Chapter 25: Complications of Pregnancy Flashcards

1
Q

what are the 3 most common causes of hemorrhage during the first half of pregnancy?

A
  • abortion
  • ectopic pregnancy
  • gestational trophoblastic dz
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2
Q

abortion

A
  • loss of pregnancy of less than 20 weeks or a fetus less than 500 g
  • can be spontaneous or induced
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3
Q

spontaneous abortion

A
  • termination of pregnancy w/o action taken by the woman or another person
  • incidence inc with paternal age and with inc maternal age
  • most occur during first 12 weeks of pregnancy
  • most common cause: severe congential abnormalities that are incompatible with life
    • also caused by syphilis, listeriosis, toxoplasmosis, brucellosis, rubela, intraabdominal infections
  • 6 types:
    • threatened
    • inevitable
    • incomplete
    • complete
    • missed
    • recurrent
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4
Q

threatened abortion

A
  • first sign is vaginal bleeding
    • other S/S are uterine cramping, persistent backache, feelings of pelvic pressure
  • mgmt:
    • bleeding during 1st half of pregnancy is considered a threatened abortion
    • report bleeding and given detailed hx about bleeding and other symptoms
    • U/S exam is done and test hCG levels
    • should limit sexual activity until bleeding as ceased
    • count perineal pads and note quantity/color
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5
Q

what problems may result from a pregnancy that does not end in spontaneous abortion after early bleeding?

A
  • prematurity
  • SGA infant
  • abnormal presentation
  • perinatal asphyxia
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6
Q

inevitable abortion

A
  • ROM and cervix dilates
    • incomplete evacuation–>infection/sepsis
  • mgmt:
    • natural expulsion is common
      • vacuum curettage: removal of uterine contents with vacuum–>clear uterus if natural process is not effective
      • D&C: used if pregnancy is more advanced or bleeding is excessive
        • involves stretching the cervical os to scrape/suction uterus
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7
Q

incomplete abortion

A
  • some but not all of products of conception are expelled
    • S/S: active uterine bleeding, severe abdominal cramping, cervix opened
  • mgmt:
    • retained tissue prevents uterus from contracting firly, so profuse bleeding occurs
      • MUST first stabilize CV state
    • draw blood specimen for type and cross
    • insert IV for fluid replacement and drug administration
    • D&C done to remove tissue
      • D&E done if the pregnancy is more advanced w/ a larger amount of tissue
      • may need to administer oxytocin or methylergonovine to help stop bleeding
      • D&C cannot be done after 14 wks gestation b/c of danger of excessive bleeding
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8
Q

complete abortion

A
  • occurs when all products of conception are passed from uterus
    • after passage, uterine contractions and bleeding subsides and cervical os closes
    • uterus feels small
    • negative pregnancy test
  • only have to intervene if excessive bleeding or infection occur
  • woman should rest and watch for bleeding, pain, fever
    • do not have sex until follow up with HCP
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9
Q

missed abortion

A
  • occurs when fetus dies during first half of pregnancy but is retained in the uterus
    • when fetus dies, early signs of pregnancy disappear (nausea, breast tenderness, urinary frequency)
    • uterus stops growing and dec in size which reflects absorption of amniotic fluid and maceration of fetus (discoloration, softening, and tissue degeneration)
  • mgmt:
    • U/S confirms fetal death
      • no fetal heart activity can be found
      • hCG will be decreasing
    • D&C or D&E are done
      • PGs or misoprostol may be needed to induce contractions to expel the fetus
    • 2 complications:
      • infection
      • DIC
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10
Q

recurrent spontaneous abortion

A
  • 3 or more spontaneous abortions
  • primary causes: genetic or chromosomal abnormalities and anomalies of the reproductive tract (such as bicornuate uterus) or incompetent cervix
  • mgmt:
    • examine woman’s body for anomalies
    • genetic screening for woman and partner
    • cerclage: procedure to prevent early dilation of cervix may be done if abortions caused by cervical incompetence
    • RhoGAM can be given to woman with Rh negative blood
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11
Q

nursing considerations for abortion

A
  • psychological care: help them to grieve, answer questions
  • listen to the woman and observe how she behaves
  • convey acceptance of the feelings expressed
  • teach that grief may last from 6 mos to one year
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12
Q

