate
7. Expulsion-shoulders and rest of body delivered
STAGE 3:
Time from birth of baby until placenta completely delivered
Placenta separates and is expelledone of two surfaces presents:
1. Schultze: SHINY fetal side
2. Duncan: DULL maternal side
STAGE 4:
1-4 hours after birth in which mothers body goes through readjustment. Vital signs stable.
Lochia scant progressing to moderate rubra

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FETAL ASSESSMENT DURING LABOR AND DELIVERY:

FHR:
1. Normal: 110-160 with slight variability (change in FHR over a brief period of seconds to
minutes)
2. Acceleration: brief rise in FHR may occur with fetal stimulation (increased O2 demand) or
uterine contractions (due to brief hypoxia)indicates a healthy fetal autonomic nervous
system.
3. Decreased variability: may indicate fetal sleep or more serious fetal problems such as
sedation from drugs, fetus < 32 weeks with immature neurologic control of HR, neurological
damage, fetal anomalies of the heart, fetal dysrhythmias, or hypoxia with acidosis.
4. Absence of variability: SERIOUS WARNING SIGN
INITIATE continuous electronic monitoring (CEM) if anomaly noted:
1. HX previous stillbirth at 38 weeks or more
2. Complication of pregnancy:
a. Preeclampsia
b. Placenta previa
c. Other
3. Induction of labor
4. Preterm labor
5. Decreased movement of fetus
6. Fetal signs of distress (nonreassuring)
7. Meconium staining of amniotic fluid
8. Maternal fever
9. Placental complications (inadequate oxygenation of fetus)
IF internal probe attached:
1. Mom must be confined to bed
2. Membranes have ruptured
3. Cervix must be dilated to 2cm or >
4. Presenting fetal part must be against cervix
DECELERATIONS: decreases in FHR from baseline that occur early, late, or at variable times
during contractions
1. Early decelerations:
a. At onset or early stage of contractionsecondary to compression of head by uterine
contraction
b. Peak depression of rate as the contraction peaks
c. Return to baseline rate after contraction
d. NORMAL

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2. Late decelerations: (IMMEDILATE intervention necessary)


a. Occurs at peak or after d/t decreased flow of blood and oxygen to fetus; often
secondary to compromised placenta blood flow with maternal hypotension (d/t epidural
or oxytocin) or other condition such as maternal HTN, DM, vascular disorder, or
placental abruption
b. IMMEDILATE delivery or c-section may be indicated
3. Variable decelerations:
a. Occur at different times during contraction
b. Secondary to obstructed blood flow from fetus to placentaslows FHR
c. Deceleration is ABRUPT/SUDDEN (<30 seconds)
4. NONREASSURING: if decreased or absent variability is noted with late or variable
decelerations
5. WANDERING baseline: unsteady baseline with no variability and may indicate the following:
a. Congenital defects
b. Metabolic acidosis
c. Hypoxia
d. Baby needs delivered as quickly as possible
6. Fetal Tachycardia:
a. FHR: > 160bpm
b. Hypoxia
c. Maternal dehydration
d. Maternal infection/fever
e. Maternal intake of drugs that stimulate the heart
f. IU infection and amnionitis
g. Fetal anemia
h. Maternal hyperthyroidism
7. Fetal Bradycardia:
a. FHR < 110
b. Can be harmless or may indicate distress
c. Late fetal hypoxia
d. Maternal hypotension
e. Umbilical cord depression
f. Fetal complete heart block or congenital heart block
g. Uterine hyperstimulation
h. Uterine rupture
i. Maternal hypothermia
j. Abruption placenta
ALERT: if FHR demonstrates late decelerations, position mother on left side to improve fetal
circulation

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CAPUT SUCCEDANEUM:
Result of birth trauma results in serum and blood accumulation in tissue OVER the suture lines
of scalp
1. Noted OVER sutures lines of scalp
2. Infant asymptomatic
3. Will resolve in few days
CEPHALHEMATOMA:
Result of blood vessels broken during L&D and bleeding occurs between the bone and
periosteum
1. Usually not present at birth
2. Appear within 24-48 hours
3. Normally resolves within 2 weeks to couple months
4. Infant at risk for jaundice
HYDROCEPHALUS:
Condition involving disruption of circulation and absorption of CSF, resulting in accumulation of
CSF in ventricles of brain increased ICP
1. Noncommunicating hydrocephalus: caused by obstruction of CSF flow
2. Communicating hydrocephalus: caused by disruption of CSF absorption
S&S:
1. Rapidly increasing head circumference
2. Bulging and widening of fontanels
3. Underdeveloped neck muscles
4. Shiny thin scalp
5. Distended scalp veins
6. Irritability
7. Projectile vomiting
8. Shrill cry
9. Anorexia
10. Weak sucking
11. Nuchal rigidity
12. Arnold-Chiari malformation
TX:
1. Surgical removal or bypass of obstruction using a shunt
2. Tylenol prn pain
3. VP shunt infection or malfunctions:
a. IV vanco
b. Tylenol for temp > 101.3

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ECTOPIC PREGNANCY (EP)


