hypertensive disorder characterized by HTN and proteinuria usually diagnosed after 20 weeks in a normal pregnancy \>140/90 generalized edema (esp face & hands) cure=birth vasospasm-vasoconstriction-reduced renal perfusion, endothelial damage, PVR increases Risk to newborn=IUGR, SGA (r/t placental insufficiency), reduced amniotic fluid, hypoxemia and acidosis, fetal death risk: obesity, pre-PG diabetes, 1st PG, \>35yo and teenagers, African Americans, family Hx, chronic HTN and renal disease, lupus, clotting disorders, low SEC, sickle cell trait hyperactive DTRs, hyper-reflexia +4 (normal is +2), clonus-can precede seizure H/A, drowsiness, mental confusion, visual disturbances (spots), numbness, tingling of hands/feet (nerves compressed by retained fluid), epigastric pain (bad!!--liver distension) restrict activity, lateral position for 1.5+ hours/day, monitor BP, daily wts, urinalysis, fetal assessment-reduced movement, growth, amniotic fluid decrease, low salt diet severe = systolic \> 160/110, or if multisystem involvement is present complications=seizures, stroke, abruptio placenta, DIC, thrombocytopenia, renal failure (decreased renal perusion-uric acid levels rise), liver failure meds=hydralazine (Apresoline)-vasodilator, increases CO, blood flow to the placenta, also nifedipine, labetalol; anticonvulsant = MgSO4-relaxes smooth muscle and reduces vasoconstriction (IV infusion)-may cause decreased FHR variability therapeutic MgSO4 is 4-8 mg/dL SE: CNS depression including respiratory depression, excreted by kidneys most seizures occur during labor or first 24 hours post partum, keep mother lateral oxytocin is OK no epidural if there are coagulation issues hypovolemia is caused by preeclampsia-fluid shift to interstitial space hypomagnesium (inverse relationship bt calcium intake and preeclampsia)

erthyrobastosis fetalis=agglutination and hemolysis of fetal erythrocytes resulting from incompatiability between maternal and fetal blood. affects fetus, causes no harm to mother Mother has indirect Coombs test to determine if she is sensitized (developed antibodies) as a result of previous exposure to Rh-positive blood; if negative Coombs is repeated at 28 weeks RhoGAM at 28 weeks to prevent sensitization from small leaks of fetal blood across the placenta; prevents formation of active antibodies RhoGAM again after birth if baby is Rh + direct Coombs tests baby's blood for antibody titer if mom's blood has + indirect coombs, monitor baby's HCT-transfuse for HCT \<30 causes hemolysis and hyperbilirubinemia; erythroblastosis fetalis

Loss of pregnancy before the fetus is viable (\<20 weeks or \<500g) spontaneous or induced spontaneous abortions increase with parental age most spontaneous abortions occur within the first 12 weeks: severe congenital abnormalities incompatible with life; chormosomal abnormalities=50-60%, also-infection cramping Threatened abortion-first sign in vaginal bleeding (50% end in spont abortion) Missed abortion-fetus dies but is retained-absorption/maceration of the fetus; complications=DIC, infection

abruptio placentae, intrauterine fetal death, endothelial damage (severe preeclampsia and HELLP syndrome), maternal sepsis, amniotic fluid embolism hypertension consumption of plasma factors: platelets, fibrinogen, prothrombin, factors 5 and 8 placenta is a rich source of thromboplastin PT, PTT, d-dimer will be + watch for bleeding, bruising no epidural due to possible bleeding into the spinal canal potential vascular occlusion of organs from thromboemboli formation monitor VS, watch fro shock, administer O2, blood products, heparin to prevent clot formation and increase available fibrinogen, coagulation factors, and platelets

implantation of fertilized ovum in an area outside of the uterine cavity (98% are in fallopian tubes) significant cause of maternal death from hemorrhage reduces woman's chance of subsequent pregnancies due to damage/destruction of fallopian tube At risk-scarred fallopian tubes (PID, inflm, surgery-Chlamydia/gonorrhoeae, previous ectopic, IUDs, low dose progesterone agents, multiple induced abortions, age) pain/bleeding-pain may radiate to scapula hypovolemic shock if tube is unruptured - Methotrexate (folic acid antagonist), surgical management (salpingectomy=removal of the tube)