DIC

A
  • occurs when anticoagulation is occurring, inappropriate coagulation also is occurring in the microcirculation
    • tiny clots form in tiny blood vessels–>block blood flow to organs–>ischemia
  • clotting mechanisms activated inappropriately
    • consumption of platelets, fibrinogen, prothrombin, factor V and VIII occur and then they are consumed, the blood becomes deficient in clotting factors and can’t clot
  • labs results establish dx: fibrinogen and platelets dec, PT and PTT may be prolonged
  • tx: correct the cause
    • blood replacement
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13
Q

dz that cause DIC fall into 3 major groups:

A
  • infusion of tissue thromboplastic into the circulatino, which consumes other clotting factors
    • ie placetal abruption, prolonged retention of a dead fetus
  • conductions characterized by endothelial damage:
    • ie severe preeclampsia
    • ie HELLP: hemolysis, elevated levels of liver enzymes, and low platelet levels)
  • nonspecific effects of some dz:
    • ie maternal sepsis, amniotic fluid embolism
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14
Q

nursing considerations of DIC

A
  • if have a dz that inc risk of DIC, nurse should observe for bleeding from unexpected sites
    • sites for IV insertion or lab work, nosebleeds, or spontaneous bruising
  • if coagulation studies are abnormal, an epidural block may be contraindicated
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15
Q

ectopic pregnancy

A
  • implantation of fertilized ovum in an area outside the uterine cavity
  • can lead to maternal death from hemorrhage
  • leads to scarring of fallopian tubes
  • pelvic infection (chlamydia and gonorrhea), failed tubal ligation, and hx of ectopic pregnancy in risk
    • also inc risk: IUDs, low dose progesterone contraceptives, assistive reproductive technology
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16
Q

manifestations of ectopic pregnancy

A
  • missed menstrual period
  • positive pregnancy test
  • abdominal pain
  • vaginal spotting
  • signs can depend on exactly where the implantation takes place
    • if in distal fallopian tube, can support embryo longer, so may experience normal early signs of pregnancy
    • if in proximal fallopian tube, can rupture tube in 2-3 weeks and cause sudden, severe pain in lower quadrants and abdominal hemorrhage which causes radiating pain under the scapula
      • hypovolemic shock is a concern
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17
Q

mgmt and nursing considerations for ectopic pregnancy

A
  • mgmt depends on if tube is intact or ruptured
    • goal is to preserve tube and improve chance of future fertility
    • methotrexate can be used to inhibit cell division of developing embryo
    • surgical mgmt if unruptured–>linear salpingostomy to salvage the tube
    • surgical mgmt if ruptured–>control bleeding and prevent hypovolemic shock
      • when CV is stable, salpingectomy (removal of tube) w/ ligation of bleeding vessels may be required
  • nurses should focus on early identification of hypovolemic shock, pain control, and psych support
    • administer analgesics
    • teach about SEs of methotrexate: n/v
    • edu about refraining from drinking alcohol, taking vits with folic acid, and having sexual intercourse
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18
Q

what are the 2 main causes of hemorrhage after 20 weeks of gestation?

A
  • placenta previa
  • placental abruption
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19
Q

placenta previa

A
  • implantation of uterus in the lower uterus–>placenta closer to the internal cervical os
  • 3 types depending on how much the internal cervical os is covered by the placenta: total, partial, marginal
    • marginal: placenta implanted more than 3 cm from internal cervical os
    • partial: lower border of placenta w/in 3 cm of internal cervical os but does not completely cover os
    • totaL: completely covered os
  • more common in: older women, multiparas, women who have had C?S, and women who have had suction currettage
  • inc risk if: African/Asian ethnicity, cigarette smoking and cocaine use, and male fetus
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20
Q

clinical manifestations of placenta previa

A
  • classic sign is sudden onset of painless uterine bleeding in second half of pregnancy
    • results from tearing of placental villi from uterine wall
  • dx by U/S
    • do not manually exam vagina until location and position of placenta verified
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21
Q