Zygote implanted outside of uterus, usually in fallopian tubes
Prognosisembryo cannot develop
Maternalpossible hemorrhage if not terminated before tube ruptures
POTENTIAL CAUSES:
1. PID
2. Endometriosis
3. Prior surgeryscar tissues
4. Presence of IUD
SIGNS & SYMPTOMS:
1. Amenorrhea
2. Sudden unilateral, abdominal LQ stabbing pain
3. Vaginal bleedingpossible
4. Symptoms of pregnancy
5. N&V may increase with rupture
6. Shoulder painreferred pain from irritation of diaphragm or phrenic nerve by blood
7. Hypotension, tachycardia, and pallorsecondary to shock
TESTS:
1. Hgb & Hct decreases with bleeding
2. HCG elevatedconfirming pregnancy
3. Progesterone level elevated
4. USempty womb
5. WBC elevated
TREATMENT:
1. Methotrexateto stop cell division & enlargement of zygote to prevent fallopian tube
rupture
2. Salpingostomysurgical excision of portion or entire FT
DRUG ALERT:
1. SE of methotrexatestomatitis, suppression of RBC production, oral lesions, anemia,
thrombocytopenia, bleeding, infection
2. Birth control should be used while on methotrexate
NURSING INTERVENTIONS:
1. Assess for signs of reaction to methotrexate:
a. Dizziness
b. Seizures
c. N&V
d. GI hemorrhage
e. Anemia
f. Urinary retention
g. Renal failure
2. Educate pt
3. Postop care for surgery
4. VS
5. Urine output
6. Skin color
7. Replace fluid loss

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8. CULTURAL CONSIDERATIONS: some may consider to be death of a child and may


require zygote and tube be disposed of in a special manner
GESTATIONAL TROPHOBLASTIC DISEASE:
Villi in placenta begin to degenerate and become swollen and filled with fluidgrape-like
clusters
Embryo does not develop beyond the cell duplicationbecomes mole-like mass
Complete moleno fetus
Partial molewith genetic material derived from fertilized ovum
SIGNS & SYMPTOMS:
1. Vaginal bleeding around 16th week
2. Rapid uterine growth beyond normal expected pregnancy growth
3. Hcg levels elevated
4. Hyperemesis
5. US reveals growths but no fetus
6. Clear vaginal drainage
7. PIH prior to 20th weekedema, HTN, proteinuria
TESTS in EARLY PG:
1. HISTORY
2. Hormone levels elevatedhcg
3. Genetic testingespecially if mom/dad > 35 years old
4. Blood typing & Rh factor
5. US
NURSING INTERVENTIONS:
1. Assess for RF or S&S:
a. RAPID increase in fundal height measurements
b. Vaginal bleeding
c. Severe hyperemesis
d. HTN
e. Edema
2. CONTRACEPTION to avoid pregnancy for at least 12 months to allow monitoring for
increasing HCGcould indicate malignancy
3. Very importantfollow-up visits & testing
4. Malignancy may developCHORIOCARCINOMAspreads to lungs, vagina, pelvis, brain,
liver, intestines, kidneyscan occur weeks to years after a pregnancy
TREATMENT:
1. D&C to remove all products of conception
2. Postop care to monitor for infection or hemorrhage

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SPONTANEOUS ABORTION:
TYPES:
Abortionfetus lost before 20 weeks; less than 500g or less than 25cm
Threatened abortionvaginal bleeding before 20 weeks without dilation of cervix
Inevitable abortionvaginal bleeding & dilation of cervixno expulsion of products
Incomplete abortionexpulsion of some products before 20 weeks, but not allsepsis risk
Complete abortioncomplete expulsion of all POC (products of conception) before 20 weeks
Missed abortion: death of embryo or fetus before 20 weeks with complete retention
Septic abortionsigns of infectionchills, pain, fever or hypothermia, vaginal discharge,
hypotension possible, oliguria, RD from sepsis
Recurrent abortiontwo or more previous miscarriages
TEST RESULTS:
Urine positive for Hcgbut without progressive increase as expected
Absent or low serum Hcgabortion complete
USEmpty uterus or partial POC
CAUSES:
Chromosomal abnormalities
Infectionbacteriuria & chlamydia
Maternal anatomical defects
Endocrine disorders
Maternal systemic diseaseLupus
Exposure to fetotoxic agents
Trauma
Alcohol/drug abuse
SIGNS & SYMPTOMS:
Bleeding
Cramping
Abdominal pain
Decreased symptoms of pregnancy
Cervical changes
TREATMENTS:
Bedrest to reduce cramping & bleeding
Abstain from sexual intercourse to prevent infection
Medical induction of labor and evacuation of POCfor late abortion16 weeks or after
D&C after 12 weeks
Antibiotics as prescribed
NURSING INTERVENTIONS:
Assessment for risk factors
Monitor for signs of retained productsbleeding, signs of infection
Monitor for uterine rupture
Emotional support and/or refer to counseling

