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NUR ADN 29 > Week 4 Antepartum/pregnany Risks > Flashcards

Week 4 Antepartum/pregnany Risks Flashcards

1
Q

The many factors contributing to complications of the Antepartum period

A

Heart disease
High blood pressure
Diabetes
Kidney problems
Autoimmune diseases
Sexually transmitted diseases
Cancer
Trauma - Violence

Multiples
Life style issues (smoking, drinking, drugs, poor nutrition)
Placental or uterine issues
Preterm labor
Maternal age
Blood disorders

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2
Q

What is the most common complication seen in L&D?

A

Preterm Labor

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3
Q

Define late preterm labor

A

34-36.6 weeks

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4
Q

Define preterm

A

Anything before 33.6 weeks

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5
Q

Risk Factors for preterm Labor

A

Risk factors = 25%, 75% is unknown
Infections
Diabetes
Hypertension
multiple gestation
premature ROM
fetal conditions
poor prenatal care
drug or alcohol use
smoking
age of mother

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6
Q

Preterm labor drugs

A

•magnesium sulphate (IV; will slow down contractions in mom & neuro protection/brain bleed for baby)
•Betamethasone (surfactant/mature baby lungs!)
•procardia (PO; slow preterm contractions)
•indocin (PO; slow/control contractions)
•Terbutaline (Sub-Q; elevated HR, anxiety attack, but knocks contractions out!)

Procardia, indocin, terbutaline are heart meds. They may work to slow contractions but they also relax the heart!

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7
Q

Magnesium sulfate side effects

A

MgS04- Assess for respiratory depression, n/v, depression of CNS, low urine output, ALOC

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8
Q

Terbutaline side effects

A

Terbutaline- Non FDA approved. Causes rapid heart rate in both mother and fetus, dyspnea, cardiac arrhythmias, headache, anxiety and restlessness

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9
Q

Procardia side effects

A

Procardia - flushing, dizziness, HA, nausea tachycardia, mild hypotension, glucose levels raised

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10
Q

Indocin side effects

A

Indocin - use under 32 weeks, no longer than 48-72 hours. (If used over 32 weeks -risk of baby heart valves not closing and causes heart problems)
Cause Gl bleeds, epigastric pain, nausea, increased BP. Not for asthma or aspirin sensitive patients

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11
Q

Side effects on baby when using Tocolytics

A

Baby: constriction of ductus arteriosus, impaired renal function, decreased AFI > cord compression

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12
Q

Placenta previa

A

•Implantation and growth of the placenta over the vagina opening.

•classic sign: sudden onset of painless uterine bleeding

absolute indication for c-section

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13
Q

What do we do if vaginal bleeding is present (suspecting placenta previa)

A

•no vaginal exams
•no pitocin
•get ultrasound to see where placenta location is first

  • vaginal exam could rupture placenta accidentally*
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14
Q

Placenta Abruption

A

“Premature separation of a normally implanted placenta”

•usually always a c-section (they’re bleeding internally)

•visible or sealed bleeding

•contractions will go crazy and start to freak baby heart rate out. They’re in distress

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15
Q

Etiology and risks for placenta abruption

A

Etiology: Unknown

Risk factors include:
-Maternal Hypertension* (#1)
-Cigarette smoking
-Short umbilical cord
-Abdominal trauma (MVA, assault)
-Previous history of placental abruption
-Maternal use of cocaine or amphetamines

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16
Q

Which can be prevented? Placenta previa or placenta abruption? How?

A

-Placenta previa cannot be controlled

-Placenta abruption can be prevented by Pt controlling BP, not smoking, not doing drugs (cocaine makes HR skyrocket)

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17
Q

Clinical manifestations for placenta Abruption

A

Classic Symptoms And Signs

-Vaginal bleeding
-Abdominal pain
-Uterine irritability or hypercontractile state

•Other Signs And Symptoms
-Back pain (especially with posterior placentas)
-Idiopathic preterm labor
-Fetal distress or fetal unrecognized fetal demise
-Coagulopathy or DIC
-Shock - hypovolemic or septic

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18
Q

Pregnancy induced HTN (PIH)

A

“A multi-organ disease process that develops in pregnancy & regresses in the postpartum period”

3 stages:
•1st & most common = Preeclampsia
A) mild
B) severe

•2nd = Eclampsia

•3rd = HELLP syndrome

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19
Q

What is considered Gestational HTN?