vital signs and urine output indicate cardiovasculr status rising pulse rate and respiratory rate falling urine output, O2 sats BP falls later in hypovolemic shock pale color skin and mucous membranes cold, clammy skin weak peripheral pulses falling H&H, BP restlessness, tachy, agitation, change in LOC 16 to 18 guage catheters for blood and fluid replacement

hemorrhagic condition of late pregnancy implantation of the placenta in the lower uterus total, partial, marginal (placenta is \>3cm from internal cervical os) placentas tend to move up during course of PG Risk factors: age, multipara, previous c-section, previous suction and currettage, previous placenta previa, African, Asian, smoking, cocaine, male fetus S/S=painless uterine bleeding in last half of PG, bright red blood no manual examinations or stimulation of contractions, stool softeners, type and cross, tocolytics PRN presentation of baby is often transverse

Separation of a normally implanted placenta before the fetus is born hemorrhage may be apparent or concealed maternal complications=hemorrhage, hypovolemic shock, DIC fetal complications=asphyxia, excessive blood loss, prematurity Risk factors: cocaine use (vasoconstriction), maternal HTN, smoking, multigravida status, short umbilical cord, abd trauma, PROM, previous history, age, autoimmune coagulopathies S/S=bleeding, uterine tenderness, uterine irritability with frequent, low intensity contractions, poor relaxation between contractions, abd and low back pain, high uterine resting tone, non-reassuring fetal HR, signs of hypovolemic shock, fetal death, increased fundal height, boardlike abd (tetanic), persistent late decels, decreasing variability, absence of accels Marginal-separates at edges Partial-separates at center (may not bleed) Complete-total separation Maternal VS q15 min faster onset than placenta previa

progression of preeclampsia to generalized (grand mal) seizures. provide low-sensory environment seizure precautions=padded side rails, O2 and suction equipment seizures start with facial twitching...rigidity of the body...tonic-clonic movements...last about 1 minute breathing stops during generalized seizures--fetal brady, loss of variability, late decels followed by fetal tachy MgSO4 is drug of choice blood volume is severly reduced-risk for poor placental perfusion pulmonary edema due to fluid shift HF due to impeded forward blood flow renal blood flow is reduced-oliguria cerebral hemorrhage due to HTN and coagulation defecits Lasix for pulmonary edema O2 by face mask 8-10 L/min Digoxin kept side lying-prevent aspiration, improve placental circulation aspiration of gastric contents=leading cause of morbidity causes uterine irritability-monitor for ROM, signs of labor and abruptio placentae

hemolysis, elevated levels of liver enzymes and low platelet levels syndrome associated with preeclampsia Risk for: hemorrhage, pulmonary edema, hepatic rupture S/S-RUQ pain, N/V, severe edema ICU mgt req'd, seizure prevention, BP mgt, pulmonary edema, ascites induction NOT c-section