mgmt and nursing considerations of placenta previa

A
  • mgmt: evaluate women to determine amount of hemorrhage and monitor the fetus
    • also must consider gestational age
    • maintain stable CV status for mother
    • try to delay birth to inc birth weight and also administer corticosteroids to mother to speed maturation of fetal lungs
    • home care criteria:
      • no evidence of active bleeding, bed rest, short distance from hospital, can verbalize risks
    • no intercourse to prevent disruption of fetus
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22
Q

placental abruption

A
  • separation of normally implanted placenta before the fetus is born
  • occurs in cases of bleeding and formation of a hematoma on maternal side of the placenta
    • as the clot expands, further separation occurs
  • dangers for woman: hemorrhage, hypovolemic shock, clotting abnormalities (DIC)
  • dangers for fetus: asphyxia, excessive blood loss, prematurity
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23
Q

etiology of placental abruption

A
  • inc risk: cocaine use (due to vasoconstriction–>abruption), maternal HTN, cigarette smoking, multigravida status, short umbilical cord, abdominal trauma, premature ROM, hx of previous premature separation, maternal age
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24
Q

manifestations of placental abruption

A
  • bleeding: may be evident vaginally or concealed behind placenta
  • uterine tenderness localized at site of abruption
  • uterine irritability w/ frequent low intensity contractions and poor relaxation b/w contractions
  • abdominal or low back pain that is described as dull/aching
    • may be suffen and severe or intermittent and difficult to distinguish from labor contractions
  • high uterine resting tone identified with intrauterine pressure catheter
    • uterus becomes boardlike and tender
  • also may show: nonreassuring FHR, back pain, signs of hypovolemic shick
  • amniotic fluid may be a port wine color
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25
Q

nursing considerations and mgmt of placental abruption

A
  • mgmt:
    • if mild and under 34 weeks, bed rest, tocolytic use, administration of corticosteroids
    • if fetal compromise of excessive bleeding: immediate delivery
      • blood products for replacement and 2 large bore IV placed for fluid replacement
  • may be very frightening b/c of pain and apprent danger
    • if C/S is necessary, woman may feel pwerless and nurse should help explain what is going on
    • excessive bleeding and fetal hypoxia are major concerns and nurse should monitor for these
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26
Q

hyperemesis gravidarum (HEG)

A
  • most n/v in pregnancy should end by 13-14 weeks
  • HEG is persistent, uncontrollable vomiting that begins in first weeks of pregnancy and may continue throughout pregnancy
    • can have serious consequences (morning sickness is self limiting and has no seirous complications):
      • loss of 5% or more of pre-pregnancy weight, dehydration, acidosis from starvation, elevated levels of blood and urine ketones, alkalosis from loss of HCl in gastric fluids, and hypokalemia
      • short term hepatic dysfunction w/ elevated liver enzymes
      • deficiency of vit K–>coagulation disorders
      • deficiency of thiamine–>encephalopathy
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27
Q

etiology of HEG

A
  • cause is not known, but more common among unmarried white women, during first pregnancies, and in multifetal pregnancies
  • possible causes include allergy to fetal proteins, elevation of pregnancy hormones, maternal thyroid dysfunction, h. pylori
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28
Q

clinical manifestations of HEG

A
  • persistent n/v
  • weight loss
  • thirst
  • oliguria
  • dry mucous membranes/skin
  • poor skin turgor
  • constipation
  • lethargy
  • inc urine specific gravity (>1.025)
  • hypovolemia: hypoTN and tachycardia
  • labs: inc BUN and hct, dec Na/K/Cl
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29
Q

therapeutic mgmt of HEG

A
  • should first exclude other causes of persistent n/v
  • lab studies include H&H which may be elevated b/c of dehydration
    • electrolytes: dec Na, K, and Cl
    • elevated Cr
  • tx:
    • correct dehydration: IV fluids may be necessary
    • antiemetics: ondansetron, promethazine, H2 receptor antagonistis, PPIs, metoclopramide
    • improve nutrition:
      • vitamin B6 (pyridoxine)
      • diet
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30
Q