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INCOMPETENT CERVIX:
Painless dilation of cervix without uterine contractionsunable to contain fetusnormally
around 20 weeks
SIGNS & SYMPTOMS:
Vaginal drainage or bleeding
ROM
Pelvic pressure
Expulsion of fetus and POC
TESTS:
USfunneling or shortening of cervix
TREATMENTS:
Cerclage: purse string suture of cervix to close the cervix
Usually removed at 37 weeks of gestation
New cerclage needed with each pregnancy
NO new cerclage needed if left in place and c-section completed
NURSING INTERVENTIONS:
VS
Observe for vaginal drainage or bleeding or c/o pressure
Strict bedrest
Avoid dehydrationcan stimulate contractions
Educate signs of preterm labor
Home health care nurse
f/u visits

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PRETERM LABOR (PTL):
Labor between 20-36 weeks
CAUSES/RISK FACTORS:
Abnormal cervical length
Prior history of preterm birth or PTL
Infection
Non-white race
Abdominal trauma
Cervical incompetence
Cervical dilation
Bleeding after 12 weeks
Uterine abnormality
Stress
Prolonged standing
Inadequate weight gain
Clotting disorders
Pregnancy within 6-9 months of previous one
SIGNS & SYMPTOMS:
Uterine contractions: 4 in 20 minutes or 8 in one hour at 20-37 weeks
Cervical dilation of > 1 cm or effacement of 80% or greater at 20-37 weeks
Cervical shortening before term is abnormal
TESTS RESULTS:
Cervicovaginal swab fetal fibronectin (fFN) (fetal protein not normally found in vaginal tract
after 22 weeks)high predictor of PTL
Hyperglycemiauncontrolled DM
Thyrotoxicosiselevated thyroid hormones
CBC, CRP, vaginal and urine culturesto detect infections
US: short cervical length & determine fetal status
MANAGEMENT:
BedrestSide lying position to maintain uterine blood flow
IV infusion if dehydration
Tocolysisto hault labormost common magnesium sulfate or Brethine (terbutaline sulfate)
CCBnifedipine (Procardia) may be effective in arresting PTL
NURSING INTERVENTIONS:
Assess for risk factors
Monitor at-risk mothers for uterine activity and educate on S&S of PTL
PT EDUCATION:
S&S PTL
Bedrest
Side lying position
Avoid overexertion
Stop sexual intercourse
Empty bladder every 2 hoursminimum

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Drink 2-3 quarts of water daily


Avoid caffeine
Minimize stress
When to call PCP

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HELLP SYNDROME:
A form of gestation HTN with severe preeclampsia with hepatic dysfunction in addition to
coexisting hematologic conditions

HHEMOLYSISblood cell death


E-Elevated Liver
EEnzymes
L-Lowless than 100,000
P-platelets
Very serious

SIGNS & SYMPTOMS:


Rapidly deteriorating liver function and thrombocytopenia
Elevated bleeding and clotting time
Petechiae
Bleeding gums
DIC
N&V with epigastric pain
TESTS:

Elevated ALT, AST


CBCsevere anemialow Hcg & Hctsecondary to hemolysis
CMPelevated Creatine & abnormal electrolytes possible if renal damage
Abnormal PT/PTT

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DISSEMINATED INTRAVASULAR COAGULATIONDIC:


Clotting & coagulation occur at same time
Relase of thromboplastin uses up available fibrinogen & platelets profuse bleeding & IV
clotting
Often secondary condition associated with the following:
1. Abruption placenta
2. Gestational HTN
3. Missed abortion
4. Fetal death in utero
SIGNS & SYMPTOMS:
Suspected when usual measures to stimulate uterine contractions fail to stop bleeding
Oozing from IV site
Petechiae
Ecchymosis
Oliguria
Restlessness
Decreasing pulse pressure with continued bleeding
ASSESS FOR SIGNS OF PP HEMORRHAGE:
Boggy uterus
Uterine fundus above umbilicus
Excessive lochia
Fundus displacednot midline
Tachycardia
Hypotension
Change in LOC
TESTS RESULTS:
Hgb & Hctlow
Fibrinreduced
Plateletsreduced
D-dimerincreased
ABGO2 low
PT/PTTprolonged
TREATMENTS:
IV blood products and/or albumin
Pitocin may be indicated
Methergineto contract uterus(contraindicated with HTN)
Recombinant-activated factor VIIa given IV for reversal of DIC symptoms
NURSING INTERVENTIONS:
Prevention of PPH:
1. Fundal massageprevent atony
2. Oxytocin
3. Early clamping of umbilical cord & deliver of placenta may prevent uterine atony & PPH
4. Baseline labs

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5. Vitamin K or Recombinant-activated factor VIIa as ordered


Management of PPH:
1. Uterine massage
2. Maintain large-bore IV access
3. IV fluids and blood products as ordered
4. Foley catheter
5. Pulse oximetry
6. Administer oxygen
7. Elevate legs to increase venous return
8. Education
9. Monitor perineal blood lossweigh each pad
10. VS q 15 minutes until stable

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MULTIPLE GESTATION:
MONOZYGOTICidentical twinsone fertilized evum, same sex, identical in appearance
(maternal twins)
DIZYGOTIC: fraternal twinstwo separate ova (eggs) have been fertilized by two different
sperm, two chorions, two amnionsmost common
TWINShigh-risk pregnanciesLevel III facility

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