A

Gestational HTN = happens after 20 weeks

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20
Q

What puts patients into Preeclampsia?

A

•Mild: Proteinuria

•Severe: proteinuria & Critical BP (160/110)

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21
Q

What is the criteria moving from preeclampsia to eclampsia?

A

When the patient has a grand mal seizure

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22
Q

Preeclampsia signs

A

-Hypertension-sustained B/P 140/90 or
30mmHg systolic or 15 mmH diastolic from BL

-Generalized edema-legs, face and hands(fast weight gain)

-Proteinuria must be present to diagnose!

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23
Q

Tx for preeclampsia

A
  • Home Care
    -Activity restriction (Stay
    stay off feet)
    -Blood Pressure checks
    -Fetal Surveillance (non-stress tests, ultrasounds, fetal kick counts)
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24
Q

Explain severe preeclampsia

A

B/P is 160/110 or higher (only 1 part of the BP needs to be high to have a problem)*

-Proteinuria is more than 500mg/day (3+ or >)
-Elevated liver enzymes (enlarged liver-AST/ALT)
-Oliguria occurs (500ml or < in 24 hrs.)
-Other S/S are usually present: headache, epigastric pain, visual disturbances (high BP)

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25
Q

Meds for severe preeclampsia

A

-Hospitalization, seizure prevention
-Antihypertensive meds: (IV PUSH; Apresoline, Labetalol)
-Anticonvulsant medications:(IV DRIP MgS04 do mag toxicity checks!)
-May have labor induced
-Postpartum assessments should be continued for at least 48 hrs. or until s/s show recovering.

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26
Q

What is the cure for preeclampsia?

A

Delivery of the placenta

27
Q

Magnesium Sulfate

A

-Given IV infusion 4g loading dose followed by 2 g/H, until a serum level of magnesium is at 3.5-7 mEq/L

*Must watch for clinical signs of toxicity
a) Absent DTRs
b) Respirations less than 12/minute, shortness of breath, or respiratory arrest.
c) Chest pain
d) Urinary output less than 30 ml /hour.

antidote for magnesium toxicity is calcium gluconate 1 g IV over 3 minutes

28
Q

RN care for preeclampsia

A

1) Monitor for s/s of impending seizures (Hyperreflexia and/or clonus(cogwheel click foot reflex issue), increasing s/s of cerebral irritability, epigastric pain)

2) Quiet environment to lower BP (limit visitors, close blinds, lay on left side)

3) Prepare the room: pad the bedrails, bed in low position, suction equipment & O2, at bedside.

29
Q

Eclampsia manifestations

A

Clinical Manifestations: Generalized, or grand mal seizures(last 1- 1 ½ min.)
Respirations usually cease during seizure but resume afterwards.

never leave seizing patient

-Roll on side
-Watching airway
-suction
-o2
-delegation for help

30
Q

If seizure occurs …

A

-Remain with the woman & press emergency call button
- Turn woman on her side. Protect from injury
- Note time & sequence of seizure
- Insert airway following the seizure and suction mouth & nose, apply 02 prn
- Notify physician
- Administer meds as directed per physician (active= Valium, Magnesium Sulfate= prevention)

31
Q

HELLP Syndrome

A

-Hemolysis (destruction of RBC’s)
-Elevated Liver function tests
-Low Platelets

This is a life-threatening variation of preeclampsia Involves hepatic dysfunction, characterized by
Hemolysis, elevated liver enzymes, and low platelets.

A diagnosis of HELLP is associated with poor perinatal outcomes:
-placental abruption
-renal failure
-hepatic rupture
-preterm birth
-fetal and maternal death

32
Q

Hellp Syndrome manifestations/management

A

-Clinical Manifestations: Liver s/s (epigastric pain, n/v, liver tenderness and swelling)

-Laboratory data shows decreased Hct, increased Liver enzymes (Bilirubin, AST, ALT), Thrombocytopenia (platelet count < 20,000/mm), abnormal clotting studies (PT, INR)

Management: MgS04, antihypertensive drugs, induction of labor or C/S

*No liver palpation, can cause it to rupture

33
Q

Pathophysiology of preeclampsia

A

*Generalized Vasospasm from abnormal placenta. Vasospasm results in impeded blood flow to all the body organs, and elevated B/P.