Test 3 Flashcards by Liz Hall

Preeclampsia

hypertensive disorder
characterized by HTN and proteinuria
usually diagnosed after 20 weeks in a normal pregnancy
>140/90
generalized edema (esp face & hands)
cure=birth
vasospasm-vasoconstriction-reduced renal perfusion, endothelial damage, PVR increases
Risk to newborn=IUGR, SGA (r/t placental insufficiency), reduced amniotic fluid, hypoxemia and acidosis, fetal death
risk: obesity, pre-PG diabetes, 1st PG, >35yo and teenagers, African Americans, family Hx, chronic HTN and renal disease, lupus, clotting disorders, low SEC, sickle cell trait
hyperactive DTRs, hyper-reflexia +4 (normal is +2), clonus-can precede seizure
H/A, drowsiness, mental confusion, visual disturbances (spots), numbness, tingling of hands/feet (nerves compressed by retained fluid), epigastric pain (bad!!–liver distension)
restrict activity, lateral position for 1.5+ hours/day, monitor BP, daily wts, urinalysis, fetal assessment-reduced movement, growth, amniotic fluid decrease, low salt diet
severe = systolic > 160/110, or if multisystem involvement is present
complications=seizures, stroke, abruptio placenta, DIC, thrombocytopenia, renal failure (decreased renal perusion-uric acid levels rise), liver failure
meds=hydralazine (Apresoline)-vasodilator, increases CO, blood flow to the placenta, also nifedipine, labetalol; anticonvulsant = MgSO4-relaxes smooth muscle and reduces vasoconstriction (IV infusion)-may cause decreased FHR variability
therapeutic MgSO4 is 4-8 mg/dL SE: CNS depression including respiratory depression, excreted by kidneys
most seizures occur during labor or first 24 hours post partum, keep mother lateral
oxytocin is OK
no epidural if there are coagulation issues
hypovolemia is caused by preeclampsia-fluid shift to interstitial space
hypomagnesium (inverse relationship bt calcium intake and preeclampsia)

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Rh Incompatability

erthyrobastosis fetalis=agglutination and hemolysis of fetal erythrocytes resulting from incompatiability between maternal and fetal blood.
affects fetus, causes no harm to mother
Mother has indirect Coombs test to determine if she is sensitized (developed antibodies) as a result of previous exposure to Rh-positive blood; if negative Coombs is repeated at 28 weeks
RhoGAM at 28 weeks to prevent sensitization from small leaks of fetal blood across the placenta; prevents formation of active antibodies
RhoGAM again after birth if baby is Rh +
direct Coombs tests baby’s blood for antibody titer
if mom’s blood has + indirect coombs, monitor baby’s HCT-transfuse for HCT <30
causes hemolysis and hyperbilirubinemia; erythroblastosis fetalis

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Abortion

Loss of pregnancy before the fetus is viable (<20 weeks or <500g)
spontaneous or induced
spontaneous abortions increase with parental age
most spontaneous abortions occur within the first 12 weeks: severe congenital abnormalities incompatible with life; chormosomal abnormalities=50-60%, also-infection
cramping
Threatened abortion-first sign in vaginal bleeding (50% end in spont abortion)
Missed abortion-fetus dies but is retained-absorption/maceration of the fetus; complications=DIC, infection

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DIC

abruptio placentae, intrauterine fetal death, endothelial damage (severe preeclampsia and HELLP syndrome), maternal sepsis, amniotic fluid embolism
hypertension
consumption of plasma factors: platelets, fibrinogen, prothrombin, factors 5 and 8
placenta is a rich source of thromboplastin
PT, PTT, d-dimer will be +
watch for bleeding, bruising
no epidural due to possible bleeding into the spinal canal
potential vascular occlusion of organs from thromboemboli formation
monitor VS, watch fro shock, administer O2, blood products, heparin to prevent clot formation and increase available fibrinogen, coagulation factors, and platelets

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Ectopic Pregnancy

implantation of fertilized ovum in an area outside of the uterine cavity (98% are in fallopian tubes)
significant cause of maternal death from hemorrhage
reduces woman’s chance of subsequent pregnancies due to damage/destruction of fallopian tube
At risk-scarred fallopian tubes (PID, inflm, surgery-Chlamydia/gonorrhoeae, previous ectopic, IUDs, low dose progesterone agents, multiple induced abortions, age)
pain/bleeding-pain may radiate to scapula
hypovolemic shock
if tube is unruptured - Methotrexate (folic acid antagonist), surgical management (salpingectomy=removal of the tube)

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Gestational Trophoblastic Disease

(Hydatidiform Mole)

trophoblasts (peripheral cells that attach to fertilized ovum to the uterine wall) develop abnormally
grow rapidly
complete=no fetus present, or partial in which some fetal tissue/membranes are present
age, Asian women, prior molar pregnancy
may become malignant=choriocarcinoma
higher levels of hCG, HEG, early preeclampsia
contraception for at least 1 year