nursing considerations for HEG

A
  • monitor V/S and monitor I&Os
  • daily weights
  • monitor U/S for growth
  • monitor urine for ketones which can indicate fat stores being broken down to meet energy needs
  • monitor for signs of dehydration: dec fluid intake, dec urine output, inc urine SG, dry mucous membranes/skin, skin turgor
  • monitor labs: BMP, H&H
  • to reduce n/v:
    • small portions of food
    • do not eat foods with strong odors
    • carbs are more easily digested
    • take soups and liquids b/w meals
    • sit up after meals
  • maintain nutrition and fluid balance
    • eat every 2-3 hours
    • salt the food to replace chloride lost in HCl thru vomit
    • consume K and Mg rich foods
    • IV fluids and TPN if needed
  • social support:
    • allow verbalization of impact
    • explore reluctance to accept pregnancy
    • recognize lack of support available
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31
Q

gestational trophoblastic dz

A
  • AKA hydatidiform mole–>developmental anomaly of the placenta
  • occurs when trophoblasts develop abnormally, so the abnormality of the placenta develops, and if present, a fetus will have a fatal chromosomal abnormality
  • inc risk at both ends of reproductive life and inc risk among Asian women
    • inc risk if have already had one GTD
  • presents as an edematous grapelike cluster on U/S
  • may or may not be malignant
    • may develop into choriocarcinoma
32
Q

clinical manifestations of GTD

A
  • higher levels of hCG than expected for gestation
  • characteristic snowstorm U/S pattern that shows the vesicles and absence of a fetal sac or fetal hear activity
  • uterus larger than expected for gestational age
  • vaginal bleeding: varies from dark brown spotting to profuse hemorrhage
  • excessive n/v (HEG) which may be related to elevated hCG
  • early development of preeclampsia (usually not diagnosed until 24 weeks in “normal” pregnancy)
33
Q

mgmt of GTD

A
  • medical mgmt:
    • evacuation of trophoblastic tissue of the mole
    • continuous f/u of the woman to detect malignant changes of any remaining trophoblastic tissue
  • CXR, CT scan, or MRI can be used to detect metastatic dz
  • may need CBC, type and screen in case transfusion is needed
  • mole usually removed by vacuum aspiration followed by curettage
    • then give oxytocin to contract uterus, but should AVOID oxytocin before evacuation b/c tissue can become embolized if given before
  • f/u to check for malignancy
34
Q

four categories of HTN during pregnancy

A
  • gestational HTN: BP elevation after 20 weeks of pregnancy NOT accompanied by proteinuria
    • may progress to preeclampsia
    • if persists after birth, then called chronic HTN
  • preeclampsia: systolic BP of 140 or greater OR diastolic BP of 90 or greater after 20 weeks gestation accompanied by significant proteinuria
    • edema is present but non-specific for pre-eclampsia
  • eclampsia: progression of preeclampsia to generalized seizures
  • chronic HTN: elevated BP was known to exist before pregnancy or before 20 weeks
35
Q

preeclampsia: risk factors

A
  • major cause of perinatal death and IUGR
  • risk factors:
    • 1st pregnancy
    • 1st pregnancy for father of baby or man who has previously fathered one preeclamptic pregnancy
    • age >35
    • anemia
    • hx of PIH
    • chronic HTN
    • obesity
    • DM
    • multifetal pregnancy
    • African Americans
36
Q

patho of preeclampsia

A
  • result of generalized vasospasm
    • peripheral vascular resistance inc b/c some women are sensitive to Ang II and may have a dec in vasodilators
    • vasospasm dec diameter of blood vessels–>endothelial damage–>circulation to body organs is dec
  • ratio of thromboxane to prostacyclin increases
  • only cure is to deliver the baby
37
Q

patho of altered metabolism related to pre-eclampsia: thromboxane vs. prostacyclin