34
Q

Effect of preeclampsia on Kidneys

A

Glomerular damage, proteinuria
(allows protein to leak through)

•Loss of protein causes fluid shift to interstitial space, results in edema.
-Rapid weight gain
-Decreased urinary output

35
Q

Effect of preeclampsia on the liver

A

Impaired liver function causes increased liver enzymes (AST/ALT)

•hepatic edema causes:
-epigastric pain (swelling liver)
-nausea/vomiting
-decreased blood glucose

36
Q

Effect of preeclampsia on the Neuro system

A

Arterial vasospasm causes minor cerebral hemorrhages, resulting in:
(Early signs of seizure)
-HA’s
-visual disturbances
-hyperactive DTR

-Numbness or tingling in hands or feet
-Cerebral vasospasms can lead to seizures

37
Q

Effect of preeclampsia on baby

A

Infarcts occur in placenta because of decreased blood flow

Can Lead to IUGR or fetal demise

Mom is at risk for placenta abruption

38
Q

Gestational Diabetes

A

•A Carbohydrate intolerance
develops or is first recognized in pregnancy
• Diabetes is the most common medical complication
• Usually 5 out of every 200 will develop gestational diabetes

39
Q

Explain GDM A 1&2

A

GDMA 1 is being managed with diet & exercise

GDMA 2 is being managed with meds

40
Q

Maternal Effects of GDM

A

*If mom is diabetic the Risk of PIH = 4x greater
-DKA (Diabetic Ketoacidosis)
-Polyhydramnios (increase in fluid/baby pee; caused by fetal hyperglycemia & consequent fetal diuresis) PTL, placenta abruption, cord prolapse, anomalies)
-Increased risk for difficult birth and C/S d/t Macrosomia

41
Q

Glucose challenge test

A

Done in the 27-28th UNLESS Pt has previous diabetic Hx they will do it earlier 24-28 weeks.

If they fail any aspect of the test, they’re + for GDM.

Test:
•lower than 140= normal
•greater than 190 = GDM
•140-190 need 3 hr test

42
Q

What is the maintenance goal for GDM?

A

Fasting = 70-90
1 hr after meals = less than 120

43
Q

Fetal effects of GDM

A

-Increased Risks for Spontaneous AB or Perinatal death
-Congenital malformations 2-4 x’s higher than general population (neural tube, cardiac, and limb defects)
-Preterm labor and preterm birth
-Variations in fetal size- Macrosomia (hard time controlling BG -low)

At Birth lungs & other organs weren’t made to withstand weight of bigger baby yet: Hypoglycemia, Hypocalcemia, Hyperbilirubinemia, Polycythemia, Respiratory Distress Syndrome (RDS)

44
Q

Cardiac disease in pregnancy

A

Cannot be prevented :/ significant cause of maternal mortality.

Two major categories:
•Rheumatic (scarring & stenosis of heart valves, mitral valves prolapse)

•Congenital (born with it, most common in US)

45
Q

Peripartum (during) & postpartum (after) cardiomyopathy

A

-A rare condition in healthy women develops heart disease in the last weeks of pregnancy or up to 5 months postpartum.

-Symptoms: those of CHF-dyspnea, edema, weakness, ch pain, heart palpitations.

-Additional signs: cyanosis, clubbing fingers, heart murmur, cardiac enlargement, serious dysrhythmias

-50% recover fully
-50% continue symptomatic with 20% of these women requiring cardiac transplant.

46
Q

Tx/management of cardiac in pregnancy

A

-Limit physical activity & stress
-Avoid excessive weight gain (also low sodium diet)
-Prevent anemia (give iron and folic acid)
-Prevent infection (no oral surgery, puts more stress on <3)
-Assessment for CHF (moist sounding lungs, orthopnea, dyspnea, cough, edema, tachycardia)
-Meds =Diuretics

47
Q

Intrapartum management :cardiac

A

-Minimize stresses of labor (side lying, oxygen, epidural, strict I&O)
-Fetal monitoring
-Vaginal delivery is preferred (c-section is more stress to heart) W/ vacuum extraction to minimize use of the valsalva maneuver/less pushing = less heart stress
-Cesarean Section when prolonged labor

48
Q

Postpartum management: cardiac

A

-Increased blood volume following delivery can overwhelm the heart of a woman with heart disease
-Observe strict 1&0
-Breastfeeding imposes extra demand on heart
-Daily weights
-Assist PRN w/newborn care
-Follow-up care with cardiologist

49
Q

RH Incompatibility patho

A

If mom is RH ‘-‘ mom needs Rhogam shot during 27-28th week to stop the formation of antibodies.