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Hypovolemic Shock

vital signs and urine output indicate cardiovasculr status
rising pulse rate and respiratory rate
falling urine output, O2 sats
BP falls later in hypovolemic shock
pale color skin and mucous membranes
cold, clammy skin
weak peripheral pulses
falling H&H, BP
restlessness, tachy, agitation, change in LOC
16 to 18 guage catheters for blood and fluid replacement

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Placenta Previa

hemorrhagic condition of late pregnancy
implantation of the placenta in the lower uterus
total, partial, marginal (placenta is >3cm from internal cervical os)
placentas tend to move up during course of PG
Risk factors: age, multipara, previous c-section, previous suction and currettage, previous placenta previa, African, Asian, smoking, cocaine, male fetus
S/S=painless uterine bleeding in last half of PG, bright red blood
no manual examinations or stimulation of contractions, stool softeners, type and cross, tocolytics PRN
presentation of baby is often transverse

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Abruptio Placentae

Separation of a normally implanted placenta before the fetus is born
hemorrhage may be apparent or concealed
maternal complications=hemorrhage, hypovolemic shock, DIC
fetal complications=asphyxia, excessive blood loss, prematurity
Risk factors: cocaine use (vasoconstriction), maternal HTN, smoking, multigravida status, short umbilical cord, abd trauma, PROM, previous history, age, autoimmune coagulopathies
S/S=bleeding, uterine tenderness, uterine irritability with frequent, low intensity contractions, poor relaxation between contractions, abd and low back pain, high uterine resting tone, non-reassuring fetal HR, signs of hypovolemic shock, fetal death, increased fundal height, boardlike abd (tetanic), persistent late decels, decreasing variability, absence of accels
Marginal-separates at edges
Partial-separates at center (may not bleed)
Complete-total separation
Maternal VS q15 min
faster onset than placenta previa

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Hyperemesis Gravidarum

(HEG)

persistent, uncontrollable vomiting that may continue throughout the PG, not diagnosed until 2nd trimester
wt loss of >5% of pre-PG
dehydration-low grade fever
fatigue
furrowed tongue
sp. gravity urine > 10.25
hypotension, tachy
tachypnea
acidosis from starvation
elevated blood & urine ketones
alkalosis from loss of HCl in gastric fluid
hypokalemia, hyponatremia, hypochloremia
elevated liver enzymes
deficient vit K
deficient thiamine (may cause encephalapathy)
Meds: Phenergan (antiemetic), compazine (anti-emetic/anti-schizo), benadryl, Zantac/Pepcid, esomeprazole, Reglan (antiemetic), ondansetron (Zofran)
daily weights, I&O, skin turgor
hypoglycemia can cause nausea
LOC changes
causes: unknown, increased hCG, allergy to fetal proteins, thyroid dysfunction, assoc with H.pylori, psychological factors

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Eclampsia

progression of preeclampsia to generalized (grand mal) seizures.
provide low-sensory environment
seizure precautions=padded side rails, O2 and suction equipment
seizures start with facial twitching…rigidity of the body…tonic-clonic movements…last about 1 minute
breathing stops during generalized seizures–fetal brady, loss of variability, late decels followed by fetal tachy
MgSO4 is drug of choice
blood volume is severly reduced-risk for poor placental perfusion
pulmonary edema due to fluid shift
HF due to impeded forward blood flow
renal blood flow is reduced-oliguria
cerebral hemorrhage due to HTN and coagulation defecits
Lasix for pulmonary edema
O2 by face mask 8-10 L/min
Digoxin
kept side lying-prevent aspiration, improve placental circulation
aspiration of gastric contents=leading cause of morbidity
causes uterine irritability-monitor for ROM, signs of labor and abruptio placentae

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HELLP Syndrome

hemolysis, elevated levels of liver enzymes and low platelet levels
syndrome associated with preeclampsia
Risk for: hemorrhage, pulmonary edema, hepatic rupture
S/S-RUQ pain, N/V, severe edema
ICU mgt req’d, seizure prevention, BP mgt, pulmonary edema, ascites
induction NOT c-section