A
  • thromboxane:
    • from kidney and trophoblastic tissue
    • vasoconstrictor
    • platelet aggregation
    • uterine irritability
    • dec utero placental blood flow
  • prostacyclin:
    • from placenta and endothelial cells
    • vasodilator
    • inhibits platelet aggregation
    • dec uterine activity
    • inc uterine blood flow
38
Q

patho of renal perfusion w/ preeclampsia

A
  • decreased renal perfusion occurs with pre-eclampsia which causes a reduced GFR
    • BUN, creatinine, and uric acid levels rise
    • protein leaks across glomerular membrane
      • loss of protein from kdineys reduces colloid osmotic pressure and allows fluid to shift to interstitial spaces–>edema and reduction of intravascular volume which causes inc viscosity of blood and rise in hct level
        • b/c of reduced intravascular volume, Ang II and aldosterone triggers retention of water and Na which resultsin further vasospasm and HTN–>edema worsens
39
Q

patho of liver circulation as it relates to pre-eclampsia

A
  • reduced liver circulation impairs function and leads to hepatic edema and subcapsular hemorrhage–>hemorrhagic necrosis
    • shows as elevated liver enzymes and epigastric pain occurs
40
Q

patho of cerebral circulation as it relates to pre-eclampsia

A
  • vasoconstriction of cerebral vessels leads to pressure induced rupture of thin walled capillaries–>small cerebral hemorrhage
    • S/S: HA, cisual disturbances (spots before the eyes), hyperactive DTRs
41
Q

patho of pulmonary circulation as it relates to pre-eclampsia

A
  • decreased colloid oncotic pressure can lead to pulmonary capillary leak–>pulmonary edema
    • dyspnea is primary symptom
42
Q

patho of nutritional deficiency as it relates to pre-eclampsia

A
  • low protein: protein responsible for cellular growth
  • hypomagnesemia: magnesium is a vasodilator
  • calcium: inverse relationship b/w calcium intake and incidence of eclampsia
43
Q

prenatal preventive measures for pre-eclampsia

A
  • monitor weight gain, BP, and urinary protein level
44
Q

complications of pre-eclampsia

A
  • placental abruption
  • hematologic problems: DIC, thrombocytopenia
  • CVS
  • renal failure
  • hepatic failure
  • newborn complications:
    • SGA r/t utero placental insufficiency
    • reduced amniotic fluid
    • intrauterine fetal death
45
Q

clinical manifestations of pre-eclampsia

A
  • classic signs: first sign is usually HTN
    • proteinuria (identified w/ clean catch urine specimen)
  • additional signs:
    • retina: vascular constriction and narrowing of small arteries
    • hyperactive DTRs
    • labs: liver or renal dysfunction
      • coagulation may be impaired and platelets dec
    • generalized edema: may first show as rapid weight gain
  • symptoms:
    • continuous HA
    • drowsiness
    • mental confusion
    • visual disturbances: blurred/double vision
    • numbness/tingling of hands or feet
    • epigastric pain
    • dec urinary output
46
Q

diagnostic criteria for mild pre-eclampsia

A
  • BP: 140/90 on 2 occasions 6 hours apart
  • proteinuria: 300 mg in 24 hour period, or trace to 1+/2+ by urine dipstick
  • I&O
  • transient HA
  • hyperreflexia 2+ or 3+
  • no clonus
47
Q

mgmt of mild preeclampsia

A
  • IV mag sulfate
  • antiHTN therapy
  • corticosteroids to accelerate fetal lung maturity if <34 weeks
  • activity restriction: rest frequently
    • lateral position for at least 1.5 hours/day dec pressure of vena cava and inc cardiac return and circulatory volume
  • BP: BP should be checked in same arm and in the same position 2-4 times/day
  • weight: weight each morning
  • urinalysis: urine dipstick for protein using first void daily
  • fetal monitoring: kcik counts, U/S, BPP
  • diet: need ample protein and calories
    • diet w/o salt or fluid restriction
48
Q

labs to manage pre-eclampsia

A
  • magnesium levels
  • liver fcn tests
  • CBC w/ platelets
  • LDH
  • uric acid
  • serum creatinine
  • bilirubin
  • 24 hour urine for protein and creatinine clearance
    • need to deliver if unstable or HELLP occurs
49
Q

assessment for pre-eclampsia

A
  • CHHURN:
    • Cardiovascular system
    • Hematologic system
    • Hepatic system
    • Uteroplacental system
    • Renal system
    • Neurological system
50
Q