If baby ends up being +, mom needs another Rhogam shot to protect further pregnancies.

50
Q

What is Erythroblastosis fetalis

A

Hemolysis -break down of RBC’s in RH incompatibility leading to Hydrops Fetalis

51
Q

What is Hydrop Fetalis s/s

A

-Hypoxia, apnea, anemia, heart failure
Capillary leak syndrome
-Generalized edema, fluid accumulation in visceral cavities
-Hypoproteinemia & hepatomegaly
-Heart failure
-High fatality rate

Baby becomes so swollen d/t hemolysis = system wide organ failure

52
Q

Fetal Tx/considerations for RH incompatibility

A

-Phototherapy
-IV fluids / Exchange Transfusion
-Cardiac support fInfusion of albumin
-May also occur with:
-Amniocentesis
-Spontaneous or elective abortions
-Placental problems (abruptio placenta)

53
Q

What is Trisomy 21?

A

Down syndrome

54
Q

What is Trisomy 18?

A

Edwards syndrome

55
Q

What is Trisomy 13?

A

Patau Syndrome

56
Q

What can diagnose Trisomy 21?

A

•Maternal DNA test
•CVS
•amniocentesis

*alphafetal protein NOT definitive, lots of false +’s

57
Q

Down syndrome/Trisomy 21 s/s

A

•Decreased muscle tone at birth
• Excess skin at the nape of the neck
•Flattened nose
• Upward slanting eyes
•Small ears
•Small mouth
•Wide, short hands with short fingers
•Separated joints between the bones of the skull
•Single crease in the palm of the hand
•White spots on the colored part of the eye

58
Q

Edwards syndrome/ Trisomy 18

A

A condition that causes severe developmental delays due to an extra chromosome 18.

A first trimester screening that includes a blood test and ultrasound offers early information about a baby’s risk of having it. A second trimester blood test called a quad screen can also detect it.

Symptoms include low birth weight, small abnormally shaped head, and birth defects in organs that are often life threatening.

Edwards syndrome has no treatment and is usually fatal before birth or within the first year of life.

59
Q

Edwards Syndrome/Trisomy 18 S/S

A

•unusually small head
• back of the head is prominent ears are malformed and low-set
•mouth and jaw are small (may also have a cleft lip or cleft palate
hands are clenched into fists, and the index finger overlaps the ather fingers
• Club feet (or rocker bottom feet) and toes may be webbed or fused

60
Q

Patau Syndrome/Trisomy 13

A

-Causes severe intellectual disability and physical defects.
-Many infants with this condition don’t live past their first week of life.
-Treatment varies from child to child and focuses on relieving symptoms and managing complications.

61
Q

Patau Syndrome/Trisomy 13 S/S

A

-Cleft lip/palate
-Extra fingers/toes
-Scalp defects
-Low-set ears
-Severe mental retardation
-Seizures
-Small eyes, head, and jaw
-Brain, heart and kidney defects

-heart defects/surgeries are main concern (heart may be on right side instead of left)

62
Q

Gastroschisis

A

Baby’s belly doesn’t close up & intestines fall out at birth.

Vaginal delivery, baby is normally perfectly fine including organs and body but intestines need to be wrapped in sterile fluid and they build a ‘silo.’ Placing intestines in bag above them- Slowly over time, gravity will push intestines back in and the abdominal wall will be surgically closed.

63
Q

Anencephaly

A

Brain is severely underdeveloped or not developed at all. Baby doesn’t have closed top of head.

-Can be diagnosed 10-12 weeks
-vaginal delivery
-not compatible w/life
-normally pass during birthing process, after delivery/ up to a week later.
-* good for organ donors, all other organs are viable if baby is delivered alive & can help other sick babies*

NUR ADN 29 (5 decks)

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