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Hemorrhagic Complications

abortion
ectopic pregnancy
DIC
Placenta Previa
Abruptio Placenta

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Hypertensive Disorders

of PG

Chronic-dx prior to PG, or first diagnosed in PG that persists beyond 6 wk post-partum
Gestational-develops after 20 wks, no proteinuria; BP returns to normal within 6 wks post-partum
Tx-low Na diet, methyldopa, hydralazine (apresoline)=arterial vasodilator, nifedipine (not with MgSO4), labetalol
If not taking meds-at risk for clots/stroke
Superimposed Pre-eclampsia-worse prognosis for mother & fetus, seizure activity or coma elevates disese to superimposed eclampsia; increased risk for: placental abruption, acute renal failure, IUGR, fetal demise, maternal death

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Infections that Affect PG

cytomegalovirus
rubella
varicella-zoster
herpes simplex
parvovirus
Hep B
HIV
toxoplasmosis (protozoan)
group B strep
TB

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DM in PG

blood sugar control is important-baby less likely to be hypoglycemic, jaundice, LGA (so less trauma at birth)
placental hormones cause insulin resistance so that glucose is available for the fetus
GDM-first dx during PG, may be asymptomatic, resolves after delivery, increased risk of DM later in life
DM in general-decreased insulin during 1st trimester, increased insulin 2nd trimester, increased insulin during labor (bc more energy needed), greater risk of DKA, vascular disease may progress.
complications: hydramnios, preeclampsia, ketoacidosis, vaginitis, UTI, PROM
for baby: death, congenital anomaly (cardiac), birth trauma (LGA), IUGR, respiratory distress syndrome, hypoglycemia after birth
GDM-screen 24-28 wks, 50 g glucose soln, serum glucose > 130 perform GTT test (3hours). GTT is gold standard-fasting: 1 hr > 180, 2 hr >155, 3hr>140
GDM mgt-diet, exercise, blood glucose monitoring; fetal-kick counts, NST, US for growth and/or AFI (amniotic fluid index), BPP, amniocentesis for lung maturity (lecithin-sphingomyelin ratio)
Post Delivery-mom rapidly returns to normal, newborn-monitor BS >40, assess jitteryness, prompt feeding, assess birth trauma
Newborn is used to high BS-compensates with high insulin; at birth BS goes down rapidly, but insulin remains high.

PROM

Premature ROM = prior to onset of labor (1-12 hr prior)
Pre-term ROM = rupture < 37 weeks
Prolonged ROM = membranes ruptured > 24 hr

Causes: Infections-can cause rupture (chorioamnionitis, vaginal, cervical), incompetent/short cervix, fetal abnormalities or malpresentation, overdistension of uterus (polyhydramnios, multi-fetus, big baby), previous preterm delivery with PROM, UTI, Trauma

Fetal Risks=RDS (if <37 wks), infection, sepsis, oligohydramnios (cord compression, IUGR, hypoplastic lungs, limb deformities=amniotic bands)

Near term-induce labor

Pre-term-preserve PG unless fetal distress, infection; give Betamethasone (steroids), antibiotics

Limit cerival exams, position left side lying, trendelenberg, maintain hydration, no peri-pads

Infection-fever (above 37.8), tender uterus, maternal or fetal tachy, foul oder, increased WBCs (>10,500), blood culture

Pre-Term Labor

labor > 20 wk < 37 week
contractions q10min x 30 or greater
80% effaced or 2 cm dilated

Nurse-hydrate, bed rest, lateral recumbant position, empty bladder at least q2h, administer tocolytics: MgSO4, nifedipine, monitor for infection

Tocolytics

-Beta-adrenergic agonist: Terbutaline (caution with DM, increased HR > 110, pulmonary edema)

-CCBs: Nifedipine (hold for low BP)

-Prostaglandin inhibitor: Indocin

-CNS depressant: MgSO₄

SGA/IUGR

Causes-smoking, HTN, DM
<10% on growth chart
perinatal mortality 8X that of AGA
Symmetrical (SGA)-chronic growth restriction, utero-placental insufficiency, chronic hypoxia
Asymmetrical (IUGR)-acute compromise of uteroplacental blood flow, head large for body bc brain growth spared, begins later in gestation >28 wks.
Characteristics: sparse hair, wide suture lines, scaphoid abd, loose dry skin, malnourished
Complications: perinatal asphyxia, aspiration syndrome (gasping at birth), heat loss, hypoglycemia, hypocalcemia, polycythemia (from hypoxia); later-learning difficulties.