assessment of CV system for pre-eclampsia

A
  • assess V/S:
    • BP w/ client in left lateral recumbent position
    • pulse
    • respirations
    • temp q4 hrs
    • FHR: continuously
51
Q

assessment of hematologic system for pre-eclampsia

A
  • assess for bleeding:
    • petechia
    • bruising
    • epistaxis
    • gingival bleeding
    • hematuria
    • excessive vaginal bleeding
    • conjunctival hemorrhage
    • oozing from incision/puncture site
52
Q

assessment of hepatic system w/ preeclampsia

A
  • assess n/v:
    • RUQ or epigastric pain
    • portal HTN may result in epigastric pain and may precede hepatic rupture
  • monitor lab values: liver function studies–>SGOT, SGPT, AST, ALT
53
Q

assessment of uteroplacental system w/ preeclampsia

A
  • antepartum:
    • EFM
    • NST
    • BPP
    • U/S
  • intrapartum:
    • continuous fetal monitoring
54
Q

assessment of renal system w/ preeclampsia

A
  • daily weights: inquire about weight gain
  • assess edema
  • monitor I&O and urine protein
    • notify HCP if <30 mL/hour
  • monitor lab values:
    • inc BUN, Cr, and uric acid
    • renal damage as indicated by oliguria
55
Q

assessment of neurological system w/ preeclampsia

A
  • assess neuro deficits and LOC
  • HAs from CNS irritability–>severe or continuous
  • visual disturbances: blurred vision, seeing spots of flashing lights, diplopia
  • drowsy/dizziness
  • assess DTRs and clonus q1 hr
    • patellar and/or biceps reflexes
56
Q

assessment of clonus w/ preeclampsia

A
  • clonus:
    • position client w/ legs dangling over edge of examining table
    • support leg w/ one hand and sharply dorsiflex the client’s foot w/ other hand
    • maintain dorsiflexed position for a few seconds then release foot
57
Q

negative vs. positive clonus

A
  • negative clonus (normal):
    • 0 beats
    • foot remains steady: no rhythmic oscillations when foot dorsiflexed
    • when released, foot drops to flexed position w/ no oscillations
  • positive clonus (abnormal):
    • 1-4 beats
    • rhythmic oscillations when dorsiflexed
    • similar oscillations when foot drops to plantar flexed position
58
Q

diagnostic criteria for severe pre-eclampsia

A
  • BP over 160/110 2 readings, 6 hrs apart while on bed rest
  • proteinuria >5 g in 24 hr or 3+ or higher on urine dipstick
  • elevated creatinine
  • dec platelets
  • elevated liver enzymes
  • oliguria
  • severe, unrelenting HA
  • visual disturbances present
  • n/v/epigastric pain
  • hyperreflexia w/ or w/o clonus
  • pulmonary edema or cyanosis
  • thrombocytopenia
  • fetus: growth restriction and reduced amniotic fluid volume
59
Q

HELLP syndrome

A
  • hemolysis, elevated liver enzymes, and low platelets
  • may be assoc with preeclampsia and develop during third trimester
  • client at risk for:
    • hemorrhage
    • pulmonary edema
    • hepatic rupture
  • tx: mag sulfate to control seizures and hydralazine to control BP
    • fluid replacement is managed to avoid worsening reduced intravascular volume
    • if woman is near term and has a favorable cervix, induction of labor is preferred to avoid bleeding and clotting complications
60
Q

signs of impending seizures

A
  • hyperreflexia, and possible clonus
  • inc signs of cerebral irritability (HA, visual disturbance)
  • epigastric or RUQ pain, n/v
61
Q

seizure preventive measures

A
  • reduce external stimuli
  • quiet room with door closed
  • pad door to reduce noise
  • keep lights low and noise to a minimum
  • block phone calls
  • group nursing assessments to allow woman periods of undisturbed rest
  • avoid bumping bed or startling woman
  • restrict visitors
62
Q