LGA

>90% on growth chart (4000 g at birth)
causes=genetic, mulitparas, male, GDM

IDM

(infant of diabetic mother)

hypoglycemia (due to high levels of insulin)
abdomen is bigger than head
hypocalcemia, hypomagnesemia (stress of delivery)
polycythemia-greater risk for jaundice
RDS-insulin antagonizes L/S-PG production
birth trauma (Erb Duchenne paralysis, facial paralysis), CNS injuries (intracranial hemorrhage, spinal cord injuries)

Premature Infants

lanugo
tone-not flexed
no sole creases
square window with hand
scarf sign
ear-cartilage
heel to ear (can put heel to ear)
genitalia
popliteal angle is greater (can’t bend knee as much)
c-section is less stressful
prone position
Respiratory distress is biggest worry
O2 therapy (blindness if too much)-high humidity promotes gas exchange
thermoregulation
red skin bc vessels are close to surface, no fat, lose heat
5-10 sec of apnea is ok; >20 sec =apnea,cyanosis, brady
easily over-stimulated
cluster care
lack reflexes that full term infants have
NIPS scale for pain
Renal-decreased ability to excrete drugs, can’t concentrate urine (fluid retention, overhydration), glycosuria with hyperglycemia, decr buffering capacity (metabolic acidosis)
GI-poor digestion and absorption, poor gag reflex, incompetent cardiac sphincter, small stomach capacity, high conc of whey to casein ratio, deficient of Ca and P, increased BMR and O2 req’d related to effort of sucking, feeding intolerance and necrotizing enterocolitis r/t decr blood flow to intestines
need supplemental vitamins, vit E
no weight gain expected until day 5
120 cal/kg/day
34 wks or greater for oral feeding
may have patent ductus arteriosus
intracranial bleeds
anemia due to rapid growth, shorter RBC life, low iron stores, hypocalcemia
Long-term: retinopathy of prematurity, bronchopulmonary dysplasia, speech defects, neurological defects, auditory defects

Post-term Infants

>42 weeks
placenta degenerates, less O2, nutrition
loose, dry, peeling skin, long fingernails, alert face, look old and worried
meconium staining
hypoglycemia, meconium aspiration, polycythemia (r/t hypoxia), seizure activity (r/t hypoxia), cold stress (less sub Q fat),

Alcohol During PG

* Fetal Alcohol Syndrome -includes **malformations (facial), smaller head** * Fetal Alcohol Effects -cognitive difficulties-life long affecting learning, **behavior**, relationships * affects speech, hearing, language, eating, sleeping * leading cause of mental retardation * SGA/IUGR **(growth deficits)** * difficulty blocking out repetitive stimuli * impulsivity * early on=sleeplessness, crying, abn reflexes, hyperactivity, jittery, excessive mouthing behaviors, hyperactive rooting, incr non-nutritive suck

Other Drugs during PG

* Cocaine-greatest perinatal mortality, spontaneous abortion, still birth, STDs, HIV, abruptio placenta, prematurity, LBW (vasoconstriction) * Heroin/Methadone-IUGR, prematurity, stillbirths, no congenital abnormalities, withdrawal is harder from methadone, increased risk for SIDS * intrauterine asphyxia r/t withdrawal (hyperactivity-increased O2 consumption) * intrauterine infection * S/S of withdrawal=poor weight gain, N/V, tremors, seizures, SIDS * Nursing: temp reg, monitor P&R q15 until stable, small feedings, phenobarbital (anti-seizure), right side for digestion, wt q8h, swaddle with hands near mouth, cluster care