how to prevent seizure related injury

A
  • padded side rails
  • O2 and suction equipment
  • preeclampsia box:
    • medium plastic airway
    • ambu bag w/ mask
    • ophthalmoscope
    • tourniquet
    • reflex hammer
    • syringes and needles
    • meds: mag sulfate, calcium gluconate
63
Q

how to protect a woman during a seizure

A
  • stay w/ pt and call for help
  • turn onto side during tonic phase to permit greater circulation to placenta and prevent aspiration
  • note time and sequence
    • eclampsia marked by tonic clonic seizure preceded by facial twitching
  • insert airway after seizure
  • suction mouth and nose
  • O2 by mask at 8-10 L/min
  • notify HCP
  • prepare for med administration
64
Q

administration and antidote of magnesium sulfate

A
  • administration:
    • infusion pump: piggyback into mainline IV
    • loading dose: 4-6 g then 1-3 g/hour
  • antidote: calcium gluconate–>10 mL of a 10% soln IV push over 10 min
65
Q

serum levels of magnesium sulfate

A
  • 4-8 mg/dL: therapeutic
  • 9-12 mg/dL: loss of reflexes
  • 15-17 mg/dL: respiratory and muscular paralysis
  • 30-35 mg/dL: cardiac arrest
66
Q

class and action of magnesium sulfate

A
  • class:
    • beta adrenergic agent
    • anticonvulsant
    • tocolytic
  • action:
    • CNS depressant
    • competes w/ calcium to reduce muscle excitation to slow and stop uterine activity
    • lowers seizure threshold
67
Q

maternal SEs to mag sulfate

A
  • flushing
  • HA
  • dry mouth
  • dizziness
  • lethargy
  • pulmonary edema
68
Q

fetal SEs to mag sulfate

A
  • drug crosses placenta
  • dec in FHR variability
  • hypotonia
  • lethargy
  • respiratory depression
69
Q

signs of mag toxicity

A
  • resp rate <12 breaths per min
  • maternal pulse ox reading less than 95%
  • absence of DTRs
  • sweating, flushing
  • altered sensorium: condused, lethargic, slurred speech, drowsy
  • hypoTN
  • serum magnesium value above 4-8 mg/dL
70
Q

nursing considerations with mag sulfate

A
  • monitor magnesium and calcium levels
  • monitor DTRs
  • continuous FHR monitoring
  • baseline maternal V/S, then q2-4 hours
  • assess resp status
    • RR rate: d/c if <12
    • auscultate lungs
  • monitor strict I&O
    • urinary output of 30 mL/hour
    • titrate IV and PO fluids
  • postpartum:
    • continue magnesium 24-48 hours
      • strict I&O
71
Q

respond to signs of mag sulfate toxicity

A
  • notify HCP
  • obtain mag sulfate level
  • monitor mag sulfate levels q12 hours
  • dec mag sulfate per protocol
  • monitor fetal well being
  • administer calcium gluconate as ordered
  • continue close monitoring of client
72
Q

nursing considerations with mag sulfate toxicity

A
  • monitor CNS status: changes indicate cerebral hypoxia or impending seizure
  • provide quiet, low stimulus env, limit visitors
  • provide bedrest: position client in left lateral position
  • monitor DTR and presence of clonus
  • monitor FHR and contraction pattern
  • provide adequate fluids
  • protect client from injury
    • initiate seizure precautions
    • administer seizure meds
  • prepare for delivery after stabilization of client
73
Q

super imposed pre-eclampsia

A
  • woman who has chronic HTN with pre-eclampsia superimposed
  • worse prognosis for mother and fetus
  • inc risk for:
    • placental abruption
    • acute renal failure
    • IUGR
    • fetal demise
    • maternal demise
  • closely monitor chronic HTN if proteinuria develops or when edema occurs in upper half of body
  • serum uric acid is helpful in confirming dx of superimposed PIH
74
Q

eclampsia

A
  • pre-eclampsia that has progressed to include maternal tonic clonic seizures
75
Q

support for family after an eclamptic seizure

A
  • explain what happened
  • don’t minimize seriousness
  • explain that it lasts a few min, pt is unconscious, drowsy for some time
  • acknowledge that seizure indicates worsening of condition
  • HCP will determine future mgmt
    • may include delivery